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Acute Care Block-Year 4 > Altered Conscious Level > Flashcards

Altered Conscious Level Flashcards

1
Q

what are the causes of altered conscious level?

A
  • Collapse secondary to cardiovascular disease
  • Hypoxaemia and/or hypercarbia due to respiratory failure
  • Shock due to any cause (sepsis, hypovolaemia, anaphylaxis)
  • Diabetic emergency (DKA, hyperosmolar hyperglycaemic state, hypoglycaemia)
  • Endocrine emergencies
  • Hypothermia
  • Hepatic encephalopathy
  • Uraemic encephalopathy
  • Poisoning and overdose
  • Seizures and epilepsy including eclampsia
  • Head injury
  • Acute stroke
  • Cerebral tumour or infection
  • Intracranial bleeds
  • Alcohol or substance misuse
  • Mental health conditions
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2
Q

AVPU

alert?

A

patient is aware of examiner and can respond to environment on their own, they can follow commands, open eyes spontaneously and track objects

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3
Q

AVPU

verbally responsive?

A

patients eyes don’t open spontaneously but do in response to verbal stimulus. They are able to react to verbal stimulus directly and in a meaningful way

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4
Q

AVPU

painfully responsive?

A

eyes don’t open spontaneously, only respond to application of painful stimuli by an examiner. They may move, moan, cry out

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5
Q

AVPU

unresponsive?

A

doesn’t respond spontaneously, they don’t respond to verbal or painful stimuli

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6
Q

how does AVPU scale correlate to GCS?

A
  • GCS 15 = alert
  • GCS 12-13 = verbally responsive
  • GCS 5-6 = physically responsive
  • GCS 3 = unresponsive
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7
Q

what are the features of the glasgow coma scale?

A 
eye response (4)
verbal response (5)
motor response (6)
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8
Q

what are the common causes of blackouts?

A
  • Syncope with or without seizures
  • Panic attacks
  • Epilepsy
  • Blank spells/microsleeps
  • NEAD (non epileptic attack disorder)
  • Narcolepsy
  • Hyperekplexia
  • Idiopathic drop attacks
  • Migraine without headache
  • TIA
  • POTS
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9
Q

what is syncope?

A

Loss of consciousness usually from a sudden decrease in cerebral blood flow, majority of patients seen in ‘first seizure’ clinics. Syncope often followed by ‘syncopal/hypoxic’ seizure

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10
Q

what are the types of syncope?

A 
reflex (vasovagal)
orthostatic
carotid sinus syncope
reflex anoxic attacks
cardiac
respiratory
CNS
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11
Q

describe reflex (vasovagal) syncope?

A

Most common in young
Exaggeration of normal cardiovascular response
Triggers and clinical features
• Prolonged standing, rising, emotional trauma, pain, venepuncture, sign of blood
•Gradual onset, light headedness, nausea, sweating, palpitations, greying of vision, muffled hearing, feeling distant
• Pallor, cold skin, uncoordinated jerks, rapid recovery with no confusion

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12
Q

describe orthostatic syncope?

A
  • Common in older age
  • Medications – postural hypotension
  • Autonomic neuropathy (MD, alcohol, amyloid)
  • Autonomic failure (MSA, PD)
  • Features: change in posture, rising, after meals
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13
Q

describe carotid sinus syncope?

A
  • Hypersensitivity of carotid sinus

* Attributable to neck pressure (tight collar, neck turning)

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14
Q

describe reflex anoxic attacks?

A
  • Children

* Increased vagal tone with brief asystole

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15
Q

when does cardiac syncope occur?

A
  • Can occur with no prodrome
  • In any posture
  • Can occur when awake or asleep, at rest and during activity
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16
Q

what are the causes of cardiac syncope?

A 
Structural heart disease
•	Aortic stenosis 
•	Hypertrophic obstructive cardiomyopathy
•	Mitral stenosis
•	Atrial myxoma
•	Ischaemic heart disease

Bradyarrythmias
• Complete heart block
• Sick sinus syndrome
• Swallow syndrome – in glossopharyngeal neuralgia

Tachyarryhmia
• Wolf Parkinson white
• Long ganong levine
• Long QT syndrome – congenital, acquired

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17
Q

describe respiratory syncope?

A
  • Cough synope – lead to bradyarrythmia
  • Valsalva manoeuvre – lead to bradyarrythmia
  • Breath holding spells – common in children / adults with anxiety
  • Hyperventilation – drop in CO2 -vasoconstriction
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18
Q

describe CNS syncope?

