Falls Flashcards

(107 cards)

1
Q

Key facts to ascertain in a falls history?

A

Circumstances of event, mechanism and contract

What was the patient doing when they fell

How did the fall happen

How did they feel before they fell

Was there any dizziness or light-headed feeling?

Was there a loss of conciousness (good question - remember hitting the ground?)

Any cardiac symptoms? (pallor, palpitations)

Are they weak anywhere

Has this happened before

Any near misses before?

What medication do they take (sedatives, cardiac medications, anticholinergics, hypoglycemics, opioids)

How do they normally mobilise?

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2
Q

What should examination of a patient who has had a fall focus on?

A

Functional assessment of mobility: how do they mobilize, with what and how is their gait

CVS examination (include ECG and lying standing BP (immediate, 3 and 5 mins))

Neurological examination

MSK examination - assess joints

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3
Q

What falls risk assesmement tools may be used?

A

Falls Risk Assessment Tool (FRAT) - Part 1 - falls risk status, Part 2 – risk factor checklist, Part 3 – action plan

The Berg Balance scale

Mobility Interaction Fall chart

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4
Q

Osteoporosis risk factors?

A

Older age - over 65 (female) over 75 (male)

Female (particularly post menopausal, as oestrogen is protective)

Reduced mobility and activity

BMI <18.5 kg/m2

Rheumatoid arthritis

Alcohol

Smoking

Long term corticosteroids (equivalent of more than 7.5mg of prednisolone per day for more than 3 months)

Other medications such as:
SSRIs
PPIs
Anti-epileptics
Anti-oestrogens

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5
Q

When might a patient over 75 be automatically commenced on osteoporosis treatment?

A

When they have fractured a large bone with minimal trauma

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6
Q

What condition should all falls patients be assessed for risk of?

A

Osteoperosis

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7
Q

What are osteoporosis and osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones.

Osteopenia refers to a less severe reduction in bone density than osteoporosis.

Reduced bone density makes bone less strong and more prone to fractures.

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8
Q

Why are post-menopausal women at higher risk of osteoporosis?

A

Oestrogen is protective against osteoporosis. Unless they are on HRT postmenopausal women have less oestrogen. They also tend to be are older and often have other risk factors for osteoporosis.

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9
Q

Which cells increase bone synthesis?

A

osteoBLASTS

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10
Q

Which cells increase bone resorption?

A

osteoCLASTS

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11
Q

What is the FRAX score?

A

The FRAX tool gives a prediction of the risk of a fragility fracture over the next 10 years. This is usually the first step in assessing someone’s risk of osteoporosis.

It involves inputting information such as their age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) for a more accurate result but it can also be performed without the bone mineral density.

It gives results as a percentage 10-year probability of a:

Major osteoporotic fracture
Hip fracture

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12
Q

How is bone mineral density measured and where is the reading key for classification and management of osteoporosis?

A

Bone mineral density (BMD) is measured using a DEXA scan, which stands for dual-energy xray absorptiometry.

DEXA scans are brief xray scans that measure how much radiation is absorbed by the bones, indicating how dense the bone is.

The bone mineral density (BMD) can be measured at any location on the skeleton, but the reading at the hip is key for the classification and management of osteoporosis.

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13
Q

How can BMD be represented, what do the scores mean and which is most clinically important?

A

T score - most clincally important.
Number of standard deviations below mean BMD for a healthy young adult.

Z score
Number of standard deviations below mean BMD for the patient’s age.

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14
Q

What T score (at the hip) indicates normal BMD?

A

More than -1

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15
Q

What T score (at the hip) indicates osteopenia (less severe reduction in bone density than osteoporosis)?

A

-1 to -2.5

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16
Q

What T score (at the hip) indicates osteoperosis?

A

Less than -2.5

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17
Q

What indicates severe osteoporosis in terms of T score and clinical picture?

A

Less than -2.5 AND a fracture

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18
Q

Which patients should have a FRAX score calculated?

A

Women aged > 65
Men > 75
Younger patients with risk factors such as a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and rheumatoid arthritis.

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19
Q

What are the possible outcomes of a FRAX score without BMD measurement?

