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Y5 Nervous System > List I - Act Core Conditions > Flashcards

List I - Act Core Conditions Flashcards

1
Q

What is a TIA?

A
  • Temporary inadequacy of the of the circulation in part of the brain that clinically resembles a stroke, except that it is transient and reversible (it must completely return to normal)
  • If TIA within last 7 days but completely resolved - 300mg aspirin + PPI and refer urgently for assessment within 24 hrs
  • Duration is no more than 24 hours
  • Most last <30 mins
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2
Q

How many people have a TIA?

A
  • 50/100,000 in the UK
  • More common increasing age
  • M>F
  • TIA will often preceed a stroke 15%
  • Black race higher risk
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3
Q

What are the risk factors for TIA?

A
  • HTN
  • Smoking
  • DM
  • Heart disease - valvular, ischaemic, AF
  • Peripheral arterial disease
  • Polycythemia vera - increased RBC’s
  • Carotid artery occlusion/bruit
  • COCP - previous VTE risk, migraine with aura, coagulopathies
  • Hyperlipidaemia
  • Excess alcohol
  • Cocaine / IVDU
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4
Q

What is thrombus?

A
  • Local occlusion
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5
Q

What is embolus?

A
  • Throw off a clot to somewhere else
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6
Q

Where do emboli occur?

A
  • Carotids - bifurcation
  • Heart - AF, mural thrombosis
  • MI
  • Atrial myxoma
  • Valve disease
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7
Q

How do TIA’s present?

A
  • Carotid territory - unilateral weakness/sensory symptoms arm, leg, face
  • Dysarthria
  • Broca’s dysphagia - expressive speech
  • Amaurix fugax (fleeting loss of vision) - unilateral retinal ischaemia
  • Vertebrobasilar territory
  • Homonymous hemianopia
  • Bilateral visual impairment (occipital lobe)
  • Hemiparesis
  • Hemisensory
  • Diplopia/vertigo/vomiting/dysarthria/dysphagia/ataxia
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8
Q

What does the left (dominant hemisphere do in most people)?

A
  • Speech - Broca’s

* Language

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9
Q

What does the right (non-dominant hemisphere do)?

A
  • Spatial awareness
  • Facial recognition
  • Visual imagery
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10
Q

What is the acronym for remembering the cerebellar examination?

A
  • DANISH
  • Dysdiadochokinesia
  • Ataxia (gait and posture)
  • Nystagmus
  • Intention tremour
  • Slurred, staccato speech
  • Hypotonia/heel-shin test
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11
Q

How do you clerk a patient with suspected TIA?

A
  • Nature of event
  • Witnessed
  • Happened before
  • Time from onset is essential to determine eligibility for acute stroke treatments such as tissue plasminogen activator (tPA)
  • If time is unclear as what time the person was last known to be unaffected
  • If the person awoke with symptoms the time of onset is defined as when the patient was last awake and symptom free
  • Recent surgery - heart or carotids
  • Prev stroke or CAD - simultaneous cardiac
  • HTN
  • DM
  • Significant illnesses - hypercoagulable state or vasculitis
  • Drug abuse - cocaine
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12
Q

How do you assess a patient with suspected TIA?

A
  • A-E assessment
  • Vital signs - BP, HR, O2, temperature, RR
  • Full neurological - CN, upper and lower peripheral nerves, ataxia
  • Cardiovascular - HR, BP in both arms, carotid bruit, peripheral pulses, look for signs of heart failure, arrhythmias (AF), murmurs, valvular heart disease, endocarditis
  • FAST test can be used for rapid assessment - Face, Arm, Speech Test
  • Fundoscopy to identify intraocular haemorrhage (1/7 present in people with aneurysmal SAH)
  • Check blood glucose to rule out hypoglycaemia (<3.3mmol/L)
  • ECG to rule out arrhythmias
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13
Q

What blood examination should you do for suspected TIA?

A
  • FBC, ESR, U&E, lipids, glucose, sickle cell, syphillis
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14
Q

What is the secondary care management of TIA?