A 
Rare
Raised intracranial pressure
•	3rd ventricle colloid cyst
•	Chiari malformation
•	Obstructive hydrocephalus
Autonomic dysreflexia
•	Intermittent massive hypertension
Diencephalic attacks
•	Post head injury or hypoxia
•	Hypertension, sweating, tachycardia, loss of consciousness
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19
Q

what are the behavioural differential diagnosis of seizures/blackouts?

A
  • Hyperventilation

* Psychogenic non epileptic attacks

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20
Q

what are the cerebrovascular disorder differential diagnosis of seizures/blackouts?

A
  • TIAs
  • Migraine
  • Transient global amnesia - Transient memory loss, Hours, Repeated questions, rare, stress, occurs once
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21
Q

what are the movement disorder differential diagnosis of seizures/blackouts?

A
  • Dystonia
  • Myoclonic jerks
  • Startle disorders
  • Tremor disorders
  • Choreoathetosis/ballismus
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22
Q

what are the sleep disorder differential diagnosis of seizures/blackouts?

A
  • Narcolepsy – sleep in inappropriate situatons
  • Cataplexy – REM sleep intrusion into wakefulness
  • Sleep apnoea – common, under recognised
  • Parasomnias – occur in first few hours of sleep
  • Periodic limb movements of sleep
  • REM behaviour disorder (dissociation of REM sleep and atonia) – act out dream
  • Night terrors- children
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23
Q

what are the toxic, metabolic, infectious differential diagnosis of seizures/blackouts?

A
  • Hypoglycaemia
  • Recreational drugs
  • Phaeochromocytoma
  • Carcinoid syndrome
  • Porphyria
  • Hyper-ammonaemia
  • Ketosis
  • Lactic acidosis
  • Organic acidosis
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24
Q

differential diagnosis of seizures/blackouts

vertigo?

A
  • BPPV – common, positional
  • Menieres disease (progessive deafness)
  • Vertebrobasilar insufficiency (rare, over diagnosed)
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25
Q

describe non epileptic attack disorder?

A
  • Usually dissociative phenomenon and not malingering
  • Some sufferers have epilepsy as well
  • Occur in people with learning difficulties as often as rest of population
  • Sufferers often have other ‘unexplained’ medical symptom conditions
  • Common to have history of abuse and complex psycho/social problems
  • Can sustain significant injuries during attacks
  • Usually occur in company
  • Patient often reluctant to discuss symptoms
  • Attacks are variable and not stereo typed
  • Might verbalise during attacks and show some awareness, may respond to communication, patient is ‘suggestible’
  • Normal pupil size
  • Movements are flailing, arched back, pelvic thrusting
  • Eyelids are clenched with resistance to eye opening
  • Rapid recovery.
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26
Q

describe typical signs/symptoms of a patient with cerebrovascular syncope?

A

reaches maximum deficit in seconds without altered awareness unless massive stroke

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27
Q

describe typical signs/symptoms of onset in a patient with syncope due to seizures?

A

deficit may evolve over a few minutes

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28
Q

describe typical signs/symptoms of onset in a patient with syncope due to migraine?

A

deficit evolves over minutes to an hour with or without headache, should not cause altered awareness. May start as visual aura getting worse, followed by other facial sensory symptoms which can involve arm, legs and progress dysphasia etc this deficit happens graduallt in stroke it would be sudden

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29
Q

what kind of symptoms are seen in a patient with syncope due to migraine compared to ischaemia?

A
  • Migraine causes positive visual symptoms

* Ischaemia causes negative visual symptoms

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30
Q

describe postural orthostatic tachycardia syndrome POTS?

A
  • Uncommon but real entity
  • Diagnosis often missed – thought to be psychogenic
  • Characterised by orthostatic tachycardia
  • Measure heart rate supine, then standing – immediately after 1 min and then after 3 mins
  • Does not cause drop in BP
  • Can cause loss of consciousness
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31
Q 
SEIZURE
1. trigger
2. prodrome
3. onset
4. duration
5. convulsive jerks
6. incontinence
7. lateral tongue bite
8. colour
9. postictal recovery
10 postictal confusion
11. seziure at night from sleep
A
  1. rare (flashing, hyperventilation)
  2. common (aura, dejavu)
  3. may be sudden
  4. 1-2 mins
  5. common (prolonged)
  6. common
  7. common
  8. pale (partial seizure), red/blue
  9. slow (confused)
  10. common
  11. common
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32
Q 
SYNCOPE
1. trigger
2. prodrome
3. onset
4. duration
5. convulsive jerks
6. incontinence
7. lateral tongue bite
8. colour
9. postictal recovery
10 postictal confusion
11. seziure at night from sleep
A
  1. common (upright, bathroom, blood, needle, exertion)
  2. almost always (nausea, sweating, palpitation, light headed, visual greying)
  3. gradual (mins)
  4. 1-30 secs
  5. common (brief)
  6. common
  7. rare
  8. very pale
  9. rapid
  10. rare
  11. rare (unless cardiac)
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33
Q

