Transient LOC and Persistent LOC (Coma) Flashcards
Causes LOC
Toxic/Metabolic
- Hypoxia, hypercapnia, sepsis, hypotension
- Drug intoxication, poisoning (CO)
- Renal or liver failure
- Hypoglycaemia, DKA
Neurological
- Trauma
- Epilespy (seizures)
- Infection (meningitis, encephalitis)
- Tropical (malaria, typhoid, rabies)
- Tumour
- Vascular (stroke, SAH, SDH)
What would you ask someone about when trying to determine a cause of transient LOC?
Individual account
- History preceding events - Context/timing, posture
- Event itself
- What happened afterwards
Witness account
- What happened before
- What happened during
- What happened after
What are the main groupings of precipitants to syncopal events?
- Reflex - Neurocardiogenic - micturition, cough
- Orthostatic - dehydration, medication related, endocrine, autonomic nervous system
- Cardiogenic - arrhythmias, AS
Why can proping someone up who is having a syncopal event cause the event to prolong?
Decreased cerebral perfusion which is corrected by lying flat. If propped up, this prolongs the cerebral hypoperfusion
What are causes of a provoked seizure?
- Alcohol withdrawal
- Drug withdrawal
- Within a few days of head injury
- Within 24 hours of stroke
- Within 24 hrs neurosurgery
- Severe electrolyte disturbances
- Eclampsia
What are causes of sudden LOC?
- Epilepsy
- Syncope
- Non-epileptic attacks (pseudoseizures)
- Panic attacks and hyperventilation
- Hypoglycaemia
- Drop attacks
- Hydrocephalic attacks
- Basilar migraine
- Severe vertigo
- Cataplexy, narcolepsy, sleep paralysis
How woud you distinguish syncope from a seizure?
Syncope often presents with LOC + sympatoms and signs of sympathetic overdrive e.g. gradual pallor, cold sweat, feeling nauseous, tachycardia etc. Those who experience syncope (for whatever cause) can be incontinent, and recover quite quickly
Seizures lack features of sympathetic overdrive, and can be incontinent, can frequently suffer some sort of injury, and recovery is slow.
What are causes of syncope?
- Neurocardiogenic syncope (vasovagal)
- Cardiac syncope (Stokes–Adams attacks)
- Situation syncope - Micturition syncope, Cough syncope
- Postural hypotension
- Carotid sinus syncope
What is vasovagal syncope?
Syncope due to sudden reflex bradycardia with vasodilatation of both peripheral and splanchnic vasculature (neurocardiogenic or vasovagal syncope).
What are precipitants vasovagal syncope?
- Emotion
- Prolonged standing
- Pain
- Fear
- Venesetion
What are prodromal features of a vasovagal syncope?
Brief episode of:
- Dizziness
- Light-headedness
- Pallor
- Nausea
- Sweating
- Feeling of heat
- Visual grey-out
What are features of the blackout seen in vasovagal syncope?
-
Usually lie still
- Can have jerking/twitching movments
- Pallor
- Can be incontinent
- No tongue biting
How long do vasovagal attacks last?
Approximately 2 minutes
Why can brief clonic jerks occur in vasovagal syncope?
Cerebral hypoperfusion
What are features following a vasovagal attack?
Tiredness - differentiated from post-ictal by lack of drowsiness/confusion
What are cardiogenic causes of syncope?
- Cardiac arrhythmias
- Aortic stenosis
- Hypertrophic cardiomyopathy
What are Stoke-Adams attacks?
Transient arrhythmias causing decreased CO and LOC. Patient falls to the ground with no warning, is pale, with a slow or absent pulse. Recovery occurs in seconds - patient fluses, pulse speeds up, and consciousness is regained
Anoxic clonic jerks can occur
What is micturation syncope?
Syncope that occurs during or after urination - usually in men at night
What is cough syncope?
Occurs when venous return to the heart is obstructed by bouts of severe coughing
What is effort syncope?
Syncope brought on by exercise - often cardiac cause underlying e.g. aortic stenosis, HOCM
What is carotid sinus syncope?