A

Low risk – reassure

Intermediate risk – offer DEXA scan and recalculate the risk with the results

High risk – offer treatment

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20
Q

What are the possible outcomes of a FRAX score with BMD measurement?

A

Treat

Lifestyle advice and reassure

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21
Q

Management of osteopetrosis?

A

Lifestyle changes

Optimize falls risk factors

Pharmacology: bisphosphonates + vitamin D and calcium

If bisphosphonates are contraindicated, not tolerated or ineffective: Denosumab, strontium ranelate, raloxifene or HRT may be considered

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22
Q

What lifestyle changes are advised in patients with osteoperosis?

A

Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption

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23
Q

Vitamin D and Calcium role in treatment of osteoporosis?

A

NICE recommend calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium.

An example of this would be Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).

Patients with an adequate calcium intake but lacking sun exposure should have vitamin D supplementation.

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24
Q

What are bisphosphonates, with examples?

A

Firstline treatment of osteoperosis

They work by interfering with osteoclasts and reducing their activity, preventing the reabsorption of bone.

Alendronate 70mg once weekly (oral)
Risedronate 35 mg once weekly (oral)
Zoledronic acid 5 mg once yearly (intravenous)

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25
What are the important side effects of bisphosphonates?
Reflux and oesophageal erosions. Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this. Atypical fractures (e.g. atypical femoral fractures) Osteonecrosis of the jaw Osteonecrosis of the external auditory canal
26
Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating - why?
Prevent reflux and oesophageal erosions
27
Other options if bisphosphonates are contraindicated, not tolerated or not effective in the management of osteoporosis?
Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts. Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction. Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus. Hormone replacement therapy should be considered in women that go through menopause early.
28
Management of low risk osteoporosis patients?
Low-risk patients not being put on treatment should be given lifestyle advice and followed up within 5 years for a repeat assessment.
29
How should patients taking bisphosphonates to manage osteoporosis be followed up?
Patients on bisphosphonates should have a repeat FRAX and DEXA scan after 3-5 years A 'treatment holiday' should be considered if their BMD has improved and they have not suffered any fragility fractures. (This involves a break from treatment of 18 months to 3 years before repeating the assessment.)
30
What might put someone at risks of falls?
Frailty Polypharmacy Gait and balance Co-morbid conditions Previous falls Pain – e.g. lower limb or foot Cognitive impairment – reduction in verbal ability, processing speed and immediate memory Urinary incontinence – rushing to the toilet at night
31
What should a falls risk assessment be based around?
1) History and examination 2) Drug review – involve the patient’s GP and/or pharmacist here 3) Specific review of medical risk factors: Vision Syncope Cardiovascular Cerebrovascular Diabetes 4) Functional and mobility assessment 5) Psychological effects of the fall May reduce mobility to decrease risk of fall but this may cause muscle weakness and joint stiffness It is therefore important to encourage or develop techniques to assist with coping with anxiety.
32
Tests to assess a patient's balance?
Timed Up and Go (TUG) test 180-degree turn
33
A systems enquiry may identify other relevant information that may relate to falls, what might this include?
General - weight loss, fatigue (constitutional symptoms) CVS - chest pain, palpitations Respiratory - SOB, cough Neuro - LOC, seizures, sensory or motor disturbance Genitourinary - dysuria, urgency, incontinence MSK - joint pain, muscle weakness
34
Particularly relevant PMH in a falls history?
General - Diabetes, visual/hearing impairment, anaemia CVS - Cardiovascular disease, arrythmias Respiratory - COPD Neuro - Parkinsons, epilepsy, stroke, dementia, peripheral neuropathy Genitourinary - incontinence, recurrent UTI GI - diverticulitis, chronic diahrea, alcoholic liver disease MSK - arthritis, chronic pain, fractures