DISSOCIATIVE SEIZURE

  1. incontinence
  2. post ictal confusion
  3. ictal crying
  4. asynchronous arm and leg movement
  5. recurrent status
A
  1. common
  2. rare
  3. occasional
  4. common
  5. common
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34
Q

DISSOCIATIVE SEIZURE

  1. multiple unexplained symptoms
  2. multiple surgical procedures and investigations
  3. on treatment for psychiatric condition
  4. history of abuse
  5. situational (anger frustration)
A

all common

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35
Q

DISSOCIATIVE SEIZURE

  1. induced by suggestion
  2. onset
  3. duration
  4. retained consciousness
  5. pelvic thrusting, back arching
A
  1. common
  2. gradual
  3. prolonged
  4. common
  5. common
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36
Q

DISSOCIATIVE SEIZURE

  1. fighting, need to be held, may injure others
  2. eyes closed
  3. resisting eye opening
  4. occurs only in company
  5. tongue bite/injury
A
  1. common
  2. common
  3. common
  4. common
  5. rare
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37
Q

EPILEPTIC SEIZURE

  1. incontinence
  2. post ictal confusion
  3. ictal crying
  4. asynchronous arm and leg movement
  5. recurrent status
A
  1. common
  2. common
  3. very rare
  4. rare
  5. rare
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38
Q

EPILEPTIC SEIZURE

  1. multiple unexplained symptoms
  2. multiple surgical procedures and investigations
  3. on treatment for psychiatric condition
  4. history of abuse
  5. situational (anger frustration)
A

all rare

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39
Q

EPILEPTIC SEIZURE

  1. induced by suggestion
  2. onset
  3. duration
  4. retained consciousness
  5. pelvic thrusting, back arching
A
  1. less common
  2. sudden
  3. seconds - minutes
  4. rare
  5. rare
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40
Q

EPILEPTIC SEIZURE

  1. fighting, need to be held, may injure others
  2. eyes closed
  3. resisting eye opening
  4. occurs only in company
  5. tongue bite/injury
A
  1. rare
  2. rare
  3. rare
  4. rare
  5. common
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41
Q
  1. what is epilepsy?

2. what is seizure?

A
  1. a disorder characterised by a tendency to recurrent seizures
  2. represents an episode which occurs when there is a sudden, excessive, disordered discharge of cerebral neurones
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42
Q

describe the tradditional classification of epileptic seizures?

A
  • Focal (partial) vs generalised (at onset) – with descriptive or anatomical localisation
  • Simple vs complex (complex = alteration in awareness)
  • Idiopathic vs symptomatic
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43
Q

what is the role of the frontal lobe?

A
  • Intellectual function
  • Praxis
  • Inhibition
  • Bladder continence
  • Saccadic eye movement (eye deviate away from area of brain)
  • Motor function (extension of limb, spread of movement from arm to limb)
  • Expression of language
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44
Q

what is the role of the temporal lobe?

A
  • Memory
  • Smell
  • Hearing
  • Vestibular
  • Emotion
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45
Q

what is the role of the occipital lobe?

A

vision

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46
Q

what is the role of the parietal lobe?

A
  • Sensory integration

* Receptive language

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47
Q

what are the types of generalised seizure under the old classification?

A
  • Atonic
  • Tonic – stiffness of limbs
  • Clonic -jerking
  • Tonic clonic
  • Myoclonic – sudden twitchy jerk of body
  • Absence
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48
Q

what are the 3 levels in the 2017 classification of epilepsy and seizures?

A
  • define seizure type
  • Define epilepsy type
  • Define syndromic diagnosis
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49
Q

what are the types of seizure?

A
  • Focal or generalised or unknown at onset
  • Simple or complex
  • Does seizure remain focal or does It evolve into a bilateral seizure (previously refered to as focal seizure with secondary generalisation)
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50
Q

describe a seizure of focal onset?

A
  • motor: automatisms, hyperkinetic, myoclonic, atonic, clonic, tonic
  • Non motor onset: autonomic, behaviour arrest, cognitive, emotional, sensory
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51
Q

describe a seizure of generalised onset?

A
  • Motor: tonic clonic, clonic, tonic, myoclonic, atonic, epileptic spasms
  • Non motor: typical, atypical, myoclonic, eyelid myoclonia
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52
Q

describe a seizure of unknown onset?

A
  • Motor: tonic clonic, epileptic spasms

* Non motor: behaviour arrest

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53
Q

what are the types of idiopathic generalised epilepsy?