Syncope due to vagal response caused by pressure over the carotid sinus baroreceptor in the neck e.g. due to tight collar
What are pseudoseizures?
Usually there are bizarre thrashing, non-synchronous limb movements, but there can be extreme difficulty in separating these attacks from seizures. EEG videotelemetry is valuable.
What types of migraine can cause loss of consciousness?
- Basilar migraine
- Familial hemiplegic migraine
What might suggest that someone has lost consciousness due to hypoglycaemia?
Prior seconds/minutes of hunger, shaking, sweating and darkening of visual fields. Following confusion, loss of consciousness +/- convulsions or hemiparesis can occur
What might indicate that syncope has been caused by a panic attack?
- Hyperventilation
- Dizziness
- Chest pains/tightness
- Feeling like your choking
- Tingling in face/extremities
- Palpitations
- Trembling
- Feeling of dissociation
What can cause drop attacks?
Mostly benign, but can be caused by:
- Hydrocephalus
- Cataplexy
- Narcolepsy
If someone had an episode of LOC and had presented to GP/A&E, what would you do?
- History - story of the attack - before, during, after
- Exmination - Cardiovascular (including BP), neurological
What investigations would you consider doing in someone who had had an episode of LOC?
Based on presenting complaint
- Bloods - U+E’s, FBC, Mg2+, Ca2+, Glucose, ABG, LFTs, renal function, blood cultures
- ECG
- EEG
- CT/MRI
- CO
- Toxicology screen
- Blood glucose
What are the four main mechanisms that can affect the ascending reticular activating system leading to alteration of consciousness?
- Brainstem lesion
- Brainstem compression - coning, posterior fossa mass lesion, hydrocephals
- Diffuse brain dysfunction - metabolic/toxic causes
- Massive cortical damage - Meningitis, hypoxic ischaemic damage after MI
What are causes of reduced GCS?
- Causes of raised ICP
- Hypoxia/Hypercapnia/sepsis/hypotension
- Drug intoxication/renal or liver failure
- Hypoglycaemia
- Ketoacidosis
- Seizures
- Fluctuation in degenerative diseases - Lewy Body dementia
What is the meaning of obtunded?
A greatly reduced level of consciousness. The patient is not yet comatose but is close, arousing only with very strong stimulus.
How would you assess consciousness level?
- Observation - spontaneous movements, seizure-like activity (AVPU)
- Depth of coma - GCS
- Brainstem function/reflexes
- Lateralization of pathology
- Review other causes of decreased GCS - temp, BP, HR, cardiovascular, respiratory (O2, CO2), drugs, toxins
- Neurological limbs exam - motor response, tone, reflexes, seizures
What clinical features indicate someone is coning?
Cushing’s triad
- Increasing blood pressure
- Declining heart rate
- Irregular breathing
Can a single focal hemisphere (or cerebellar) lesion produce a coma?
No - unless brainstem is compressed
What is the progression from awake and alert to coma?
Alert -> Lethargy -> Stuporous -> Obtunded -> Coma
What does consciousness depend on?
- Intact ascending reticular activating system - acts as the alerting or awakening element of consciousness
- Functioning cerebral cortex of both hemispheres - determines the content of that consciousness
What are the commonest causes of Coma?
- Metabolic disorders
- Drugs/toxins
- Mass lesions
- Trauma
- Stroke
- CNS infection
Why might you smell someones breath if they were unconscious?
- Alcohol
- Fetor hepaticus
- Ketones
- Uraemia
If someone had bilateral fixed dilated pupils, what might this indicate in a comatose patient?
- Brainstem death
- Barbituate overdose
- Hypothermia
What might a single, fixed dilated pupil indicate in a comatose patient?
Coning/Uncal herniation
What might bilateral pinpoint pupils indicate in a comatose patient?
- Opiate overdose
- Pontine lesion/stroke
What might a loss of Doll’s eye reflex indicate?
- Deep coma
- Brainstem lesions
- Brain death
What would you look for on examination of someone who appeared comatose?