A
  • Aspirin 300mg with 24hrs and be seen in specialist clinic
  • PPI
  • > 1/52 ago - see within 7 days in a specialist clinic
  • Confirmed TIA - 75mg clopidogrel daily, high dose statin, modify BP
  • Usually require further investigations - echo, carotid dopplers (70%) 72 hr ECG
  • MRI - pick up an area of ischaemia
  • Argument for full cardiac investigations - biggest cause of death after TIA is stroke
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15
Q

What should patients be made aware of after TIA?

A
  • Cannot drive for 1 month following TIA
  • Notify DVLA
  • Multiple TIA’s over a short period require 3 months free before can resume driving
  • Lorry drivers cannot drive for a year
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16
Q

What is the definition of ischaemic stroke?

A
  • Sudden loss of blood circulation to an area of the brain resulting in residual neurological deficit lasting more than 24hrs or leading to death
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17
Q

Where can people most often have a stroke??

A
  • ACA - supplies medial portions of the frontal and parietal lobes, anterior portions of the basal ganglia and anterior internal capsule
  • MCA - supplies lateral portions of frontal and parietal lobes, anterior and lateral portions of the temporal lobes. Perforating branches - globus pallidus, putamen and internal capsule. It is the dominant source of vascular supply
  • PCA - supplies the cortical branches, posterior and medial temporal lobes and occipital lobes. Also supplies the perforating branches which supply the thalamus and brain stem
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18
Q

Where is stroke most common?

A
  • MCA
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19
Q

What is the pathophysiology of a stroke?

A
  • Ischaemic neuron depolarised as ATP depleted and membrane ion-transport systems fail
  • Na+/K+ impaired - intracellular Na+
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20
Q

What is the possible outcome of an ACA stroke?

A
  • Disinhibition
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21
Q

What is the possible outcome of MCA stroke?

A
  • Speech impairment
  • Contralateral hemiparesis
  • Contralateral homonimous heminopia
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22
Q

What is the possible outcome of PCA stroke?

A
  • Movement problems?

* Locked in?

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23
Q

What is the possible outcome of lacunar stroke?

A

*

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24
Q

What are the important differentials for stroke?

A
  • ALWAYS exclude hypoglycaemia
  • CNS tumour
  • Subdural bleed
  • Todd’s/Bell’s palsy
  • Consider drug overdose
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25
Q

What is the window for stroke treatment with thrombolysis?

A
  • 4.5 hours (ideally 3)
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26
Q

What is the management of stroke?

A

Normal limits of the following should be maintained:

  • Oxygen
  • BM control
  • Temperature
  • Hydration
  • BP control - only give antihypertensives if haemorrhage, BP >200, MI, dissection, pre-eclampsia
  • CT scan to rule out haemorrhagic stroke - non-contrast 1st
  • Give 300mg aspirin orally or rectally as soon as possible if haemorrhagic stroke has been ruled out
  • Thrombolysis - consider reduction in >185/110
  • If cholesterol is >3.5 mmol/l patients should be commenced on a statin - many physicians will delay treatment until after at least 48 hrs due to the risk of haemorrhagic transformation
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27
Q

What is the name of the thrombolysis drug administered for stroke and how many have it?

A
  • Alteplase

* ~11%

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28
Q

Who gets haemorrhagic strokes?

A
  • Tumour
  • High blood pressure
  • Ischaemic transformation
  • Trauma
  • Aneurysm
  • AV malformations
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29
Q

What is the management of haemorrhagic stroke?

A
  • Aim for good BP control
  • Reverse anticoagulants
  • Refer to neurosurgery - use their guidance
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30
Q

How does a subarachnoid haemorrhage present?

A
  • Worse headache ever in 1/3 patients
  • Thunder clap headache
  • Head ache can last 1-2/52
  • Of 100 patients presenting with sudden headache only 1 have SAH
  • Vomiting
  • Seizure/confusional state
  • Meningism
  • 10-15% patients have warning signs in prior 3 weeks - sentinel bleeds
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31
Q

How does subarachnoid haemorrhage happen?

A
  • Usually due to a burst berry aneurysm
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32
Q

Who gets a subarachnoid haemorrhage?

A
  • 6-9 / 100,000
  • 85% bleed from intracranial aneurysms
  • PCKD
  • Mean age 50 years
  • F>M 6:1
  • Connective tissue disorders - Ehlers Danlos, Neurofibromatosis T1
  • First degree relative increases chance by x7
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33
Q

What is a ‘star fish of death’?