A
  • Childhood absence epilepsy
  • Juvenile absence epilepsy
  • Juvenile myoclonic epilepsy
  • Generalised tonic clonic epilepsy
  • Genetic generalised epilepsy
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54
Q

name some epilepsy syndromes?

A
  • West syndrome
  • Dravet syndrome
  • Lennox gastaut
  • Unvericht-lundborg syndrome
  • Self limiting syndromes eg benign Rolandic epilepsy
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55
Q

what are the likely causes of epilepsy with an age of onset 0-2 years?

A

birth trauma
congenital defects
familial epileptic syndrome/channelopathy

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56
Q

what are the likely causes of epilepsy with an age of onset 2-12 years?

A

idiopathic generalised epilepsy, trauma, infections, accidental poisoning

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57
Q

what are the likely causes of epilepsy with an age of onset 12-30 years?

A

trauma, alcohol and toxins

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58
Q

what are the likely causes of epilepsy with an age of onset over 50 years?

A

trauma, alcohol and toxins, tumours, CVAs

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59
Q

what are the likely causes of epilepsy with an age of onset over 70 years?

A

trauma, alcohol and toxins, tumours, CVAs, dementia

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60
Q

describe vaccine encephalopathy?

A
  • LD/epilepsy following on vaccination in childhood
  • Rarely family history
  • SCN1a gene abnormality in 11/14 and 8/8 in second series
  • Presents with severe myoclonic epilepsy of childhood
61
Q

describe idiopathic generalised epilepsy?

A
  • Most start in childhood and adolesnce
  • Is there history of absences
  • Any myoclonus
  • Any family history
  • Sleep deprivation/ excess
62
Q

describe focal (partial) seizures?

A
  • 85% of seizures of adult onset

* Aura or complex behaviour post seizure may indicate primary focus

63
Q

what invesitgations are of use in epilepsy?

A
  • History
  • Bloods – metabolic derangement
  • Brain imaging
  • EEG
  • ECG
64
Q

describe EEG?

A
  • Often only as good as the timing of the test: frequent false negatives
  • Standard awake and sleep EEG
  • Ambulatory EEG
  • Video EEG telemetry
  • Cortical mapping
  • Depth elecotrode EEG
65
Q

describe the role of brain imaging in epilepsy?

A
  • Always required in focal onset epilepsy
  • Should be done in idiopathic generalised epilepsy?
  • CT or MRI? MRI better if possible
66
Q

what are the different components of epilepsy treatment?

A
  • Counselling and education
  • Drugs
  • Non drugs
  • Surgery
67
Q

what are triggers for seizures?

A
  • Lack of sleep
  • Psychological and emotional stress
  • Medications
  • Metabolic derangement
  • Hormonal changes - oestrogen
  • Alcohol and recreational drugs
  • Stimulants – caffeine
68
Q

what are the important considerations prior to initiating drug treatment for epilepsy?

A
  • Was this definitely epileptic seizure
  • Is there underlying recurrent structural cuase
  • Is there focal active epileptiform activity on eeg
  • Patient choice – can they afford to have anoter seizure
  • Counsel adequately – drugs can be hit and miss, to find best for individual, side effects, aim balance between control and side effects
69
Q

name some drugs used in the treatment of epilepsy?

A 
Vigabatrin
lamotrigine
gabapentin
topiramate
oxycarbazepine
tiagabine
levetiracetam
pregabalin
zonisamide
lacosamide
retigabine
perampanel
brivaracetam
70
Q

describe the action of phenytoin and carbamezapine?

A

as cell membrane is depolarised, sodium channels open, but fewer channels open as depolarisation progresses, those that are not open are activated and must be hyperpolarised before they can be activated. Phenytoin and carbamezapine bind to and block channels in inactivated state and prolong inactivation and prevent propagation of seizure activity. Allows for these drugs to inhibit neuronal firing under abnormal conditions of neural excitation, while having little effect on normal neurones

71
Q

describe the action of retigabine?

A

voltage gated potassium channels are important determinants of neuronal activity. Mutations in KCNQ2 underlie some forms of inherited epilepsy. Opening of these channels stabilises the resting membrane potential and controls the subthreshold electival excitability in neurons, thus preventing the initiation of epileptiform action potentials

72
Q

what are the 2 categories of calcium channel blockers?

A
  • Voltage regulated calcium channel – subtypes T,L and N eg ethosuximide and valproate reduce t-type cell current in thalamic neurones (important mechanism for inhibiting absence seizures
  • Receptor regulated calcium channels – including glutamate receptor subtype NMDA
73
Q

describe epileptic medication acting on GABA receptors

A

mediating CNS inhibition, regulated chloride channel. Benzodiazepines work by prolonging the chloride channels open time. Benzodiazepines work by increasing its frequency of opening and also work on benzodiazepine receptors. Valproate may have presynaptic effects on GABA too

74
Q

describe the mechanism of action of perampanel?

