Head Injury and Coma

Question 1

What does consciousness depend on?

Answer 1

Consciousness dependent on ARAS (Brainstem to
Thalamus, determines Arousal) and Cerebral
Cortex (Determines content of Consciousness);
Impaired function causes Coma

Question 2

What is coma?

Answer 2

State of Unarousable Unresponsiveness –
Exists on a continuum, quantified by GCS; Coma is
defined as GCS ≤8

Question 3

What are disorders of consciousness?

Answer 3

Minimal Awareness with Wakefulness= Minimally Conscious, No Awareness with Wakefulness =Vegetative State; Not Awake =Comatose
o Prolonged DOC (>4 Weeks), Permanent
VS is typically >6 months if non-TBI and >12 months if TBI was causative; Permanent MCS is harder to determine

Question 4

What is delirium?

Answer 4

Confusional State of Reduced

Attention; Altered Behaviour, Cognition, Orientation, Fluctuating LOC

Question 5

Mechanisms of Coma

Answer 5

• Discrete lesion of Brainstem (ARAS) or Thalamus
• Brainstem Compression – Supratentorial Mass Lesion leading to Coning (esp Posterior Fossa)
• Diffuse Brain Dysfunction – Metabolic (35%)/Toxic (25%)
• Massive Cortical Damage – Extensive Damage to Cerebral Cortex and Cortical Connections E.g. Meningitis, Hypoxic/Ischaemic Damage

Question 6

Initial Management of Comatose Patient

Answer 6

• ABC + Blood Glucose Monitoring; Treat Seizures with Buccal Midazolam or IV Phenytoin
• Fever and Meningism – IV Antibiotics
• IV Naloxone (For Opioid OD) or Flumazenil (For
Benzodiazepines OD); Thiamine for ETOH XS
• General examination and GCS

Question 7

Fundoscopy

Answer 7

Papilloedema and Subhyaloid
Retinal Haemorrhage (Seen in SAH)

Question 8

Pupils

Answer 8

o Fixed Pupil Dilatation (Surgical Oculomotor Palsy – Affects the outer parasympathetic fibres first)
o Bilateral Midpoint Reactive Pupils – Normal Pupils; Metabolic Comas
o Bilateral Fixed Dilatation – Cardinal Sign of Brain Death; Deep Coma of any cause,
particularly Barbiturate intoxication and Hypothermia
o Bilateral Pinpoint Pupils – Pontine Lesions and Opiate Overdose

Question 9

Causes of Disconjugate Eyes (Divergent Ocular Axes)

Answer 9

Brainstem Lesions

Question 10

Causes of Conjugate Gaze Deviation

Answer 10

Away in FEF seizure, Towards in FEF damage, Away from Lesions in Brainstem and Towards Weak Limbs

Question 11

Causes of Vestibulocular Reflex

Answer 11

Lost in Brainstem Lesions and Death

Question 12

Causes of Windscreen Wiper Eyes

Answer 12

Light Coma or Extensive Cortical Damage in Deep Coma

Question 13

Ddx for Coma

Answer 13

• Psychogenic Coma
• Locked-In Syndrome – Complete paralysis except Vertical Eye Movements and Blinking (Oculomotor Sparing) due to Ventral Pontine Infarction (Bilateral Foville’s Syndrome); Functioning Cerebral Cortex, Unable to communicate except through eye movements
• Severe Paralysis – Myasthenia Gravis Crisis, Severe Guillain-Barré Syndrome

Question 14

Investigations in the Comatose Patient: Bloods and Urine

Answer 14

Blood Alcohol, Salicylates, Urine Toxicology (Benzodiazepines, Narcotics, Amphetamines)

Question 15

Investigations in the Comatose Patient: Biochemistry, Metabolic and Endocrine

Answer 15

• Biochemistry – Urea, Electrolytes, Glucose, Calcium, Liver Biochemistry
• Metabolic and Endocrine Studies – TSH, Cortisol; ABG – Acidosis, CO2 Retention

Question 16

Investigations in the Comatose Patient: Other Investigations

Answer 16

Other Investigations include those for Cerebral Malaria, Porphyria

Question 17

Investigations in the Comatose Patient: Neuro

Answer 17

• CT Brain Imaging; MRI also useful but challenging to monitor patient
• LP – Only after risk assessment e.g. Mass Lesion; Useful to look for undiagnosed Meningoencephalitis/Infections, Subarachnoid Haemorrhage
• EEG – Diagnosis of Metabolic Coma, Encephalitis and Non-Convulsive Status Epilepticus

Question 18

Management of the Comatose Patient

Answer 18

• Skin care/Pressure Ulcer Prophylaxis, Oral Hygiene, Eye Care, Fluids (NG or IV), Feeding (Fine Bore NGT or PEG), Catheterisation if needed; Rectal Evacuation
• Prognosis depends on cause of coma; Metabolic and Toxic have best prognosis when corrected; Failure to recover leads to Vegetative State or Minimally Responsive State

