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Geriatrics for OSCEs

Geriatrics for OSCEs. Andriana Harris Michelle Ting. OSCE stations. Histories Patient has become confused on the ward; please take a history from the relative and discuss what you would do next Patient has presented to GP/ A&E after a fall, please take a history and elicit the cause

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Geriatrics for OSCEs

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  1. Geriatrics for OSCEs Andriana Harris Michelle Ting

  2. OSCE stations • Histories • Patient has become confused on the ward; please take a history from the relative and discuss what you would do next • Patient has presented to GP/ A&E after a fall, please take a history and elicit the cause • Patient has presented to GP with a tremor, please take a history and answer the questions at 6m • Prescribing – do a prescription review to assess for causes of a recent fall

  3. OSCE stations • Examinations • Patient has presented with a tremor, please examine • Neuro examination • Cranial nerves – bells palsy vs stroke • Diabetic foot

  4. OSCE stations • Explanations • Please take a history and explain to a relative what their mother has, and explain the next steps (delirium) • Please explain Parkinson's to this patient who has been recently diagnosed • A patient has suffered a TIA/ stroke, please explain this to them and give them lifestyle advice and medication information • DVLA station – truck driver

  5. OSCE stations • Data interpretation • Stroke • 62 year old man presented to A&E with sudden onset of weakness on the left side of body. PMH Hypertension, migraine, diabetes, ex-smoker • On examination he had L facial droop , dysphasia and L hemiplegia. Otherwise general physical examination was normal. • O2 sats 97% • HR 114 • RR 14 • BP 130/80 • Temp 37.5 • Glucose 6.5 • GCS 15

  6. Atrial Fibrillation – absent P waves, irregular R – R intervals CT Brain - Hypodensity in the Right MCA Region

  7. Important aspects of the geriatric history • Important to get the patient’s baseline and compare it to their current symptoms • Social history • Living arrangements • Personal, domestic and community ADLs • Mobility • Cognition and mood • Continence • Nutrition • If in hospital, try to assess harm free care • VTE risk

  8. Confusion assessment When did the confusion start? – acute or chronic Has the patient had change in his/her functional activities? How is the patient’s attention span? Are they any changes in the patient’s behaviour? What is the patient’s mood? Has the patient been forgetful? PMH – CVA, psychiatric history Drug hx - any recent changes in medications? Known IVDU/EtOH intake?

  9. Confusion differentials • Delirium • Hyperactive – predominantly restless and agitated • Hypoactive – predominantly drowsy and inactive • Dementia • Depression

  10. Delirium

  11. Delirium • Risk factors • Age 65 or older, dementia, hospitalisation, acute illness/injury, post operative status, poor nutrition, underlying psychiatric disorder, Hxof substance abuse • Causes • Metabolic disorders • Electrolyte abnormalities, acid-base disturbances, hypoxia, hypoglycaemia/hyperglycaemia, uraemia • Pain • Infections • Decreased cardiac output • Dehydration, acute blood loss , acute MI , congestive heart failure • Stroke • Medications • Opioids, BZDs, steroids • Intoxication (alcohol etc.) • Transfer to unfamiliar surroundings • Miscellaneous • Faecal impaction, urinary retention

  12. Delirium examination • Abbreviated Mental Test Score (AMTS) • A – E assessment (incl. vital signs) • Mental State Examination if relevant • Delirium detection specific: Confusion Assessment Method and 4-AT • CAM • Acute onset and fluctuating course • Inattention • Disorganised thinking • Altered level of consciousness

  13. Delirium investigations • Bedside • Urine dipstick – UTI • ECG – MI • ABG – hypoxia/hypercarbia? • Bloods • FBC – infection • U&Es, - UTI, electrolyte imbalance • LFTs – GI pathology • ECGs – MI? • B12, folate • Imaging • CXR – pneumonia? • CT Brain – stroke?

  14. Management of delirium Review drug chart – reduce polypharmacy and withdraw contributory drugs Address acute medical issues – infection, metabolic disorders, hypoxia, hydration and nutrition, dehydration and constipation, pain Reorientation strategies – encourage family involvement, eyeglasses and hearing aids, mobility Normalise sleep wake cycle – try to provide uninterrupted sleep at night Regular monitoring of AMTS Pharmacological management – for patients with severe agitation/severe psychotic sx – haloperidol 0.25-0.5mg PO/IM BD (usually < 1 week, CI – Parkinsonism)

  15. Delirium prognosis May take several weeks to resolve Cognitive decline may persist Mortality 2X of non delirious patients with similar medical conditions FU in community after episode as increased risk of future dementia

  16. Stroke • Definition: sudden onset of neurological deficits of a vascular basis with infarction of CNS tissue lasting more than 24 hours • There are 2 different types of stroke • Ischaemic • Haemorrhagic

  17. TIA Definition: sudden onset of neurological deficits of a vascular basis without infarction that resolves within 24 hours Important to recognise as they have a high early risk of stroke and MI TIA is a medical emergency

  18. Stroke/ TIA history • Onset: time when last known to be awake and symptom free • Symptoms • Weakness • Sensory disturbance • Visual disturbance • Expressive/receptive dysphasia • Dizziness, vomiting, vertigo, double vision – Posterior circulation symptoms • Course – worsening, improving or fluctuating? • Headache(SOCRATES), N&V – SAH • Loss of consciousness – Seizure • Recent head/neck trauma – SDH, EDH, Dissection • Risk factors for developing stroke – AF, IHD, HT, Diabetes, Smoking, Excess ETOH