A

AMPA receptors

reduces neuronal hyperexcitation by selectively targeting glutamate activity at post synaptic AMPA receptors

75
Q

what medications are used for primary generalised seizures?

A
  • Sodium valproate (not in reproducing age women) - lamotrigine
  • ethosuximide (absence) then try topiramate
  • levetiracetam then try clonazepam/clobazam
  • perampanel/brivaracetam
  • phenytoin/phenobarbitone
  • rufinamide/vigabatrin
76
Q

what medications are used for focal seizures?

A
  • Carbamazepine retard vs lamotrigine then sodium valproate
  • levetiracetam then pregabalin
  • gabapentin
  • zonisamide
  • lacosamide
  • topiramate then perampanel
  • brivaracetam then phenytoid
  • phenobarb
  • tiagabine
  • felbamate
  • vigabatrin
77
Q

describe the effect of antiepileptic medication on the foetus?

A
  • Reactive metabolites
  • Altered folate metabolism
  • Compromise of embryo-fetal circulation
  • Inactivation of histone deacetylase
  • Disruption of developmental control genes-PAX genes
  • Major malformations, minor abnormalities, psychomotor development (sodium valproate) , intrauterine growth
  • First trimester most vulnerable
  • Higher doses and combination increase risk
  • Folic acid 5mg daily
  • Uncontrolled epilepsy carries 3% risk of teratogenecty
  • Seizure recurrence might utweigh risks of teratogenic medication (driving, occupation, child care, self confidence
78
Q

what are the potential issues with antiepileptic medications while breast feeding?

A

not an issue with medication but may cause tiredness/sleep deprivation that could trigger seizure

79
Q

what epileptic medication cause sedation, memory loss?

A

topiramate

phenobarbitone

80
Q

what epileptic medication cause ataxia, chorea?

A

phenytoin

carbamazepine

81
Q

what epileptic medication cause personality change?

A

topiramate

levetiracetam

82
Q

what epileptic medication cause headaches?

A

lamotrigine

83
Q

what epileptic medication cause rash and stevens johnson sydrome?

A

phenytoin
lamotrigine
carbamazepine

84
Q

what epileptic medication cause nausea, weight gain and weight loss?

A

sodium valproate

topiramate

85
Q

what epileptic medication cause hepatic dysfunction?

A

phenytoin
carbamazepine
sodium valproate

86
Q

what epileptic medication cause leucopaenia?

A

carbamazepine

87
Q

what epileptic medication cause pancytopaenia?

A

sodium valproate

88
Q

what epileptic medication cause SIADH (low sodium)?

A

carbamazepine

oxcarbazepine

89
Q

EPILEPSY

describe vagal nerve stimulation?

A
  • When drug treatment has failed
  • 50% will have 20-90% reduction in seizures
  • Considered for frequent seizures
  • Under skin like a pacemaker
90
Q

EPILEPSY

describe role of surgery?

A
  • When drug treatment has failed
  • When definite structural abnormality (except corpus callosotomy)
  • Temporal lobectomy
  • Lesion surgery
  • Gamma knife surgery
  • Hemispherectomy
91
Q

what are other issues surrounding a patient with epilepsy?

A
  • Depression
  • Pregnancy/ contraception/ breast feeding
  • Driving and employment
  • SUDEP-sudden unexplained death in epilepsy
  • Non epileptic attack disorder
92
Q

what are the features suggestive of epileptic seizures?

A
  • bitten tongue
  • head turning to one side during event
  • no memory of abdominal behaviour that was witnessed before, during or after the episode by someone else
  • unusual posturing
  • prolonged limb jerking
  • confusion or drowsiness after event
  • prodromal deja vu or jamais vu
93
Q

what are the features not suggestive of epileptic seizures?

A
  • prodromal symptoms that on other occasions have been abolished by sitting or lying down
  • sweating before the episode
  • prolonged standing that appeared to precipitate the event
  • pallor during episode
94
Q

describe patient assessment after first seizure?

A
  • document detailed description of event
  • vital signs (BP, temp)
  • full neurological examination
  • signs of injury
  • posisble underlying causes, including electrolyte disturbance, hypoglycaemia, haed injury, alcohol withdrawal, CVA
95
Q

what investigations would you perform in a patient following a first seizure?

A

ECG
urine Hcg if childbearing age
FBC
VBG

96
Q

if a patient presents to ED following a seizure when is CT indicated?