A
  • SAH with blood white around the circle of Willis
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34
Q

What are the investigations for SAH?

A
  • Bloods
  • LP
  • ECG - QT prolongation, Q waves, ST elevation
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35
Q

What is the management of SAH?

A
  • Manage ICU if required
  • Refer to specialist unit
  • Prevent vasospasm
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36
Q

What risks are there post SAH?

A
  • Re-bleeding
  • 40% over subsequent 4 weeks
  • Clipping - craniotomy - MCA
  • Coiling - femoral catheterisation - PCA
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37
Q

What further management strategies are required for SAH?

A
  • Prevent seizures
  • Ventricular drainage - hydrocephalus
  • Secondary prevention - HTN & smoking
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38
Q

What presentation would make you suspect a TIA?

A
  • Sudden onset, focal neurological deficit which has completely resolved within 24 hours of onset and cannot be explained by another condition such as hypoglycaemia
  • Most resolve within 1 or 2 hours but can persist for 24 hours
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39
Q

What are focal neurological deficits?

A
  • Unilateral weakness or sensory loss
  • Dysphagia
  • Ataxia, vertigo or incoordination
  • Syncope
  • Sudden transient loss of vision in one eye (amaurosis fugax)
  • Homonymous hemianopia
  • Cranial nerve defects
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40
Q

What presentation would make you suspect a stroke?

A
  • Sudden onset, focal neurological deficit which is ongoing or has persisted for longer than 24 hours and cannot be explained by another mechanism such as hypoglycaemia
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41
Q

What are the possible features of stroke to look for?

A
  • Confusion or altered consciousness
  • Headache - sudden, severe associated with a stiff neck, sentinel headaches may occur in the preceding weeks
  • Weakness - sudden loss of strength in the face or limbs
  • Sensory loss - paraesthesia or numbness
  • Speech problems such as dysarthria
  • Visual problems - diplopia or vision loss
  • Dizziness, vertigo or loss of balance
  • Nausea and/or vomiting
  • Horners syndrome (miosis, ptosis and facial anhidrosis)
  • Difficulty with fine motor co-ordination and gait
  • Neck or facial pain
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42
Q

How can posterior circulation stroke symptoms present?

A
  • Symptoms of acute vestibular syndrome - acute persistent, continuous vertigo or dizziness with nystagmus, nausea or vomiting, head motion intolerance and new gait unsteadiness
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43
Q

What are the differential diagnoses for stroke and TIA?

A
  • Toxic/metbolic disturbance - hypoglycaemia, drug and alcohol toxicity
  • Dizziness - syncope, peripheral vestibular disturbance - vertigo or dizziness
  • Neurological conditions such as - seizure, migraine with aura, demyelination, peripheral neuropathy (bells palsy), Spinal epidural
  • Trauma
  • Infection
  • Space occupying lesion - tumour, subdural haematoma
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44
Q

How should a person be managed with suspected acute stroke?

A
  • Arrange emergency admission to acute stroke facility
  • Ensure the ambulance understands the urgency of the situation
  • Inform hospital on arrival - time of onset, symptom evloution, current condition and medications
  • Do not start with antiplatelet treatment until haemorrhagic stroke has been ruled out by a brain scan
  • While awaiting transfer monitor condition ABC
  • Give O2 if sats are less than 95% and there are no contraindications
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45
Q

How should a person with suspected TIA be managed?

A
  • If the TIA is within the last week
  • 300 mg aspirin immediately (with PPI cover)
  • Arrange urgent assessment (within 24 hours) by a specialist stroke physician
46
Q

How should a person with suspected TIA be managed if it occurred more than a week ago?

A
  • Refer for specialist assessment as soon as possible within 7 days
  • Assess for AF and other arrhythmias
  • Advise all patients on recognition and who to call if symptoms occur
47
Q

What criteria or system is used to classify stroke?

A
  • Bamford classification
48
Q

According to Bamford classification - what is a total anterior circulation stroke (TACS)?

A
  • All three need to be present:
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphagia, visuospatial disorder)
49
Q

According to Bamford classification - what is a partial anterior circulation stroke (PACS)?

