HEAD INJURY

Trauma

Unit S5 - June 20 2024

Introduction
Athul
•Introduction
•Head injury accounts for 3–4% of emergency department attendances, with around 1500 cases per 100 000
population per year.
•INTRACRANIAL PRESSURE
•Normal cerebral blood flow (CBF) is about 55 mL/min for every 100 g of brain tissue. Ischaemia results when
this rate drops below 20 mL/min.
•Flow depends on cerebral perfusion pressure (CPP), which is the diference between the mean arterial pressure
(MAP) and the intracranial pressure (ICP): CPP (75–105 mmHg) = MAP (90–110 mmHg) – ICP (5–15 mmHg)
•The Monro–Kellie doctrine and herniation syndromes Alexander Monro observed in 1783 that the cranium is a
rigid box’ containing a ‘nearly incompressible brain’. Any expansion in the contents, especially haematoma and
brain swelling, may be initially accommodated by exclusion of fuid components, venous blood and cerebrospinal
fuid (CSF).
•Uncontrolled increases in ICP result in
cerebral herniation
•Cerebellar tonsillar herniation leads to
compression of vasomotor centre and
respiratory centre producing Cushing's
triad: hypertension,bradycardia,
respiratory abnormalities
•CLASSIFICATION OF HEAD INJURY
•The severity of head injury is classifed
according to the postresuscitation
Glasgow Coma Scale (GCS) score as it
is the GCS score – and in particular the
motor score – that is the best predictor of
neurological outcome.
Minor and mild head injury
Benet

•A ‘lucid interval’ that may precede delayed

deterioration due to an expanding intracranial
haematoma
•Decisions on imaging and discharge are best
made guided by published criteria
•Patients who do not meet all the discharge
criteria will need admission for a further period
of observation and/or brain imaging.
Non accidental injury
•Head injury in children and vulnerable adults may be due to abuse
•Signifcant fndings include :-
• Delayed presentation
•Injuries of disparate age
•Retinal haemorrhages
•Bilateral chronic subdural haematomas
•Multiple skull fractures
•Neurological injury without external signs of trauma.
 Concussion, second impact syndrome
and postconcussive syndrome
•Concussion is defned as the alteration of consciousness as a result of closed head injury
•It is generally used to describe mild head injury without imaging abnormalities
•Amnesia, confusion, headaches and somnolence are typical features of concussion
•Second impact syndrome following an apparently trivial repeat injury comprises malignant
brain swelling that can quickly progress to coma and death
•It occurs rarely
•Post-concussive syndrome is a loosely defined constellation of symptoms persisting for a
prolonged period after injury.
•report somatic features such as headache, dizziness and disorders of hearing and vision
 Moderate and severe traumatic brain injury
Bhagya
•Resuscitation and evaluation
•Resuscitation is performed according to advanced trauma life support (ATLS) guidelines beginning with management of airway with cervical spine control and
proceeding to assess and manage breathing and circulation.
•History
•Obtained from witness and paramedics
•High energy mechanism of injury require careful clinical and radiological exclusion associated multisystem and spinal injury.
•In RTA, extraction time and evidence of hypoxia is important
•Neurological progression
•Check for any loss of consciousness at time of injury and duration.
•GCS score and pupil response should be recorded
•Important to assess extent of amnesia
•Past medical history
•Medical background including allergies and medication
•History of anti platelet and anti coagulant agents should be recorded
Examination- primary survey
•Ensure adequate oxygenation and circulation
•Blood glucose level should be measured to
avoid hypoglycaemia
•Check pupil size and response
•Record it in millimetres and reactivity
documented as present, sluggish or absent.
•Neurological deficits
•An assessment to exclude neurological deficits
should be done.
Secondary survey
Biya
•Head
• Inspection and palpation of the scalp-evidence of hematoma or lacerations
• Face-evidence of fractures(maxilla, orbital rim etc.)
• CLINICAL EVIDENCE OF SKULL BASE FRACTURES
➢ Battle’s sign- Bruising over the mastoid process
➢ Raccoon or panda eyes- Bilateral periorbital bruising
➢ CSF Rhinorrhoea and otorrhoea
➢ Hemotympanum(Blood in tympanic cavity)or overt bleeding from ear(TM rupture)
• Complete examination of the cranial nerves -associated nerve damage- eg:- facial or vestibulocochlear nerve damage
• Signs of Midbrain or brainstem dysfunction-
• GAZE PARESIS(inability of the eye to look across beyond the midline)
• DYSCONJUGATE GAZE(inability of the Figure Eyes to work together) or roving eye movements.
• Inspect the conjunctiva and cornea of the eyes, and the retina using an ophthalmoscope, looking for hyphaema (blood in the anterior chamber of the eye), papilloedema or retina
detachment
• Re evaluation of GCS score and pupil status
Neck and spine
• Cervical spine injury must be presumed in the context of head injury until actively excluded.
• Spinal Pathology – Peripheral nerve examination,+Documentation of limb tone, power,
Reflexes and sensation
• Log Rolling Of Patient- Thoracic or Lumbar deformity
• Per rectum examination- Anal tone,sensation in awake patient, anal wink-Sphincter
contraction in response to a pinprick stimulus
• Priapism- prolonged, rigid erection of penis in the absence of appropriate stimulation.
 Surgical pathologies
Head injury - SKULL VAULT FRACTURES
• Closed linear fractures are managed conservatively- no surgical intervention
• Open or Comminuted fractures -Debridement and prophylactic antibiotic therapy
• Depressed skull fractures- high incidence of infection, neurological defcit and late-onset epilepsy-
need exploration and elevation
• Fractures that involve the air sinuses should generally be managed as open fractures, using broad-
spectrum antibiotics with or without exploration.
SKULL BASE FRACTURES
• Signs
• CSF leak will generally resolve spontaneously but persistent leak can result in meningitis so
repair may be required
Head injuries - contd.
Extradural hematoma , Chithu