A
  • age >60
  • recurrent seizure
  • fever or immunocompromised
  • recurrent new neurological symptoms
  • persistent focal neurological signs
  • post trauma
  • confusion >1 hour
  • signs of raised intracranial pressure
  • known/suspected occupying lesion, malignancy, anticoagulation, alcoholism, TB
97
Q

what should be given if seizures are thought to be alcohol related?

A

pabrinex IV

98
Q

what are the differential diagnosis for seizures?

A
  • Eclampsia
  • Nonepileptic seizures/ pseudoseizures
  • Syncope
  • Acute dystonic reactions
  • Rigors
  • Cardiac disorders (e.g. Dysrhythmias, Long QT syndrome, HOCM)
99
Q

what is the pneumonic SICK DRIFTER mean as causes of seizures?

A
  • Substrates (sugar, oxygen)
  • Isoniazid overdose
  • Cations (Na, Ca, Mg)
  • Kids (eclampsia)
  • Drugs (CRAP: Cocaine, Rum (alcohol), Amphetamines, PCP)
  • Rum (alcohol withdrawal)
  • Illnesses (chronic seizure disorder or other chronic disorder)
  • Fever (meningitis, encephalitis, abscess)
  • Trauma (epidural, subdural, intraparynchymal hemorrhage)
  • Extra: toxocologic (TAIL: Theo, ASA, Isoniazid, Lithium) and 3 Anti’s: (Antihistamine overdose, Antidepressant overdose, Anticonvulsants (too high dilanitin, tegretol) or benzo withdrawal.
  • Rat poison (organophospates poisoning – not actually rat poison!)
100
Q

define status epilepticus?

A

state of prolonged, uncontrolled seiures, potentially life threatening and if untreated mortality approaches 30%. A single seizure persisting greater than 30 mins (5 mins without intervention), multiple seizures of shorter duration without a full neurological recovery in between seizures. Most seizures lasting longer than 5 mins will go on for 30 mins. Average seizure in adults is less than 1 minute. Neuronal injury can occur after 5 mins
Impending status epilepticus = continuous or intermittent seizures persisting beyond 5 mins without neurological recovery

101
Q

what is established status epilepticus?

A

seizures longer than 30 mins without full neurological recovery between them

102
Q

what is refractory SE?

A

persistence of convulsions despite adequate doses of 2 IV agents

103
Q

what is the pathophysiology of status epilepticus?

A

Rapid abnormal electrical discharges from cerebral neurones. Due to imbalance between excitatory and inhibitory neurotransmitters (glutamate and GABA).
Prolonged seizures can result in tachycardia, hypertension, hyperglycaemia, lactic acidosis

104
Q

what investigations should be done for status epilepticus?

A
  • IV cannula
  • Urea, electrolytes, magnesium, calcium, FBC
  • Blood gas
105
Q

what is the prehospital management of status epilepticus?

A
  • ABCDE

* Benzos – diazepam (rectal) or midazolam (biccal or intranasal)

106
Q

what is the management of status epilepticus in hospital?

A
  • Benzos - Prevent propogation of seizure / Diazepam, lorazepam, midazolam
  • Hydantoins - Phenytoin – prevent seizure recurrence / Fosphenytoin – inactive prodrug of phenytoin
  • Paraldehyde – second line
  • Barbituates – not standard first line. Phenobarbital, thiopental, pentobarbital
  • Others: propofol ,levetiraetam, midazolam
107
Q

ACUTE POISONING

airway management?

A

may need intubation (consider naloxone IV if unresponsive – opiate overdose this may correct airway), patient may be unconscious and therefore lose protective factors to airway. Benzo overdose/alcohol can also cause unconsciousness

108
Q

ACUTE POISONING

breathing

A

consider naloxone if unresponsive and sats <95% if this doesn’t work and patient still hypoxic on oxygen consider intubation. Patients who have drunk corosives can have breathing problems (pneumonitis)

109
Q

ACUTE POISONING

circulation?

A
  • ECG – broad complex tachycardia – tricyclics – (bicarb), digoxin
  • Prolonged QTc – risk factor for torsaddes - check toxbase (national poisoning database)
  • Low BP – IV fluid resuscitation, add vasopressors if cardiac depressants/anti hypertensives, check toxbase
110
Q

ACUTE POISONING

disability and detect and correct

A
  • Seizures – use benzos, stop seizures, check toxbase
  • Hypoglycaemia – check BM
  • Hypo/hyperthermia – check temp, hyperthermia risks in smpathomimetics eg ectasy, cocaine – dantraline for reversal
111
Q

what is involved in risk assessment of a patient with acute poisoning?

