Head Injury and Coma Flashcards
What does consciousness depend on?
Consciousness dependent on ARAS (Brainstem to
Thalamus, determines Arousal) and Cerebral
Cortex (Determines content of Consciousness);
Impaired function causes Coma
What is coma?
State of Unarousable Unresponsiveness –
Exists on a continuum, quantified by GCS; Coma is
defined as GCS ≤8
What are disorders of consciousness?
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
What is delirium?
Confusional State of Reduced
Attention; Altered Behaviour, Cognition, Orientation, Fluctuating LOC
Mechanisms of Coma
- 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
Initial Management of Comatose Patient
• 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
Fundoscopy
Papilloedema and Subhyaloid Retinal Haemorrhage (Seen in SAH)
Pupils
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
Causes of Disconjugate Eyes (Divergent Ocular Axes)
Brainstem Lesions
Causes of Conjugate Gaze Deviation
Away in FEF seizure, Towards in FEF damage, Away from Lesions in Brainstem and Towards Weak Limbs
Causes of Vestibulocular Reflex
Lost in Brainstem Lesions and Death
Causes of Windscreen Wiper Eyes
Light Coma or Extensive Cortical Damage in Deep Coma
Ddx for Coma
- 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
Investigations in the Comatose Patient: Bloods and Urine
Blood Alcohol, Salicylates, Urine Toxicology (Benzodiazepines, Narcotics, Amphetamines)
Investigations in the Comatose Patient: Biochemistry, Metabolic and Endocrine
- Biochemistry – Urea, Electrolytes, Glucose, Calcium, Liver Biochemistry
- Metabolic and Endocrine Studies – TSH, Cortisol; ABG – Acidosis, CO2 Retention
Investigations in the Comatose Patient: Other Investigations
Other Investigations include those for Cerebral Malaria, Porphyria
Investigations in the Comatose Patient: Neuro
- 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
Management of the Comatose Patient
- 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
Vegetative State
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
Minimally Conscious State
Limited Awareness E.g. Apparent, Vague pain perception; Might
have been previously VS; Functional Brain imaging and Specialist assessment to distinguish
Types of Damage in Head Injury
• 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
Skull Fracture
Skull Fracture associated with complications including Meningeal Artery Rupture causing EDH, Dural Vein tears causing SDH, CSF Rhinorrhoea and Otorrhoea and consequent Meningitis
Mild Traumatic Brain Injury
Stunned or Dazed for seconds – minutes; No Post-Traumatic Amnesia; Might have headaches, but complete recovery
Prognosis
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
Recovery from Severe Coma
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
Late sequelae of TBI
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
Immediate Management of Head Injury
• 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
Medical Management of Head Injury
• 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
Red Flags in Mild Head Injury
- 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