•An extradural hematoma is a collection of blood between the inner table of the skull and the dura
mater .
•Usually results from rupture of an artery, vein or venous sinus, in association with a skull fracture,
the most common being middle meningeal artery due to fracture to the thin squamous temporal
bone.
•Clinical features - patients present with Lucid interval from the time of injury with headache ,
without any neurological deficit .
•Until they suddenly deteriorate due to enlarging hematoma and impeding brain herniation
•There is contralateral hemiparesis, a reduced conscious level and ipsilateral pupillarydilatation, the
cardinal signs of brain compression and herniation.
Extradural hematoma
Contd.

•On CT, extradural haematomas

appear as a lentiform (lens-shaped or
biconvex) hyperdense lesion between
the skull and the brain
•A mass efect may be evident, with
compression of the surrounding brain
and midline shift. Skull fracture also
usually evident.
•Require immediate transfer to a
neurosurgical unit for decision on
evacuation.

•A large left Extradural hematoma

Acute subdural hematoma
•two broadly distinct contexts- First, high-energy injurymechanisms result in the
rupture of cortical surface vessels with signifcant primary brain injury.
•results in an expanding haematoma with rapid deterioration and development of
signs of raised ICP reminiscent of extradural haematoma, without the lucid
interval, require prompt evacuation.
•In a second group of patients, older and often anticoagulated, a lower energy
injury leads to venous bleeding around the brain.
•present much later with a further ‘acute-onchronic’ subdural haematoma.
•Management- large : symptomatic subdurals are evacuated
Small :smaller hemorrhages must be followed as they tend to become chronic
and may enlarge over time . Right sided acute
•On ct scans :hematoma is crescent shaped on head CT and will cross suture subdural hematoma
lines
Chronic subdural hematoma
Dany
•Common cause of acute-neurological deterioration in older adults
Cerebral atrophy
stretching of the cortical–dural bridging veins
rupture
haematoma can expand by osmosis
Raised ICP or focal deficits.
•Causes -Head injury ,Antiplatelet or anticoagulant medication in trivial impacts
•Presentation:
•-Exclude coexisting electrolyte disturbance and infection may cause clinical impairment. -
•Imaging -> difuse hypodensity overlying the brain surface.
•Recent bleeding -> isodense or hyperdense, and mixed density [acute-on-chronic subdural haematoma]
•Management -administration of vitamin K , transfusion of recombinant clotting factor(if urgency) ,corticosteroid administration(small
bleed) ,BURR HOLE(major bleeding)
Traumatic subarachnoid
haemorrhage
Cerebral contusions
•Cause: Trauma •Predominant sites: regions where the brain is in
•Presentation : CT angiography contact with the irregularly ridged inside of the skull
•Traumatic subarachnoid (inferior frontal lobes and temporal poles)
haemorrhage • *Coup contre-coup* ’ contusions refer to brain
injury both at the site of impact and distant to this.
•Contusions appear heterogeneous on CT(composition
Collapse of injured brain matter interspersed with acute blood)
•Delayed evacuation done to reduce a mass effect.
Diffuse axonal injury

