Cerebral Contusion

A cerebral contusion is traumatic bruising of brain parenchyma containing variable haemorrhage, oedema and tissue necrosis.

Common locations are:

Inferior frontal lobes
Anterior temporal lobes

because the brain impacts irregular surfaces of the skull base.

Contusions can occur at:

Coup site

Directly beneath impact.

Contrecoup site

Opposite the impact as the brain moves within the skull.

A major clinical characteristic is haemorrhagic progression, often called contusion blossoming.

A relatively small lesion on initial CT can enlarge significantly during the first hours after trauma.

Noncontrast CT: first line investigation.

The important features are:

Contusion volume
Surrounding oedema
Midline shift
Basal cistern compression
Associated subdural or subarachnoid blood

Repeat CT is warranted with:

Falling GCS
New focal deficit
New pupil abnormality
Significant initial contusion at risk of expansion

MRI can demonstrate nonhaemorrhagic components and associated axonal injury but is not required for immediate surgical decisions.

Small contusions without neurological deterioration or significant mass effect can be managed with:

Close neurological observation
ICP focused treatment when severe
Serial CT according to clinical course
Early seizure prophylaxis in significant cortical injury

Correct:

Hypoxia
Hypotension
Hypercapnia
Fever
Coagulopathy

Reverse clinically significant anticoagulation promptly when haemorrhage is expanding or surgery may be required.

Surgery

Operate when a parenchymal lesion produces:

Progressive neurological deterioration
Refractory intracranial hypertension
Significant CT mass effect

Specific operative thresholds include:

GCS 6 to 8 plus frontal or temporal contusion greater than approximately 20 cm³

with either:

Midline shift at least 5 mm

Basal cistern compression

Also operate for:

Any traumatic parenchymal mass lesion greater than approximately 50 cm³, particularly when producing significant mass effect.

Procedure

Perform craniotomy and evacuate the haemorrhagic contused tissue causing mass effect while preserving viable cortex where possible.

A large decompressive craniectomy can be added when severe swelling prevents safe bone flap replacement.

Avoid unnecessarily aggressive removal of nonexpansile contused brain simply because it appears abnormal on CT.

Refractory swelling

Persistent intracranial hypertension after focal evacuation requires:

Repeat imaging
Hyperosmolar therapy
CSF drainage where appropriate
CPP optimisation
Decompressive surgery in selected patients

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Head Injury

Also known as: Traumatic brain injury, TBI, Concussion

Injury to the brain or skull from external mechanical force, ranging from mild concussion to severe TBI with structural brain damage.

Primary injury (at the moment of impact; irreversible) is distinguished from secondary injury (subsequent hypoxia, hypotension, raised ICP, seizures; potentially preventable and treatable, and the focus of emergency management).

Classified by GCS at presentation (best post-resuscitation score):

Mild: GCS 13-15
Moderate: GCS 9-12
Severe: GCS ≤8 ; requires airway protection/intubation

Pathology types: extradural hematoma (arterial, typically middle meningeal artery, biconvex on CT), subdural hematoma (venous, bridging veins, crescentic on CT), traumatic subarachnoid hemorrhage, intracerebral hemorrhage/contusion, diffuse axonal injury (shearing forces, often normal initial CT despite a severe clinical picture), skull fracture (linear, depressed, basal).

GCS assessment (Eye 1-4, Verbal 1-5, Motor 1-6) ; serial monitoring is more important than a single value
Extradural hematoma classic pattern: initial loss of consciousness → "lucid interval" → rapid deterioration as the hematoma expands; do not be falsely reassured by a lucid interval
Signs of raised ICP: headache, vomiting, deteriorating GCS, Cushing's triad (hypertension, bradycardia, irregular breathing ; a late, pre-terminal sign), unilateral then bilateral pupil dilation (uncal herniation)
Basal skull fracture signs: Battle's sign (mastoid bruising, delayed), raccoon eyes (periorbital bruising), CSF rhinorrhea/otorrhea, hemotympanum
Focal neurological deficit: localizes the lesion
Seizures: early (within 24h, common, doesn't necessarily predict epilepsy) vs. late (>7 days, higher epilepsy risk)

Red flags requiring urgent CT: GCS <15 at 2 hours post-injury, suspected open/depressed skull fracture, signs of basal skull fracture, post-traumatic seizure, focal neurological deficit, more than one episode of vomiting, age ≥65, dangerous mechanism, retrograde amnesia >30 min, anticoagulant use, GCS <13 at initial assessment.

CT head (non-contrast) : investigation of choice: identifies hemorrhage, mass effect, midline shift, skull fracture; do not delay for mild-moderate injury meeting the criteria above
C-spine imaging: high association with head injury (assess per NEXUS/Canadian C-spine rules), CT C-spine if high-risk mechanism/symptoms
GCS and pupillary response: serial reassessment is the primary monitoring tool, not a single CT
Bloods: FBC, coagulation profile (critical if on anticoagulants/antiplatelets : reverse urgently if intracranial bleed present), glucose (exclude hypoglycemia as cause of reduced GCS), alcohol level if relevant : do not attribute reduced GCS to intoxication without excluding structural injury
MRI: superior for diffuse axonal injury, not first-line acutely

Differentials for altered consciousness post-trauma: hypoglycemia, alcohol/drug intoxication, post-ictal state, hypoxia, hypotension/shock, pre-existing intracranial pathology.

Primary survey first : hypoxia and hypotension are the two most important preventable secondary insults; treat these before focusing on the head injury itself.

Airway protection: intubate if GCS ≤8, maintain C-spine precautions
Maintain cerebral perfusion: target SBP ≥110-120mmHg (a single hypotensive episode significantly worsens outcome), normocapnia, normothermia, normoglycemia

Signs of raised ICP/herniation (unilateral dilated pupil, deteriorating GCS, Cushing's triad):

Head elevation 30 degrees, midline neck position (avoid venous obstruction)
Hyperosmolar therapy: mannitol 0.5-1g/kg IV bolus, or hypertonic saline (3%) 150-250mL bolus : temporizing while arranging definitive management
Brief hyperventilation (target PaCO2 ~30-35mmHg) as a temporizing bridge to surgery only, not sustained therapy
Urgent neurosurgical referral for evacuation (extradural/subdural with mass effect, depressed skull fracture)

Other measures:

Seizure management: benzodiazepine for active seizure; consider prophylactic levetiracetam in severe TBI (reduces early post-traumatic seizures, no proven effect on late epilepsy)
Reverse anticoagulation urgently if intracranial hemorrhage (vitamin K + prothrombin complex concentrate for warfarin, specific reversal agents for DOACs where available)
Mild TBI/concussion: observation period, safety-netting advice (return if worsening headache, vomiting, drowsiness, confusion), avoid return to contact sport until symptom-free with graduated return-to-play
ICU admission for severe TBI (GCS ≤8) : ICP monitoring, ventilation, neuroprotective management (target ICP <20-22mmHg, cerebral perfusion pressure 60-70mmHg)

Disposition: discharge with head injury advice if low-risk, normal CT, and responsible adult supervision available; admit for observation if risk factors present even with a normal CT; neurosurgical transfer for any surgical lesion or GCS ≤8.

Cerebral Contusion

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management