A
  • Two of the following:
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphagia, visuospatial disorder)
50
Q

According to Bamford classification - what is a lacunar syndrome (LACS)?

A
  • One of the following
  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
51
Q

According to Bamford classification - what is a posterior circulation syndrome (POCS)?

A
  • One of the following:
  • Cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. gaze palsy)
  • Cerebellar dysfunction (e.g. ataxia, nystagmus, vertigo)
  • Isolated homonymous hemianopia or cortical blindness
52
Q

What is the criteria for thrombolysis following acute ischaemic stroke?

A
  • Thrombolysis with alteplase should only be given if:
  • Administered within 4.5 hrs of onset of stroke symptoms
  • Haemorrhage has definitely been excluded i.e. imaging has been performed
53
Q

What are the absolute contraindications to thrombolysis following acute ischaemic stroke?

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected SAH
  • Stroke or traumatic brain injury in the preceding 3 months
  • Lumbar puncture in preceding 7 days
  • GI haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120 mmHg
54
Q

What are the relative contraindications to thrombolysis following acute ischaemic stroke?

A
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
55
Q

What is the NICE recommended pre-stroke functional status a patient should have been at to be considered for thrombectomy?

A
  • Less than 3 on the modified Rankin scale

* More than 5 on the NIHSS

56
Q

Which further criteria should patients meet in order to be considered for thrombectomy?

A
  • Offer thrombectomy as soon as possible and within 6 hours of symptom onset with IV thrombolysis (if within 4.5 hrs) to people who have:
  • Acute ischaemic stroke and
  • Confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)
  • Offer thrombectomy as soon as possible to people who were last known to be well between 6 hrs and 24 hrs previously (including wake up strokes) for:
  • Confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
  • If there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion weighted MRI sequences showing limited infarct core volume
  • Consider thrombectomy together with IV thrombolysis (if within 4.5 hrs) as soon as possible for people last known to be well up to 24 hours previously (including wake up strokes) for:
  • People who have had acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (that is, basilar or PCA) shown by CTA or MRA and
  • If there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion weighted MRI sequences showing limited infarct core volume
57
Q

What is the secondary prevention management for people with strokes?

A
  • Clopidogrel recommended first line after an ischaemic stroke
  • Aspirin plus MR dipyridamole (if clopidegrel not tolerated)
  • No limit on treatment
58
Q

What is the criteria for the treatment with carotid artery endarterectomy?

A
  • Recommend if:
  • Patient has suffered stroke or TIA in the carotid territory and are not severely disabled
  • Should only be considered if carotid stenosis >70% (ECST criteria) or >50% (NASCET criteria)
59
Q

What is meningitis?

A
  • Inflammation of the meninges with an increased number of white cells in the CSF
60
Q

What are the causes of meningitis?

A
  • Infective
  • Viral - enteroviruses, adenovirus, EBV, mumps
  • Bacterial - neisseria meningitidis, strep pneumoniae, HiB, E. coli, group B strep, listeria, TB
  • Fungal - cryptococcal (immunocompromised), protozoal (amoebic, Naegleria fowleri), helminth
  • Non-infective
  • Neoplastic
  • Drugs (NSAID’s)
61
Q

What are the common non-specific signs of meningitis?

A
  • Fever
  • Vomiting/nausea
  • Lethargy
  • Irritability/unsettled behaviour
  • Ill appearance
  • Refusing food/drink
  • Headache
  • Muscle ache/joint pain
  • Respiratory symptoms/signs or difficulty breathing
62
Q

What are the less common signs of meningitis?

A
  • Chills/shivering
  • Diarrhoea, abdominal pain/distention
  • Sore throat/coryza or other ear, nose, throat symptoms/signs
63
Q

What are the more specific symptoms/signs of meningitis?

A
  • Non blanching rash
  • Stiff neck
  • Capillary refill time >2 s, cold hands and feet
  • Unusual skin colour
  • Shock and hypotension
  • Leg pain
  • Back rigidity
  • Bulging fontanelle
  • Photophobia
  • Kernig’s sign (person unable to fully extend the knee when hip is flexed)
  • Brudzinski’s sign (person’s knee and hips flex when neck is flexed)
  • Unconsciousness or toxic/moribund state
  • Paresis
  • Seizures
  • Focal neurological deficit including cranial nerve involvement and abnormal pupils
64
Q

How should adults with suspected bacterial meningitis be assessed?