A
  • Agents
  • Dose
  • Time since ingestion
  • Clinical features and progress
  • Patient factors (weight and comorbidities)
112
Q

EMERGENCY ANTIDOTES

opiate toxicity

A

naloxone

not needed if airway is protected

113
Q

EMERGENCY ANTIDOTES

correct hypoglycaemia in insulin or sulphonylureas

114
Q

EMERGENCY ANTIDOTES
arrythmias with hydrofluoric acid
temporising measure in calcium channel blocker toxicity

A

calcium gluconate

115
Q

EMERGENCY ANTIDOTES

severe TCA overdose or sodium channel blockage?

A

sodium bicarbonate

116
Q 
EMERGENCY ANTIDOTES
organophosphate poisoning (farming)
117
Q

what affect does paracetamol poisoning have?

A
  • Inhibits CNS prostaglandin synthesis
  • One metabolite is hepatotoxic (NAPQI) in high concentrations, but in low amounts is detoxified by gluthathione (GSH). Endogenous GSH is limited
118
Q

what is the treatment of paracetamol poisoning?

A

(N-acetly cysteine) replenishes GSH and is highly effective if commenced withing 8 hours of ingestion with minimal risk of subsequent organ failure

119
Q

what is the treatment of paracetamol poisoning with a known time of ingestion <4 hours?

A

activated charcoal 50G if <1 hour and >150mg/kg ingested

check paracetamol conc, VBG, LFT, INR 4 hours after ingestion and treat according to nomogram

120
Q

what is the treatment of paracetamol poisoning with a known time of ingestion 4-8 hours?

A

check paracetamol conc, U&E, LFT, INR on arrival

then treat according to paracetamol nomogram

121
Q

what is the treatment of paracetamol poisoning with a known time of ingestion of 8-16 hours?

A

start NAC treatment if >75mg/kg ingested
paracetamol concentration, U&E, LFT, INR on arrival
commence/continue/stop treatment according to nomogram

122
Q

what are the signs and symptoms of opiate overdose?

A
  • Confusion
  • Nausea
  • Vomiting
  • Decreased level of consciousness
  • Respiratory depression
  • Pin point pupils
  • Signs of recent injection in IV drug users
123
Q

OPIATE OVERDOSE INITIAL STEPS:

inspection

A
  • AVPU
  • How do they look
  • Breathing?
  • Bedside?
124
Q

OPIATE OVERDOSE INITIAL STEPS:

airway

A
  • If they can talk the airway is patent
  • Airway compromise – sea-saw breathing, accessory muscles, diminished breath sounds, added sounds / cyanosed / inspect in mouth
  • In opioid overdose airway compromise likely due to secretion or vomit or collapse of upper airway
  • If airway obstruction – anaesthetist
  • Maintain airway – head tilt, chil lift / jaw thrust / airway adjunct eg oropharyngeal / nasopharyneal airway
125
Q

OPIATE OVERDOSE INITIAL STEPS:

breathing

A
  • Resp rate likely to be reduced
  • O2 sats aim for 94-98
  • Inspection
  • Palpation
  • Percussion
  • Auscutaion
  • 400micrograms naloxone then 800micrograms upto 2 doses at 1 min intervels then increase to 2mg for 1 dose if no response. Can be given subcutaneous, IM but only if IV not possible
  • ABG
  • CXR
126
Q

OPIATE OVERDOSE INITIAL STEPS:

circulation

A
  • BP – haemodynamic compromise
  • CRT <2 Seconds
  • Pulses
  • Peripheries
  • Inspect JVP – reduced in shock
  • IV access with large bore cannula
  • IV fluids if haemodynamic compromise
  • Investigations: FBC, U&E, CRP, lactate, glucose, coagulation studies, toxicology screen
127
Q

OPIATE OVERDOSE INITIAL STEPS:

disability

A
  • AVPU, GCS
  • Drug chart for opioids, sedative, anxiolytics, antihypertensives
  • Assess pupils
  • Pinpoint - opioid
  • Dilated – TCA overdose or intracerebral pathology
  • Blood glucose
128
Q

OPIATE OVERDOSE INITIAL STEPS:

exposure

A
  • Rashes
  • Bleeding
  • Evidence of IV use
129
Q

AMITRIPTYLINE

  1. absorption
  2. distribution
  3. metabolism
  4. excretion
A
  1. Rapidly absorbed following oral administration. Time to peak levels is 2 hours
  2. Large volume of distribution (5-20L/kg). Highly bound to plasma and tissue proteins
  3. Undergoes hepatic metabolism by oxidation via Cytochrome p450 to active metabolites such as nortriptyline
  4. Mainly in the urine as metabolites. Very little is excreted unchanged
130
Q

what are the CNS effects of TCA overdose?

A

Delirium/confusion/agitation, sedation, seizures, coma (often precedes cardiovascular signs)

131
Q

what are the cardiovascular effects of TCA overdose?