35
Important social history in a patient presenting after a fall?
Alcohol intake Support at home – friends/family and carers Mobility – use of mobility aids and when (e.g. zimmer frame downstairs only)
36
Common medications that increase falls risk?
Beta-blockers (bradycardia) Diabetic medications (hypoglycaemia) Antihypertensives (hypotension) Benzodiazepines (sedation) Antibiotics (intercurrent infection)
37
Clinical examination of a patient presenting after a fall?
General: Alert and orientated, able to perform timed up and go test 1. CVS Pulse: may have irregularities such as AF or bradycardia Blood pressure – hypotension Bruits over carotid arteries (e.g. aortic stenosis, carotid stenosis) Murmurs: aortic stenosis/regurgitation, mitral stenosis 2. Resp Inspection: increased work of breathing Auscultation: coarse crackles (e.g. pneumonia) Percussion: dullness (e.g. pleural effusion) 3. Neuro Cranial nerve examination: stroke or visual impairment Power: weakness (e.g. stroke, disuse atrophy) Tone: increased in stroke Reflexes: absent (e.g. diabetic neuropathy), hyperreflexia (e.g. upper motor neuron pathology) Sensation: may be reduced secondary to upper or lower motor neuron pathology Co-ordination: may be impaired (e.g. chronic alcohol misuse leading to cerebellar degeneration) 4. GI Abdominal tenderness Organomegaly 5. MSK Check for injuries associated with falls and examine carefully the point of contact with the floor 6. ENT Is there any evidence of ear wax? Are the tympanic membranes intact?
38
What bedside investigations might you perform on a patient presenting after a fall and why?
Vital signs (may suggest sepsis or reveal a bradycardia) Lying standing blood pressure (orthostatic hypotension) Urine dipstick (infection, Rhabdomyolysis) ECG (bradycardia, arrythmias, prolonged QT) Cognitive screening such as AMT (cognitivie impairment) Blood glucose (hypoglycemia)
39
What blood test investigations might you perform on a patient presenting after a fall and why?
FBC (anemia, infection) U&Es (rhabdomyolysis, electrolyte imbalances, dehydration) Liver function (chronic alcohol use) Bone profile (calcium over supplementation, calcium abnormalities in malignancy)
40
What imaging might you perform on a patient presenting after a fall and why?
CXR (pneumonia) CT head (acute or chronic subdural bleed, stroke) ECHO (valvular heart disease such as aortic stenosis) X rays of injured limbs
41
What specialist investigations might you perform on a patient presenting after a fall and why?
Tilt table test (orthostatic hypotension) Dix-Hallpike test (BPPV) Cardiac monitoring e.g. 48 hr tape (If no symptoms during monitoring episode in hospital)
42
Potential causes of a fall: general
Mechanical: bad footwear, poor flooring, visual impairment Polypharmacy
43
Potential fall causes: CVS
Arrhythmias Orthostatic hypotension Bradycardia Valvular heart disease
44
Potential fall causes: neuro
Stroke Peripheral neuropathy Epilepsy
45
Potential fall causes: genitourinary
Incontinence Urinary tract infection
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Potential fall causes: endocrine
Hypoglycemia
47
Potential fall causes: MSK
Arthritis Disuse atrophy
48
Potential fall causes: ENT
Benign paroxysmal positional vertigo Ear wax
49
Potential interventions based on the various components of a falls risk assesment?
1 Gait - Physiotherapy 2 Visual problems - Eye test and ensure wears glasses 3 Hearing difficulties - Remove earwax, Hearing assessment 4 Medications review -Reduce unnecessary medication 5 Alcohol intake - Alcohol cessation advice, -Alcohol service referral 6 Cognitive impairment - Referral to a psychiatric team 7 Postural hypotension - Review medication, Improve hydration 8 Continence -Treat or rule out infections, Continence assessment 9 Footwear - Ensure good fitting footwear 10 Environmental hazards - Turn on lights, Take up rugs
50
Syncopal vs non-syncopal transient LOC
51
What 3 components does normal gait involve?
The neurological system - basal ganglia and cortical basal ganglia loop. The musculoskeletal system (which must have appropriate tone and strength). Effective processing of the senses such as sight, sound, and sensation (fine touch and proprioception).
52
Medications that can cause falls via postural hypotension vs other mechanisms?