- Glasgow Coma Score
- Rectal temperature
- Respiratory pattern - cheyne-stoke, Kussmaul’s breathing
- Smell breath for alcohol/ketones
- Blood pressure/pulse
- Pupils
- Eye movements - Doll’s head reflex, Fixed lateral gaze
- Fundi for papilloedema
- Lateralizing signs
- Facial drooping
- Neuro limbs - Muscle tone, Plantar responses, Tendon reflexes
What investigations would you do in someone who presented in a comatose state?
- Bloods - U+E’s, glucose, tox screen, AG, TFTs, BCs, cortisol
- ECG
- CT/MRI
- LP
- EEG
How would you assess brainstem function in a comatose patient?
Reflexes and cardiorespiratory centres
- Pupillary light reactions (CN II+III)
- Eye movements (IV, VI and VIII) - Doll’s eye reflex, dysgonjugate gaze, conjugate gaze deviation
- Corneal reflex (V + VII)
- Gag reflex (IX, X) - If intubated, gentle tugging on endo-tracheal tube
- Respiratory drive (resp. centres)
What might the following indicate in a comatose patient?
Dysgonjugate gaze - usually indicates brainstem lesion, can also be mildly dysgonjugate in metabolic coma
What can conjugate gaze deviation indicate?
Brainstem lesion
What can small, reactive pupils indicate in someone who is comatose indicate as a potential cause?
Metabolic/toxic causes
What lateralising signs might you look for in a stuporous/comatose patient?
Asymmetry of:
- Response to visual threat - in stuporous patient indicates hemianopia
- Facial tone
- Limb muscle Tone
- Decorticate/decerebrate posturing
- Response to pain
- Tendon reflexes/plantars
What is the cause of a vegetative state?
Extensive cortical damage with intact brainstem
What are features of a vegetative state?
- Normal breathing - brainstem intact
- Patient appears awake - with eye opening and sleep–wake cycles
- No sign of awareness or response to environmental stimuli except reflex movements
HIGH LEVEL OF WAKEFULNESS, LOW LEVEL OF AWAREMESS
When is a vegetative state classed as persitent?
- >12 months following trauma
- >6 months any other cause
How would GCS (eyes, verbal and motor scores) differ between a vegetative state and a coma?
Eye score is the main difference
- Vegetative - E4, M1-4, V1-2
- Coma - E1-2, M1-4, V1-2
What are features of locked in syndrome?
- Awareness present
- Sleep-wake cycle present
- Response to noxious stimuli
- Blinking preserved and vertical eye movements
What is the cause of locked-in syndrome?
Occlusion/haemorrhage leading to Ventral pontine infarct with preserved ARAS (ascending Reticular Activating System) that extends from the thalamus and influences the state of arousal
What GCS score would individuals with Locked in syndrome have?
E4, V1, M1
What are metabolic causes of coma?
- Hypo/hyperglycaemia
- Uraemia
- Hypo/Hypercalcaemia
- Hypoadrenalism/pituitarism/thyroidism
- Hypo/hypernatraemia
- Metabolic acidosis
- Hypo/hyperthermia
- Porphyria
What are causes of direct effects within the brainstem that can lead to a coma?
- Haemorrhage
- Neoplasm
- Wernicke-Korsakoffs
What are infectious causes of coma?
Diffuse brain dysfunction
- Encephalitis
- Meningitis
- Cerebral malaria
What are cardiorespiratory causes of coma?
- CO poisoning
- Hypoxic-ischaemic brain injury
- Type II resp failure - CO2 retention
What is presetiant vegetative state?
Where brainstem rvovers to a considerable state but theres no evidence of cortical function recovery
-> high level wakefullness, low level of awareness
What is locked in syndrome?
Total paralysis below CN3 nuceli
- All voluntary msucles are paralysed except for those that control eye mvoement
- Eyes canb only open/close and move up/dowb (no horizontal movement)
What is given for wernicke’s encephalopathy?
IV thiamine (IV pabrinex)
What is given for opitate intoxication
IV Naloxone
What is given for benzodiazepine intoxication?
IV Flumazenil