A

Sinus tachycardia, hypertension, hypotension (due to alpha2-adrenoreceptor blockade), broad complex tachycardia (can develop bradycardia pre-arrest)

132
Q

what are the anticholinergic effects of TCA overdose?

A

Can occur at time or presentation or be delayed and prolonged/. Agitation, restlessness, delirium, mydriasis (big pupil), dry, warm skin, tachycardia, ileus, urinary retention

133
Q

what would ABG show in a patient with TCA overdose

A

metabolic overdose

134
Q

TCA OVERDOSE

resuscitation mainstays

A
  • appropriate area for monitoring and ventilatory support
  • intubation and hyperventilation for severe overdose when decline in GCS with sodium bicarb
  • serial ECGs and blood gases
135
Q

how should ventricular arrhythmias caused by TCA overdose be treated?

A

unlikely to respond to cardioversion or defibrillation
• first line - sodium bicarbonate 2mmol/kg IV every 1-2 minutes until rhythm and perfusion restored
• second line is lignocaine 1.5mg/kg IV once pH greater than 7.5

136
Q

how should hypotension be treated in a patient with TCA overdose?

A

volume- crystalloid, sodium bicarbonate or failing this, vasopressor (noradrenaline or adrenaline) infusions

137
Q

TCA overdose

supportive care

A
  • suffice if only small ingestion
  • secure IV access
  • adequate hydration with IV fluids
  • pressure care, bladder care and DVT prophylaxis
  • cardiac monitoring should continue until toxicity reversed
138
Q

what investigations should be performed in a patient with TCA overdose?

A

ECG
paracetamol and blood glucose levels
blood gases
consider co-ingestants

139
Q

TCA OVERDOSE

decontamination

A
  • Activated charcoal can be useful for large ingestions >10mg/kg but should not be given without a definitive airway (i.e. a tube) being established prior
  • Charcoal not indicated for smaller ingestions as supportive care is often enough
140
Q

what is the antidote for TCA overdose?

A

Sodium Bicarbonate

141
Q

describe the toxicokinetics of benzodiazepines?

A
  • Rapid oral absorption
  • Highly protein bound
  • Varied Volume of distribution 0.4 – 4L/kg
  • Hepatic metabolism to active metabolites
  • Duration of effect depends on CNS tolerance and redistribution, rather than rate of elimination.
142
Q

what are the clinical features of benzodiazepine ovedose?

A
  • Onset in 1-2 hours
  • Ataxia, lethargy, slurred speech and reduced GCS
  • Profound coma rare except alprazolam or mixed ingestions
  • Apnoea indicated airway obstruction
  • Large ingestions rarely cause hypothermia, bradycardia and hypotension
  • Resolution of CNS depression occurs in 12 hours
143
Q

what are the investigations in a patient with benzo overdose?

A
  • 12 lead ECG
  • BSL
  • Paracetamol level
144
Q

what is the antidote for benzo?

A

Flumazenil – competitive benzo antagonist, indicated with; reversal of conscious sedation, accidental paediatric ingestion, aid investigation, manage airway and breathing but risk of precipitating toxidome or seizure in mixed overdose or history of epilepsy or chronic benzo use

145
Q

describe epidural haemorrhage?

A
  • Trauma to head / present with skull fracture
  • RTA / falls / assault
  • Source of blood – arterial – middle meningeal artery
  • Altered state of consuounse, headache, vomiting, confusion, sezuire, aphagia
  • between skull and dura
146
Q

describe subdural haemorrhage

A
  • Between Dura mater and arachnoid
  • RTA / falls/ assaults
  • Tearing of bridging veins
  • Coma 50%, lucid interval then progressive decline and coma
147
Q

descibre subarachnoid haemorrhage?

A
  • Blood occupies whole area
  • Cerebral artery (aneurysm) - Rupture of sacular anaurysm
  • Non aneurysm types as well
  • Sudden severe thunder clap headache
  • LOC, seizure, nausea, vomiting, mningismus (stiff neck, photophobia, headache)
148
Q

describe intracerebreal haemorrhage?

A
  • Lobar haemorrhage – specific lobes eg thalmic haemorrhage
  • Pontine haemorrhage. – in pons
  • Cerebellar haemorrhage
  • Second most common cause of stroke
  • Hypertension, brain tumour, bleeding disorders, blood use
  • Neurological signs and symptoms depend on where effected
  • Headache, nausea, vomiting, LOC
149
Q

describe intraventricular haemorrhage?

A
  • Bleeding in ventricles

* Most often secondary when intracerebral ruptures of subarachnoid heamohage extends to ventricle

Acute Care Block-Year 4 (8 decks)

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