A
  • Assess for vital signs using red flag/amber flag risk stratification criteria - if any of the high risk criteria are met active the sepsis 6 protocol
65
Q

What are the initial investigations for meningitis suggested by NICE?

A
  • FBC
  • CRP
  • Coagulation screen
  • Blood culture
  • Whole blood PCR
  • Blood glucose
  • Blood gas
  • Lumbar puncture if no signs of RICP
66
Q

How should patients with suspected meningitis be managed?

A
  • Transferred to hospital urgently
  • Pre-hospital setting e.g. GP surgery with meningococcal disease suspected give IM benzylpenicillin as long as it does not delay transit to hospital
  • Recommended antibiotics in hospital (empirical therapy)
  • <3 months - IV cefotaxime + amoxicillin
  • 3 months - 50 years - IV cefotaxime
  • > 50 years - IV cefotaxime + amoxicillin

Meningococcal meningitis
- IV benzylpenicillin or cofotaxime

Pneumococcal meningitis
- IV cefotaxime

Meningitis caused by Haemophilus influenzae
- IV cefotaxime

Meningitis caused by listeria
- IV amoxicillin + gentamicin

IV dexamethasone should also be given to reduce the risk of neurological sequelae

67
Q

How should contacts be managed in a person with suspected meningococcal meningitis?

A
  • Prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis. Prophylaxis should also be offered to people who been exposed to respiratory secretion, regardless of the closeness of contact
  • People who have been exposed to a patient with confirmed bacterial meningitis should be given prophylactic antibiotics if they have close contact within the 7 days before onset
  • Oral ciprofloxacin or rifampicin or may be used. The Health Protection Agency (HPA) guidelines now state that whilst either may be used ciprofloxacin is the drug of choice as it is widely available and only requires one dose
  • The risk is highest in the first 7 days but persists for at least 4 weeks
  • Meningococcal vaccination should be offered to close contacts when serotype results are available, including booster doses to those who had the vaccine in infancy
  • For pneumococcal meningitis, no prophylaxis is generally needed. There are however exceptions to this. If a cluster of cases of pneumococcal meningitis occur the HPA have a protocol for offering close contacts antibiotic prophylaxis.
68
Q

What is the appearance of CSF in bacterial meningitis?

A
  • Appearance - cloudy
  • Glucose - low (<1/2 plasma)
  • Protein - High (>1g/L)
  • WCC - 10-5000 polymorphs/mm3
69
Q

What is the appearance of CSF in viral meningitis?

A
  • Appearance - clear/cloudy
  • Glucose - 60-80% of plasma glucose
  • Protein - normal/raised
  • WCC - 15-1000 lymphocytes/mm3
70
Q

What is the appearance of CSF in tuberculous meningitis?

A
  • Appearance - slightly cloudy, fibrin web
  • Glucose - low (<1/2 plasma)
  • Protein - High (>1g/L)
  • WCC - 30-300 lymphocytes/mm3
71
Q

What is the appearance of CSF in fungal meningitis?

A
  • Appearance - cloudy
  • Glucose - low
  • Protein - high
  • WCC - 20-200 lymphocytes/mm3
72
Q

What is acute confusional state?

A
  • Delirium or acute organic brain syndrome

* Affects up to 30% of elderly patients admitted to hospital

73
Q

What are the predisposing factors for developing delirium?

A
  • Age >65 years
  • Background of dementia
  • Significant injury e.g. hip fracture
  • Frailty or multmorbidity
  • Polypharmacy
74
Q

What are the precipitating factors for the development of delirium?

A
  • Infection - particularly UTI
  • Metabolic - hypercalaemia, hypoglycaemia, hyperglycaemia, dehydration
  • Change of environment
  • Any significant CV, respiratory, neurological or endocrine condition
  • Severe pain
  • Alcohol withdrawal
  • Constipation
75
Q

What are the presenting features of delirium?

