ACH Flashcards
Management of an ischaemic stroke
Transfer to stroke centre
Non contrast CT head then diffusion weighted MRI
Aspirin 300mg for 2 weeks
Alteplase if within 4.5 hours (and no contraindications/no wake-up stroke)-0.9mg/Kg/hour
Thrombectomy if within 6 or up to 24 hours (limited core volume) (and required)
Carotid endarterectomy if required
Resolution of AF if required
Support care eg. SALT/ VTE prophylaxis, oxygen if sats low etc.
NB:
-Secondary prevention (clopidogrel 75mg and atorvastatin 80mg, treat modifiable risk factors)
-Anticoagulation after 2 weeks if an embolic stroke (caused by AF)
Lateral medullary syndrome
Wallenberg syndrome
Posterior inferior cerebellar artery
Cerebellar features;
ataxia
nystagmus
Brainstem features;
ipsilateral: dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss
Lateral pontine syndrome
Anterior inferior cerebellar artery
Horner’s syndrome
Facial paralysis and droop
Decreased taste (anterior 2/3 tongue)
Audiovestibular disturbance
Decreased facial sensation
Ataxia
NB- difference with posterior inferior cerebellar artery (wallenberg) is there would be no facial paralysis there and upper/lower limb involvement
Secondary prevention after ischaemic stroke
Clopidogrel 75mg (or dipyridamole 200mg BD + aspirin 75mg if contraindicated)
Atorvastatin 80mg
NB- not the same as secondary prevention following ACS
Contraindications to clopidogrel
Active bleeding
Allergy
Absolute contraindications to thrombolysis
Previous ICH
Seizure at stroke onset
Intracranial neoplasm
Suspected SAH
Stroke or traumatic brain injury in preceding 3 months
Lumbar puncture in preceding 7 days
GI haemorrhage in preceding 3 weeks
Active bleeding
Pregnancy
Oesophageal varices
Uncontrolled HTN (200/120)
Relative contraindications to thrombolysis
Concurrent anticoagulation (INR >1.7- higher the INR, the more likely they are to bleed)
Haemorrhagic tendency (ie. haemophilia)
Suspected intra cardiac thrombus
Major surgery or trauma in the preceding 2 weeks
Management of a haemorrhagic stroke
Transfer to stroke centre
Correction of coagulopathy
Reduce ICP eg. Mannitol and raised head
Surgery- craniotomy and clotting evacuation
Supportive- SALT/ VTE prophylaxis etc.
NIHSS Score
0- no Sx
1-4- minor stroke
5-15- moderate stroke
16-20- moderate to severe stroke
21-42- severe stroke
Management of a TIA
Immediate aspirin 300mg (even in community) for 2 weeks, unless patient has a bleeding disorder or is taking an AC (like aspirin)- needs to be referred for MRI head to exclude haemorrhage
Same day referral to the stroke service to be seen within 24 hours (carotid doppler/ ECG)
Lifestyle modification eg. Reduce BP (130/80), smoking cessation, diabetes review, AF management etc.