Postural hypotension: Nitrates Diuretics Anticholinergic medications Antidepressants Beta-blockers L-Dopa ACEi Other: Benzodiazepines Antipsychotics Opiates Anticonvulsants Codeine Digoxin
53
NICE recommendations: re falls assessment
Identify all individuals who have fallen in the last 12 months. As per above identify why they are at risk. For those with a falls history or at risk complete the 'Turn 180° test' or the 'Timed up and Go test'. Offer a multidisciplinary assessment by a qualified clinician to all patients over 65 with: >2 falls in the last 12 months A fall that requires medical treatment Poor performance or failure to complete the 'Turn 180° test' or the 'Timed up and Go test' Individuals who fall but do not meet these criteria should be reviewed annually and given written information on falls.
54
What is syncope?
A loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure.
55
Features suggestive of SDH?
Presentation is typically in the sub-acute phase (within 3 days to 3 weeks) or the chronic phase (>3 weeks). Clinical presentation varies but may include: Headache, nausea or vomiting, confusion, and diminished eye/verbal/motor response. There may be focal neurological signs indicative of the haematoma site. A subdural haematoma (SDH) is caused by a collection of venous blood accumulating in the potential space between the dura mater and arachnoid mater.
56
What is an SDH!?
A subdural haematoma is caused by a collection of venous blood accumulating in the potential space between the dura mater and arachnoid mater. It typically occurs in elderly patients following minor trauma, resulting in shearing forces that tear bridging veins between the cortex and dura mater.
57
SDH risk factors
Advancing age (>65 years old) Bleeding disorders or anticoagulant therapy Chronic alcohol use, and Recent trauma.
58
How is SDH diagnosed and what is seen?
In most cases CT scan is sufficient to make the diagnosis and decide on patient management. CT scan appearance: The CT scan appearance varies depending on the clot age. In the hyperacute phase (<1 hour) the clot may appear as a relatively isodense lesion, with underlying cerebral oedema. Note that patients with a SDH rarely present in the hyper-acute phase. In the acute phase (<3 days) the classic appearance is of a crescent-shaped homogeneously hyperdense extra-axial collection over the affected hemisphere. In the sub-acute phase (3 days to 3 weeks) there is organisation of the clot, and the density of the clot falls. The haematoma will therefore appear more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement. In the chronic phase (>3 weeks) the haematoma becomes hypodense relative to the adjacent cortex. Note that 15% of SDH are bilateral in adults, and 80% are bilateral in infants - remember to check both sides of the scan!
59
Vasovagal episode pathophysiology?
Vagus nerve receives strong stimulus Stimulation of parasympathetic nervous system Parasympathetic activation counteracts the sympathetic nervous system Blood vessels delivering blood to the brain relax Blood pressure in cerebral circulation drops Hypoperfusion of the brain tissue
60
Primary causes of syncope
Dehydration Missed meals Extended standing in a warm environment Vasovagal response to a stimulie such as pain/suprise/blood
61
Secondary causes of syncope
Hypoglycemia Dehydration Anaemia INfection Anaphylaxis Arrhythmias Valvular heart diease Hypertrophic obstructive cardiomyopathy
62
Syncope vs Seziure
Syncope: Prolonged upright position before the event Lightheaded before the event Sweating before the event Burning/clouding vision before the event Reduced tone during the episode Return of conciousness shortly after falling Seizure Aura (smells, tastes, deja vu) Head turning Abnomral limb positions Tonic clonic activity Tongue biting Cyanosis More than 5 mins Prolonged post-ictal period
63
Patients with a particularly high falls risk?
Lower limb muscle weakness Vision problems Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson's disease etc) Polypharmacy (4+ medications) Incontinence >65 Have a fear of falling Depression Postural hypotension Arthritis in lower limbs Psychoactive drugs Cognitive impairment
64
What kind of investigation results indicate rhabdomyalysis?
CK Raised LDH (muscle damage) Hyperkalemia (liverated from damaged muscle) Hyperphosphatemia (liberated from damaged muscle) Hyperuricaemia (liberated from damaged muscle) Hypocalcemia (calcium is taken into damaged muscle)