A
  • Memory disturbances (loss of short term > long term)
  • May be very agitated or withdrawn
  • Disorientation
  • Mood change
  • Visual hallucination
  • Disturbed sleep cycle
  • Poor attention
76
Q

What is the management of delirium?

A
  • Treat the underlying cause
  • Modification of the environment
  • Haloperidol 0.5 mg as first line sedative (or olanzapine)
77
Q

What are the assessment criteria for delirium?

A
  • DSM-IV criteria

* Short confusional assessment method (short-CAM)

78
Q

What are the CAM criteria for the assessment of delirium?

A
  • Confusion that has developed suddenly and fluctuates, and
  • Inattention — ask if the person is easily distracted or has difficulty in focusing attention, and either
  • Disorganised thinking — ask if the person’s thinking is disorganised, incoherent, illogical, or unpredictable (for example they have an unclear flow of ideas, change subject unpredictably, or have rambling or irrelevant conversation), or
  • Altered level of consciousness — ask about changes in level of consciousness from alertness to: lethargy (drowsy, easily aroused); stupor (difficult to arouse); comatose (unable to be aroused); or hypervigilant (hyper-alert)
79
Q

What are the DSM-IV criteria for the assessment of delirium?

A
  • All four features must be present:
  • Confusion that has developed over a short period of time and fluctuates and
  • Disturbance of consciousness (reduced clarity of awareness of the environment, reduced ability to focus, hold or shift attention) and
  • A change in cognition (such as memory deficit, language disturbance or disorientation) or a perceptual disturbance and,
  • Evidence from the history, examination, or investigations which is consistent with delirium, cannot be attributed to another diagnosis, and is a direct physiological consequence of a general medical condition
80
Q

What is the ICD10 for delirium?

A
  • Etiologically nonspecific organic cerebral syndrome characterised by concurrent disturbances
  • Consciousness and attention
  • Perception
  • Thinking
  • Memory
  • Psychomotor behaviour
  • Emotion
  • Sleep - wake schedule
  • Duration is variable and the degree of severity ranges from mild to severe
81
Q

How is delirium characterised?

A
  • Acute generalised psychological dysfunction that usually fluctuates
  • Most common psychiatric problem encountered by medical students when first on the wards
82
Q

How can you investigate and exclude the possibility of an organic psychiatric disorder?

A
  • Detailed history
  • Mental state examination
  • Physical examination
  • Investigations - blood etc
83
Q

What are the features of the prodromal phase of delirium?

A
  • Perplexion
  • Agitation
  • Hypersensitivity to light and sound
84
Q

What are the features of delirium itself?

A
  • Impairment of consciousness - fluctuating, worse at night
  • Mood changes - anxiety, perplexion, depression, labile affect
  • Abnormal perceptions - transient illusions, visual, auditory and tactile hallucinations
  • Cognitive impairment - disorientation (time, place), poor concentration, impaired new learning, registration, retention and recall may all occur
  • Temporal course - disturbance develops over a short period (hours to days) tends to fluctuate
85
Q

Who does delirium affect?

A
  • Patients with physical illnesses, particularly inpatients:
  • 10% general medical and surgical wards
  • 20%-30% surgical intensive care units
  • 20% severe burns patients
86
Q

How can the causes of delirium be categorised?

A

DIMSP

  • Drugs and alcohol
  • Intracranial causes
  • Metabolic and endocrine disorders
  • Systemic infections
  • Post operative states
87
Q

What are the possible drug causes of delirium?

A
  • Drug toxicity
  • Antimuscarinics
  • Anticonvulsants
  • Antihypertensives
  • Anxiolytic hypnotics
  • Cardiac glycosides
  • Cimetidine
  • Insulin
  • Levodopa
  • Opiates
  • Salicylates
  • Steroids
  • Industrial poisons - solvents, heavy metals
  • Carbon monoxide poisoning
88
Q

What are the possible intracranial causes of delirium?

A
  • Infections - encephalitis, meningitis
  • Head injury
  • Subarachnoid haemorrhage and space occupying lesions e.g. brain tumours, abscesses, subdural haematomas
  • Epilepsy and post ictal states
  • Drugs and alcohol withdrawal - anxiolytics, amphetamines, etc
89
Q

What are the possible metabolic and endocrine disorders that can lead to delirium?