•Cause : extreme acceleration of skull contents primary brain injury comatose

•pathological diagnosis made at postmortem
•CT - haemorrhagic foci in the corpus callosum and dorsolateral rostral
brainstem
•MRI - more sensitive and to evaluate for diffuse axonal injury in patients who
fail to improve neurologically.
Arterial dissection
•Cause: Trauma
•*Common:
•Carotid artery dissection

Due to skull base fractures

headache, neck pain and focal ischaemic defcits

due to occlusion by mural haematoma, thrombus and Intracranial dissection

thromboembolism.
Vertebral artery dissection

Subarachnoid bleeding
Medical management
Darshana
•Medical management strategies aim to minimise secondary brain injury through avoidance of hypoxia and
hypotension and control of ICP .
•Control of ICP
•Intubation and ventilation are required early in the management of severe brain injury for airway control.
•A bolus of mannitol or hypertonic saline may be administered to temporise ICP, for example while scanning and
transferring the patient.
•Management of the intubated patient, is guided by ICP monitoring using a bolt ICP monitor or else an external
ventricular drain inserted into the lateral ventricle, which can also contribute to ICP control by permitting CSF
drainage.
•A sustained elevated ICP exceeding 20–25 mmHg is associated with a poor outcome, and maintenance of a CPP of at
least 60 mmHg is important in preventing secondary injury.
•ICP can be controlled by simple measures, including raising the head of the bed and loosening the collar to improve
venous drainage.
•Where these measures fail, neurointensivists may seek to control brain swelling using mannitol or hypertonic saline infusions.
•Cerebral salt wasting, a poorly understood form of excretory dysregulation in association with brain insult, leads to volume
depletion and hyponatraemia.
•SIADH leads to water retention and hyponatraemia in the context of pituitary damage.
•ADH secretion may be compromised in the context of trauma, producing diabetes insipidus, resulting in hypernatraemia
•Seizures
•Seizures may occur early or late.The cumulative probability is between 2% (mild TBI) and 60% (severe TBI with exacerbating
features).
•Antiepileptics, typically phenytoin, are administered prophylactically to patients at high risk of seizures.
•Nutrition
•Enteral nutrition is preferred to intravenous parenteral nutrition.Prokinetics (e.g. metoclopramide, erythromycin) can be
administered to promote absorption.
•Outcomes and sequelae
•Rehabilitation represents a complex and prolonged multidisciplinary challenge.
•The Glasgow Outcome Scale score is used to quantify the degree of recovery achieved after head injury.
 Surgical management
Craniotomy: Bone flap is temporarily removed from the skull to access the brain. To
remove hematomas, hemorrhages etc.
Craniectomy: Excision into cranium to cut away a bone flap. Decompressive
cranirctomy can help to control ICP.
Cranioplasty: Surgical repair of a defect or deficit of skull.
Elevation of depressed fractures of skull.
Lumbar puncture to drain the CSF to control ICP.
Suturing of severe scalp lacerations.