Then clopidogrel for life (+statin)- may require carotid endarterectomy
NB- no CT head if neuroimaging required (use MRI)
Contraindications to 300mg aspirin
Patient has a bleeding disorder or is taking an anticoagulant (haemorrhagic event needs to be excluded)
Patient already takes low dose aspirin regularly
Aspirin is always contraindicated in this patient eg. Allergy
Guidelines for a carotid endarterectomy
Suffered a stroke/ TIA
Stenosis is above 70% (European guidelines)
Not severely disabled
NB- significant stenosis should be operated on within 2 weeks
Embolic TIA (or stroke)- extra medications required
Anticoagulation eg. DOAC first line (edoxaban), started 2 weeks after the event, or warfarin
NB- Antiplatelet therapy if anticoagulation contraindicated eg. Aspirin 75mg, clopidogrel 75mg
NB- these patients will still be given aspirin and clopidogrel, then anticoagulants but timing depends on whether TIA or stroke
TIA- start when imaging excludes haemorrhage
Stroke- start after 2 weeks (when no haemorrhage)
Recognised complications of thrombolysis in acute stroke
7% angioedema (increased if using an ACE-I)
6% haemorrhage
Territory affected and upper/lower limb Sx
ACA- upper < lowers (ants are on the ground)
MCA- upper > lower
Barthes index
Measure a persons daily functioning post-stroke (AODL & mobility)
Level 1- mild dependent
Level 2- moderate dependent
Level 3- severe dependent
Ischaemic vs haemorrhagic stroke
Very difficult to differentiate, but if symptoms progress (get worse), could be haemorrhagic
Stroke mimic
Seizure- post ictal paresis (can be a dense hemiparesis)
Hypoglycaemia (BM is most important initial test)
Functional
TIA
Migraine
NB- difference is that the patient loses consciousness beforehand (unlikely with stroke/TIA)
Drugs that can induce Parkinsonism
Chlorpromazine, haloperidol (anti psychotics), risperidone, olanzapine, metoclopramide (anti emetic/GORD), prochloperazine (schizophrenia, anxiety, BPPV), cyclizine (depression)
Vascular Parkinson’s
Predominant lower body signs
Dementia with Lewy bodies
Dementia, Parkinson’s, and visual hallucinations (hallucinations first)
Cognition may fluctuate (like delirium), in contrast to other forms of dementia
Multi system atrophy
Prominent early autonomic features eg. Hypotension, bladder instability, erectile dysfunction
Cerebellar signs
PSP
Early falls, truncal rigidity, vertical gaze palsy
Normal pressure hydrocephalus
Dementia, gait disorder, bladder instability
Wet wobbly wacky
Corticobasal degeneration
Asymmetrical Parkinsonism and dyspraxia, dementia, and aphasia
Parkinson’s disease with dementia
Dementia comes after initial Parkinsonism
Drug induced Parkinsonism
Rapid onset and bilateral
Rigidity and rest tremor are uncommon
Differentiate IPD and Parkinson’s plus syndromes
Poor response to levodopa
PD and neuroleptic malignant syndrome
If medication isn’t taken or absorbed regularly (eg. Due to vomiting illness/ forgetfulness etc.)
Patients need to be advised on the importance of regularly taking medication and how to spot symptoms of NMS
NB- don’t give Drug holidays for this reason/ mess with patients drugs whilst they are in hospital
Neuroleptic malignant syndrome
Hyper pyrexia, mental status changes, muscular rigidity, autonomic dysfunction
NB- raised creatinine, leukocytosis seen. AKI may develop secondary to rhabdomyolysis
Management of a tremor patient
Parkinson features- refer to movement disorder clinic
Non Parkinson features;
Review meds and check TFT’s
Propranolol
Safety net (come back if PD features develop)
Symptoms to ask in stroke or TIA history
Face
Arms
Speech
Features of narcolepsy
Hypersomnolence
Cataplexy (sudden loss of muscle tone triggered by emotion)
Sleep paralysis
Vivid hallucinations
Investigations and management of narcolepsy
Multiple sleep latency EEG
Give daytime stimulants (modafinil), and nighttime sodium oxybate
Neurofibromatosis 1
Cafe au lait spots
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas
Scoliosis
Phaeochromayctoma
Mnemonic CRABBING;
C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve
Neurofibromatosis 2
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, meningiomas, ependyomas
Treatment of neuropathic pain