A
  • Addisons disease - primary hypoadrenalism
  • Cushings syndrome - increased glucocorticoids
  • Hyperinsulinism
  • Hypothyroidism
  • Hyperthyroidism
  • Hypopituitarism
  • Hypoparathyroidism
  • Hyperparathyroidism
90
Q

What is the management and prognosis of delirium?

A
  • Investigate appropriately to determine the underlying cause
  • Treat the underlying cause
  • Episode can last 1 week to 1 month
91
Q

What are the possible infective causes of delirium?

A
  • UTI (remove unnecessary urinary catheters)
  • Pneumonia
  • Septicaemia
  • Endocarditis
  • Encephalitis
  • Meningitis
  • Cerebral abscess
  • HIV
  • Malaria
92
Q

What are the possible other causes of delirium?

A
  • Hypoperfusion states (anaemia, cardiac arrhythmias)
  • Post operative states
  • Stress and sleep deprivation
  • Change in environment
  • Faecal impaction
  • Urinary retention
  • Vitamin deficiencies (B1, B3, B12)
93
Q

What are the possible neurological causes of delirium?

A
  • Stroke
  • Sub-arachnoid haemorrhage
  • Head injury
  • Space occupying lesion
  • Epilepsy
94
Q

Which investigations are required for delirium?

A
  • Bloods - FBC, U+E’s, LFT’s, TFT’s, glucose, thiamine level, drug screen
  • Infection screen - Urine dip, MSU, sputum samples, blood cultures, lumbar puncture
  • Imaging - CXR, AXR, CT head, MRI head
  • Other - ECG, EEG, urinary drug screen
95
Q

What is characteristic of the EEG in delirium?

A
  • Slowing of the posterior dominant rhythm

* Generalised slow-wave activity

96
Q

Which simple measures can be taken to reduce the risk of delirium?

A
  • Carrying out regular cognitive screen
  • Rationalising the drug chart
  • Ensuring that sensory aids such as spectacles and hearing aids are available
  • Encouraging fluids and nutrition, correcting any electrolyte imbalances and nutritional deficiencies
  • Encouraging gentle mobilisation
  • Encouraging relatives and carers to spend time at the bedside
97
Q

If the patient is so confused and their delirium is causing them to be psychotic or very agitated, which drug can be used?

A
  • Haloperidol
  • Exception to this is if their delirium is caused by alcohol or benzodiazepine withdrawal - treatment should be with benzodiazepines
  • Doses should be kept to a minimum e.g. 0.5 mg QDS, not PRN to avoid alternating periods of agitation and sedation
  • Stopped as soon as it is no longer needed
98
Q

What are the complications of delirium?

A
  • Prolonged hospital stay
  • Accelerated cognitive decline
  • Aspiration pneumonia
  • Fluid and electrolyte imbalance
  • Malnutrition
  • Falls
  • Injuries
  • Decreased mobility
  • Pressure sores
  • One year mortality has been estimated to be as high as 50%
99
Q

What is the underlying basis for delirium?

A
  • Any form of stress which ultimately results from excessive neurotransmitter release ( especially acetylcholine and dopamine) and leads to abnormal signal conduction
100
Q

What are the 8 delirium signs?

A
  • DELIRIUM
  • Disordered thinking
  • Euphoric/fearful/depressed/angry - labile mood
  • Language impaired
  • Illusions/delusions/hallucinations
  • Reversed sleep wake cycle
  • Inattention
  • Unaware/disoriented
  • Memory deficits
101
Q

What is subarachnoid haemorrhage?

A
  • Spontaneous bleeding into the subarachnoid space (often catastrophic)
102
Q

What are the causes of a SAH?

A
  • Saccular rupture (80% - congenital weakenings)
  • AV malformation (15% - angiomas)
  • Trauma
  • Coagulopathies
  • Mycotic aneurysm (subacute bacterial endocarditis)
  • No cause found <15%
103
Q

What are the risk factors for SAH?

A
  • Smoking
  • Alcohol misuse
  • HTN
  • Post menopausal oestrogen (low)
  • M:F 3:2 once >45 yrs
  • Berry aneurysm
104
Q

How common is SAH?