  19. Stroke differentials Todd’s paresis (post-ictal) Hypoglycemia Hemiplegic migraine Space occupying lesion Subdural/extradural hematoma Bell’s palsy Encephalitis

  20. Examination • A – E assessment – stabilise the patient (neuroprotection), sit the patient up 15 – 30˚ to prevent aspiration • A – patent? • B – 15L Oxygen Non-rebreather mask, O2 sats cyanosis?, RR, Resp exam, ABG, CXR • C – BP, HR, Temp, Cardio exam, ECG • D – GCS?, Glucose?, pupils ? • E – GI exam, expose patient • Rapid diagnosing using ROSIER to differentiate between suspected stroke and stroke mimics • Cranial Nerve Examination – is it forehead sparing? Bell’s palsy vs Stroke • Upper limb and lower limb neurological Examination – expect to see UMN signs

  21. Stroke/ TIA investigations • ECG • Telemetry, Holter monitor • Transthoracic echocardiography • Vascular risk stratification – lipid profile, HbA1C • Doppler US of carotids who have stable neurological symptoms with symptomatic carotid stenosis • Be assessed and referred for carotid endarterectomy within 1 week from onset of TIA • Undergo surgery within 2 weeks

  22. Management of TIA 300 mg aspirin STAT PO/PR Aspirin 300 mg should be continued until 2 weeks after onset at which time definitive long-term antithrombotic tx should be initiated Refer to TIA clinic to be seen within the same day if high risk or 7 days if low risk (dependent on ABCD2) Don’t drive till being seen in TIA clinic Lifestyle measures High dose atorvastatin Anti-HT, anticoagulation, diabetes management Continue clopi 75mg /aspirin75 mg/MR dipyridamole 200 mg long term

  23. ABCD2 It is used to stratify the risk of having a CVA in 2 days for TIA patients Ideally should be seen on the same day in the TIA clinic if ABCD2 score≥4

  24. Management of stroke • Start aspirin 300 mg until 2 weeks after stroke starts • CT Brain before starting alteplase (if patient presents <4.5 hours since symptom onset) • NIHSS score (the higher the score, the more severe the stroke) • Frequent neuro-observations (do not treat HT unless HT crisis or EOD present) • Contact Stroke Specialist Team if available • SALT assessment • NG tube • Nutritional screen • Malnutrition universal screening tool • Physiotherapy and OT input • Encourage mobility if safe (prevents DVTs, pneumonias and pressure ulcers) • Stroke workup • Cardiac evaluation – ECG, telemetry for 24 hours • Transthoracic echo • Carotid duplex ultrasound • MRI diffusion weighted imaging – gold standard • Stroke secondary prevention • Anticoagulation if AF present • Lifestyle measures • Treat hypertension, diabetes • High dose statins (should not be started in people with acute stroke)

  25. Complications of stroke • Brain • Brain edema (raised ICP) • Haemorrhagic transformation of stroke (10%) • Seizures • Swallowing • Aspiration pneumonia • Immobility • Pneumonia • UTI • Bedsores • DVT/PE • Falls • Long term • Depression and anxiety • Cognitive impairment

  26. Falls assessment • Before • Where did it happen? • Time of day • Pattern • Symptoms before falling – “dizziness” • During • Did they lose consciousness? • Did they injure themselves? • After • How did they get help? • Were they able to get up themselves? • Complications of fall – long lie (rhabdomyolysis), fracture, head injury

  27. Dizziness • If a patient uses this term, ask them what they mean by it • “Sensation of room spinning” • This is vertigo • “Sensation of unsteadiness” • Usually comes from the patient’s legs not their head – ask about this • “Feeling faint” • Presyncope or syncope, when standing, relieved by lying • “Fear of falling” • Common, loss of confidence, anxiety

  28. Causes of falls - DAME

  29. Parkinson’s • Degeneration of dopaminergic neurones in substantia nigra (of basal ganglia) • Quadrad of classical features – tremor, rigidity, bradykinesia, postural instability • Diagnosis based on clinical symptoms but must conduct investigations to exclude other causes e.g. MRI • Non-pharmacological management • MDT approach – neuro, physio, OT, SALT, specialist nurses, GP • Supervised exercise • Home modifications

  30. Parkinson's treatment – pharmacology • Monoamine oxidase B inhibitor • Selegiline • Low potency • Mild symptoms – no functional disability • Dopamine agonists • Ropinirole, pramipexole • Moderate potency • Moderate symptoms – most patients at diagnosis • Side effects – sleep attacks, impulse control disorders • Levodopa • High potency • Severe symptoms or for the elderly • Given with peripheral decarboxylase inhibitor (carbidopa) to prevent peripheral conversion to dopamine • Side effects – wearing off phenomena, dyskinesias

  31. Explaining Parkinson's Substantia nigra in the brain sends messages down the spinal cord to control muscles – these messages are sent using a chemical called dopamine, which is made by the substantia nigra In Parkinson's, the substantia nigra is damaged and parts of it die  reduced dopamine production  messages that get sent to the muscles are either slow or abnormal Slow messages  bradykinesia  slow walking, slow speech, expressionless, micrographia Abnormal messages  rigidity and tremor Clinical diagnosis Will be referred to Parkinson's specialist with no treatment so they can assess the symptoms DVLA

  32. Parkinson’s examination Very different to a neuro examination, work down the body Try to get a bit of a history if the examiner allows you to General Face Upper limbs Lower limbs Extra features

  33. Parkinson’s Plus Neurodegenerative conditions with the quadrad of Parkinson's symptoms PLUS other symptoms that separate them from Parkinson's disease

  34. Parkinson's plus

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