Either amitriptyline, duloxetine, gabapentin, or pregabalin (if it doesn’t work, stop and try another one- all used as mono therapy)
Tramadol as a rescue therapy
Causes of delirium
PINCH ME Stroke
Pain
Infection (UTI, pneumonia, cellulitis, meningo-encephalitis)
Nutrition (hypercalcaemia, hyperglycaemia, hyponatraemia, (any electrolyte disturbance) alcohol withdrawal, B12 & folate deficiencies)
Constipation
Hydration
Medication
Environment
Stroke (acute infarct/bleed)
Features of delirium
Memory disturbance
Agitated or withdrawn (hyper or hypoactive delirium)
Disorientated
Mood change
Visual hallucinations
Disturbed sleep cycle
Poor attention
Factors favouring delirium over dementia
Impaired consciousness
Fluctuating symptoms (worse at night, periods of normality)
Abnormal perceptions (illusions and hallucinations)
Agitation
Fear
Delusions
Risk factors for falls
Lower limb muscle weakness
Vision problems
Previous falls
Balance or gait disturbance (diabetes, PD, RA)
Poly pharmacy
Incontinence
65+
Postural hypotension
Arthritis
Psychoactive drugs
Cognitive impairment
Medications that cause postural hypotension
Nitrates
Diuretics
Anticholinergic medications
Antidepressants
Beta blockers
Levodopa
ACE-inhibitors
Medications that can cause falls for other reasons
Benzodiazapenes
Antipsychotics
Opiates
Anticonvulsant
Codeine
Digoxin
Sedative agents
What tools are used to assess frailty
Evaluation of gait speed
Self reported health status
PRISMA7 questionnaire (age, sex, health problems, assistance required, walking aid use)
STOPP START
STOPP- identifies medications where their risk outweighs therapeutic benefits
START- identifies medications that may provide additional benefits eg. PPI for gastroprotection
Investigations for a confused/delirious patient
History (collateral (family, staff), notes), cognitive assessment (AMT10), thorough clinical examination (A-E with observations)
Confusion screen
-urinalysis with culture
-bloods: FBC, UE, LFT, coagulation INR, TFT,Ca, B12, folate, haemanitics, glucose, blood cultures, bone profile
-imaging: CT head if concerned about intracranial pathology, CXR (pneumonia, PE, pulmonary oedema)
Management of delirium
Supportive- same staff, gentle re orientation, clear and regular introductions, access to hearing aids and glasses, encourage independence, clocks, familiar objects and photographs, ensure lighting and noise are adequate, ask family and friends to visit
Medication- avoid where necessary, haloperidol 0.5mg IM is first line, then benzos (0.5mg lorazepam). Avoid haloperidol in PD patients (always check)- use lorazepam
Tell family and carers on discharge that delirium may never diss appear (some will be left with a degree of cognitive impairment)
How long after stroke will you see signs on CT
12 hours
Assess stroke symptoms in an acute setting (eg. AE)
ROSIER
Parkinson’s disease and inhibition
Dopamine receptor agonists are associated with inhibition eg. Ropinirole
Thrombectomy guidelines
Acute ischaemic stroke
6-24 hours, if limited infarct core volume demonstrated on scans
Levodopa side effects
Dyskinesia
On off effect
LESS EFFECTIVE OVER TIME
Postural hypotension
Cardiac arrhythmias
Nausea and vomiting
Psychosis
Reddish discolouration of urine upon standing
What to check for in a man with osteoporosis
Testosterone
Management of osteoporosis
Offer bone protection if T score less than -2.5
Offer prophylactic bisphosphonates to those with a T-score < -1.5 if they are on steroids / going to be on steroids for 3 or more months (even if <65 years-old)
NB- if they cannot tolerate alendronate, try risedronate
NB- no bisphoshpanates below eGFR 35, try denosumab instead
Cabergoline (dopamine agonist)
Associated with pulmonary fibrosis
3 H’s when classifying a stroke
High function (speech, apraxia, neglect)
Hemianopia
Hemi loss (sensory or motor)
TACS
3/3 H’s
PACS
2/3 H’s
Lacunar stroke (Lacunar)
1/3 H’s
Posterior circulation stroke (POCS)
Occipital- isolated CONTRALATERAL homonymous field defect
Cerebellar- IPSILATERAL cerebellar signs
Brain stem- IPSILATERAL cranial nerve palsy
ACA occlusion
Contralateral arm and leg hemiplegia and sensory loss
Apraxia
MCA occlusion
Contralateral lower facial, arm, leg hemiplegia and sensory loss
Contralateral homonymous hemianopia
Dysphasia (dominant hemisphere)
Contralateral neglect (non dominant hemisphere)