Question 19

Vegetative State

Answer 19

Extensive Cortical Damage; Brainstem intact so breathing normal; Appears awake with eye opening and sleep-wave cycles; No awareness of environment
Persistent VS – No recovery >12 months when Trauma is cause, >6 Months if others

Question 20

Minimally Conscious State

Answer 20

Limited Awareness E.g. Apparent, Vague pain perception; Might
have been previously VS; Functional Brain imaging and Specialist assessment to distinguish

Question 21

Types of Damage in Head Injury

Answer 21

• Poor division of damage as Concussion (Transient Coma for hours followed by apparent total recovery) from Contusion (Bruising with Prolonged Coma, Focal Signs and Lasting Damage)
o Diffuse Axonal (Shearing/Rotational Stresses on Deceleration, often Contrecoup),
o Neuronal and Axonal Damage from Direct Trauma
o Cerebral Oedema and Raised ICP, Cerebral Hypoxia and Ischaemia

Question 22

Skull Fracture

Answer 22

Skull Fracture associated with complications including Meningeal Artery Rupture causing EDH, Dural Vein tears causing SDH, CSF Rhinorrhoea and Otorrhoea and consequent Meningitis

Question 23

Mild Traumatic Brain Injury

Answer 23

Stunned or Dazed for seconds – minutes; No Post-Traumatic Amnesia; Might have headaches, but complete recovery

Question 24

Prognosis

Answer 24

Duration of Unconsciousness and Post-Traumatic Amnesia grades severity; PTA >24h = Severe
• GCS has prognostic value – GCS <5/15 at 24hrs implies serious injury, with 50% Mortality or Vegetative/Minimal Conscious State

Question 25

Recovery from Severe Coma

Answer 25

Recovery from Severe Coma takes many weeks/months; Often in first few weeks,
intermittently restless or lethargic with focal neurological deficits
o Awareness improves over time, however Amnesia takes longer to recovery
o PTA is a predictor of outcome; >1/52 implies persistent organic cognitive deficit is inevitable, although recovery of function is possible

Question 26

Late sequelae of TBI

Answer 26

include Incomplete Recovery (Cognitive Impairment, Hemiparesis, etc), Post-Traumatic Epilepsy, Post-Traumatic Syndrome (Vague Headache, Dizziness and Malaise that follow even minor head injury; Depression), BPPV, Chronic SDH, Hydrocephalus
o Chronic Traumatic Encephalopathy – ‘Punch-Drunk Syndrome’ of Cognitive Impairment, Extrapyramidal and Pyramidal signs typically seen in Boxers

Question 27

Immediate Management of Head Injury

Answer 27

• A (plus C spine recautions), B (plus O2) C (Treat shock) D (Note Pupils), E• Check Ears and Nose for CSF leaks; Blood behind TM might indicate Skull Base Fracture;
Battles Sign (Bruising over Mastoid), Racoon Eyes (Periorbital Bruising) are late and unreliable
• Access spinal injury; Access GCS accurately and repeatedly;
o GCS 15 – 13 Mild, 12 – 9 Moderate, <8 Severe
• Pupils – Size and Reactivity every few minutes until stable, especially if unconscious
• Cord/Long Tract Signs – Tone, Power, Reflexes, Sensory; Priapism and Anal Tone
• Hypotension plus Bradycardia indicates Sympathetic disruption in Cervical cord injury
• If Coma, Depressed Fracture or Suspicion of Intracranial Bleed, CT Imaging and Neurosurgeon
discussions essential

Question 28

Medical Management of Head Injury

Answer 28

• Avoid Hypotension – SBP>90mmHg; Even a single episode associated with worse outcomes in severe TBI; Avoid Hypoxia – Sats >90%
• Treat Hypovolaemia (=Cerebral Hypoperfusion), but do not overload (Avoid Cerebral Oedema); Do not use Glucose Preparations (Damaging to Cerebral Tissue)
• Hyperventilation – Temporising measure to reduce Acute Elevations of ICP (Reduces PaCO2
hence causing Cerebral Vasoconstriction) o Avoid in first 24h; Might lead to increased ischaemia worsening injury
• Mannitol – 20% solution causes Osmotic Diuresis, which reduces ICP; Avoid Systemic Hypotension when using
• Ventilation for Severe TBI might be required; ICP monitoring if possible; Early Therapeutic Hypothermia reduces ICP, and is used in specialised Neurotrauma centres
• CSF Leaks – Prophylactic Antibiotics, Vaccinations; Drugs to reduce CSF production; Possible
Surgical Repair might be required to reduce risk of Meningitis

Question 29

Red Flags in Mild Head Injury

Answer 29

• Difficult to Awaken and Excessive Sleepiness
• Convulsions or Seizures, Confusion or Strange Behaviour
• Bleeding or Watery Discharge from Nose
• Severe Headache, Incontinence
• Weakness or Loss of Sensation
• Visual Problems – Pupil discrepancy, Nystagmus, Diplopia
• Tachy or Bradycardia, Unusual Breathing Pattern