A
  • 9/100,000 per year
  • Age range 35-65 yrs
  • In primary care only 25% with thunder clap headache will have SAH (50-60% have no cause)
105
Q

What is the pathophysiology of SAH?

A
  • Berry aneurysm
  • Common sites - junction of posterior communicating internal carotid, anterior communicating anterior cerebral, bifurcation of MCA
  • 15% are multiple, some are hereditary
  • Associations - PCKD, coarctation of the aorta, Ehlers-Danlos syndrome
  • Meningism
  • Signs of meningism occur as leaking blood irritates the meninges
  • Focal neurological signs
  • False localising effect of raised ICP, co-existent intracerebral haemorrhage, vessel spasm from blood irritant
106
Q

What are the presenting clinical features of SAH?

A
  • Sudden (often in seconds) occipital thunder clap headache
  • Vomiting, collapse, seizures, coma/drowsy, RICP (in days)
  • Sentinel headache (warning) prior headache from small leak of offending aneurysm (6%)
  • PMH - bleeding disorders, HTN, previous SAH, endocarditis, menopause, PCKD, coarctation
  • SH - smoking and alcohol
  • FH - SAH

Signs

  • Neck stiffness
  • Photophobia
  • Kernigs +ve (6h to develop)
  • Retinal/subhyaloid haemorrhage
  • Papilloedema
  • Pupil changes of 3rd nerve palsy (posterior communicating)
  • Intracerebral haematoma

Systemic features

  • Low HR
  • HTN
  • Fever (hypothalamic damage)
  • Sometimes associated with pulmonary oedema/arrhythmias
107
Q

What are the differential diagnoses for SAH?

A
  • Meningitis
  • Migraine
  • Intracerebral bleed
  • Cortical vein thrombosis
108
Q

What are the appropriate investigations for SAH?

A
  • Imaging - CT scan (detects >90% within first 48 hrs), then followed by CT angiogram with contrast
  • LP - Indications (if CT -ve and no contraindications >12 hrs post-onset of headache)
  • CSF uniformly bloody early on, becoming xanthochromic (yellow more diagnostic than bloody tap) after several hours (due to break down of Hb products like bilirubin)
109
Q

What are the principles of management of SAH?

A
  • Refer immediately to neurosurgery
  • Regular CNS observations - chart BP, pupils, GCS
  • Repeat CT if deteriorating
  • Maintain cerebral perfusion - keep well hydrated (aim for SBP >160mmHg - therapy if HTN is very severe - nimodipine 60mg/4h po for 3 wks or 1mg/hr IVI (CCB shown to decrease vasospasm as a consequence of morbidity from cerebral ischaemia
  • Further management - catheter/CT angiography with contrast to identify single vs multiple aneurysms - surgery
  • Surgical management
  • Endovascular coiling, preferable to surgical clipping where possible (as 7% increase in survival over 7 yrs but increase in risk of bleeding)
  • Intracranial stents/balloon remodeling - allow therapy of wide necked aneurysms/AV malformations/fistulae (microcatheters can now traverse tortuous vessels)
110
Q

What are the potential complications of SAH?

A
  • Risk of re-bleeding (commonest cause of death in 20% often in first few days)
  • Cerebral ischaemia (commonest cause of morbidity - vasospasm - permanent CNS deficit - surgery not helpful at the time/may be useful later)
  • Hydrocephalus (from blockage of arachnoid granulations - requires ventricular/lumbar drain)
  • Hyponatraemia - common, do not fluid restrict
111
Q

What is the mortality/morbidity of SAH?

A
  • Grade I - No signs 0%
  • Grade II - Neck stiffness/cranial nerve palsies 11%
  • Grade III - Drowsiness 37%
  • Grade IV - Drowsy with hemiplegia 71%
  • Grade V - Prolonged coma 100%

Other information - most mortality in first month, if survive this, 90% survive 1 yr +

112
Q

What is the prevention of SAH?

A
  • Surgery - only if young (<45 yrs), aneurysm >7mm diameter, especially if at junction of internal carotid posterior communicating or at rostral basilar artery bifurcation, uncontrolled HTN or PMH of bleeds, +/- previous SAH

Y5 Nervous System (2 decks)

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