Initial management for a patient who becomes unresponsive several hours after a fall/head injury
Insert an oropharyngeal airway and call anaesthetics for definitive airway management
What investigation can aid IPD diagnosis
single photon emission computed tomography (SPECT), especially if trying to distinguish ET and IPD
Management of PD
Refer to movement disorder clinic/ neurologist (don’t start treatment before they have seen the movement disorder specialist- will remove any signs and Sx)
Conservative- physiotherapy, support groups, SALT assessment, occupational therapy
Medical;
-If the motor symptoms are affecting the patient’s quality of life: levodopa (usually combined with a decarboxylase inhibitor eg. carbidopa (co-carbeldopa) or benserazide (co-benyldopa)) and a MAO-B inhibitor (sometimes a dopamine agonist too)
-If the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived eg. bromocryptine), levodopa or monoamine oxidase B (MAO‑B) inhibitor (selegiline)
Surgical- DBS
NB- drooling: glycopyrronium, orthostatic hypotension (midodrine), nausea- domperidone
COMT inhibitor
entacapone
Dopamine receptor agonists
bromocriptine, ropinirole, cabergoline, apomorphine
Pulmonary fibrosis, hallucinations, impulse control, daytime somnolence
MAO-B inhibitor
selegilline
Antimuscarinics
procyclidine, benzotropine, trihexyphenidyl (benzhexol)
block cholinergic receptors
now used more to treat drug-induced parkinsonism rather than idiopathic Parkinson’s disease
help tremor and rigidity
Amantadine
SE- ataxia, slurred speech, confusion, dizziness and livedo reticularis
Discontinuing benzodiazepines
Switch to diazepam slowly
Reduce dose by 1/8 every 2 weeks
When 1mg reached, stop completely
Features of a benign essential tremor
Fine tremor
Symmetrical
More prominent on voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep
Differentials for a tremor
Benign essential tremor
Parkinson’s disease
Multiple sclerosis
Huntington’s Chorea
Hyperthyroidism
Fever
Medications (e.g. antipsychotics, lithium, salbutamol)
DT’s
Areas a benign essential tremor affects
Voluntary muscles
Hand tremor
Head tremor
Jaw tremor
Vocal tremor
Investigations for a tremor
Bedside- thyroid, neuro, and PD exams
Bloods- FBC UE TFT’s folate B12
Imaging- not needed, SPECT if I wanted to differentiate BET and PD
Vertebral wedge fracture investigation
X ray
Ondansetron
5-HT3 antagonists used mainly in the management of chemotherapy-related nausea. It mainly acts in the chemoreceptor trigger zone area of the medulla oblongata.
Adverse effects- constipation, prolonged QT interval
Bisphosphonate treatment holiday
Repeat DEXA scan and FRAX score now and stop the bisphosphonate if low risk, T score is now >-2.5, and review in two years
The duration of bisphosphonate treatment varies according to the level of risk. Some authorities recommend stopping bisphosphonates at 5 years if the following apply:
patient is < 75-years-old
femoral neck T-score of > -2.5
low risk according to FRAX/NOGG
Weber’s stroke syndrome
affects medial portion of midbrain
ipsilateral III palsy
contralateral limb weakness (not sensory loss)
DVT and subsequent stroke
Do an echocardiogram to rule out ASD/VSD (that’s the only way you can have an embolic stroke following a DVT, if the thrombus can get into the opposite side of the circulation)
Anti-emetics in PD
domperidone
AF post stroke
following a stroke or TIA, warfarin or a direct thrombin or factor Xa inhibitor should be given eg. apixaban
Antiplatelets should only be given if needed for the treatment of other comorbidities (eg. clopidogrel)
3 stroke syndromes
Weber’s
Wallenberg’s (lateral medullary)
Lateral pontine
Respiratory secretions and bowel colic
Hyoscine bromide and glycoporronium
Agitation and confusion at the end of life
Underlying causes of confusion need to be looked for and treated as appropriate, for example hypercalcaemia, infection, urinary retention and medication. If specific treatments fail then the following may be tried:
first choice: haloperidol
other options: chlorpromazine, levomepromazine
In the terminal phase of the illness then agitation or restlessness is best treated with midazolam
Anticholinergics and dementia meds
work in opposite ways to one another so will reduce each others efficacy
