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.

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

Cauda Equina Syndrome

Also known as: CES

Cauda equina syndrome is compression of the lumbosacral nerve roots below the conus medullaris producing variable dysfunction of:

Bladder
Bowel
Saddle sensation
Sexual function
Lower limb motor and sensory pathways

The commonest cause is a large central lumbar disc prolapse, but other causes include:

Lumbar spinal stenosis
Tumour
Epidural abscess
Epidural haematoma
Trauma
Postoperative haematoma
Severe spondylolisthesis
Inflammatory disease

CES is a spinal surgical emergency because prolonged compression can produce permanent bladder, bowel, sexual and motor disability.

Practical clinical classification

CES suspected

Red flag symptoms without objective major sphincter dysfunction.

Incomplete CES, CESI

Neurogenic urinary dysfunction is present but voluntary bladder emptying remains possible.

Features can include:

Altered urinary sensation
Loss of desire to void
Poor stream
Need to strain
Saddle sensory change

CES with retention, CESR

The patient has painless urinary retention with overflow or loss of effective voluntary bladder control.

CESR generally has a poorer neurological recovery than CESI.

Do not wait for complete urinary retention before obtaining emergency imaging.

High value red flags are:

Bilateral sciatica
New saddle or perineal numbness
New urinary difficulty
Reduced awareness of bladder filling
Poor urinary stream
Urinary retention
New faecal incontinence
Reduced anal tone
New sexual dysfunction
Bilateral or progressive leg weakness

A patient can have CES without every classical feature.

Examination

Document:

Hip, knee and ankle motor power
Great toe extension
Dermatomal sensation
Saddle sensation
Lower limb reflexes
Anal tone
Voluntary anal contraction where appropriate
Bladder function

Do not overrely on digital rectal examination. Normal anal tone does not reliably exclude CES.

Bladder scan

Measure post void residual where available.

A PVR greater than approximately 200 mL increases concern for neurogenic bladder dysfunction.

However, a low PVR does not safely exclude incomplete CES when saddle symptoms or neurological deficits are present.

Emergency MRI lumbar spine: diagnostic investigation of choice.

When clinical suspicion is moderate or high, obtain MRI urgently rather than observing for progression.

Service standards support MRI in the next available emergency slot, aiming within approximately 4 hours of request for suspected acute CES.

If MRI is contraindicated or impossible:

CT myelography can demonstrate compressive pathology

but it is invasive and requires specialist availability.

Do not delay emergency spinal referral while waiting for routine outpatient imaging.

Immediate management

Keep the patient:

Nil orally if urgent surgery is likely
Adequately analgesed
Under serial neurological observation

If urinary retention exists:

Insert a urinary catheter and document the drained volume.

Catheterisation treats retention but does not treat the nerve compression.

Disc related CES

Once MRI confirms a surgically remediable disc prolapse producing cauda equina compression, perform urgent decompression as soon as safely possible.

Operations include:

Lumbar laminotomy or laminectomy
Discectomy
Adequate decompression of affected roots

Do not delay an available decompression simply to reach an arbitrary 24 or 48 hour threshold.

Outcome generally worsens as established severe sphincter dysfunction persists for longer. Surgical care should therefore proceed without avoidable delay.

CESI

Incomplete CES has meaningful potential for preservation or recovery of bladder function.

Treat urgently before progression to painless retention.

CESR

Established urinary retention is a more severe injury but remains an indication for urgent decompression.

Do not deny surgery because the patient has already developed retention.

Recovery can continue for months after decompression.

Epidural abscess

If CES is caused by infection:

Obtain blood cultures
Start appropriate IV antibiotics
Perform urgent surgical drainage when there is neurological deficit or significant compression

A practical empirical regimen is:

Vancomycin IV plus ceftriaxone 2 g IV every 12 to 24 hours

with broader Gram negative coverage when risk factors warrant.

Epidural haematoma

Urgently reverse anticoagulation and decompress when the haematoma produces significant neurological dysfunction.

Malignant CES

Treat according to spinal oncological compression principles with:

Urgent MRI
Dexamethasone when appropriate
Surgical decompression and stabilisation in suitable patients

Urgent radiotherapy where surgery is inappropriate

Postoperative care

Document postoperative:

Saddle sensation
Motor function
Bladder emptying
Bowel function

Patients with persistent neurogenic bladder need:

Urology input
Intermittent catheterisation where appropriate
Urodynamic assessment later
Renal protection

Bowel dysfunction can require a structured bowel programme.

Sexual dysfunction should be addressed rather than omitted from long term follow up.

Prognosis

Motor recovery can occur relatively early.

Bladder, bowel and sexual recovery may continue for many months.

Poorer prognostic features include:

Complete painless urinary retention before decompression
Severe saddle anaesthesia
Longstanding dense neurological deficit
Severe bilateral weakness

Even severe deficits do not prove that recovery is impossible, so long term rehabilitation and bladder management remain essential.

Head Injury

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management