65
What is a fragility fracture?
Fracture resulting from falling from standing height or lower at walking speed or slower (low intensity) Dose not include pathological fractures, fractures of digits, or skull fractures
66
Where do fragility fractures most commonly occur
Vertebra Proximal Renee Distal radius Humerus
67
Which groups of patients should be assessed for fracture risk and FRAX score
Women over 65 Men over 75 Patients with risk factors (prv fragility fractures, long term steroid use, fhx or hip fracture l secondary causes of osteoperosis)
68
Hypocalcemia
Muscle weakness Tingling sensation Spasam Tetany
69
What treatment can be considered in lieu or oral bisohosphinates in patients with low eGFR
Denosumab
70
What are the NICE criteria for imaging in a head injury?
Clinical evidence of a skull fracture Retrograde amnesia of over 30 minutes Focal neurological deficit Seizure GCS < 13 at any time GCS < 15 2 hours after injury More than one episodes of vomiting Loss of consciousness and amnesia in any patients who: - Are over 65 - Suffered a dangerous mechanism of injury (great height, RTC) - Have evidence of coagulapathy (including on warfarin therapy)
71
NICE falls guidance - multifactoral risk assement
identification of falls history assessment of gait, balance and mobility, and muscle weakness assessment of osteoporosis risk assessment of the older person's perceived functional ability and fear relating to falling assessment of visual impairment assessment of cognitive impairment and neurological examination assessment of urinary incontinence assessment of home hazards cardiovascular examination and medication review.
72
Falls definition
Inadvertently coming to rest on the ground or other lower level with or without LOC other than as a consequence of overwhelming external force, sudden onset paralysis, epileptic seizure, excess alcohol intake
73
‘Unconscious’ causes of collapse
Trauma Metabolic Infection Neurological: SAH, epilepsy, CVA
74
TLOC causes of collapse
Transient, self limited, no external trauma: Syncope Epilepsy (TIA or subclavian steel syndrome)
75
Causes of collapse - apparent unconsciousness
Falls (dizziness, vestibular, accidental (externsic factor)) Psychogenic pseudo syncope (PPS) Psychogenic non epileptic seizures (PNES) Dissociative attacks
76
Falls causes - extrinsic vs extrinsic
Intrinsic: Cardiac - BP HR IHD Sensory - vision, hearing Medical illness MSK - weakness arthritis osteoperosis feet Neuromuscular - gait balance, position sense PD Central processing - delirium, depression, dementia Extrinsic: Drugs Obstacles Inappropriate footwear Dim lighting
77
Why does a history of falls often lead to a cycle of further falls
Reduced strength balance, vision or judgement Fall injury loss of pride and confidence Reduce activity leading to further reduced - especially if damage, strength, balance, vision or judgement and thus more falls
78
What to ask in collateral/witness history following a fall
Posture before Appearance/colour Any movement Tongue biting/incontinence Duration Post event confusion Focal
79
Common associated symptoms with falls
Weak legs Fatigue General unwellnes Weight gain Swollen ankles SOB Off balance Trios Falls whilst not using aids
80
What might you assess in a falls patients
Falls and syncope, neurological MSK cardiac and vestibular history & directed examination Drug/polypharmacy review - Appropriate investigations (BLUE - normal bloods, lying standing, UTI, ecg clear?), X ray, CT, MRI, tilt table, DEXA scan - Bone health osteoperosis review (Ca2+ and vitamin D - measurement and replacement, fragility fracture, bisphosphonates , refer to metabolic bone clinic )
81
Falls evaluation algorithm
82
Therapy services: OT and PT assessments
PT: Gait analysis Walking aid assesments Muscle power Joint range of movement Dizziness Balance Outcome measures OT: Personal ADL Domestic ADL Transfers Environmental issues Outcome measures Joint: Sensory Motor presentation Vision Cognitive and psychological Footwear Confidence
83
Falls prevention programme: roles of therapy and education
Therapy: modified Otago - strength and balance work Falling safety Walking aid usage Postural change Home environment Education: Nutrition Continence Pharmacy Staying active
84
OT and PT outcome measures
10m walk test Timed up and go 180 turn (no. steps) Tinetti gait and balance
85
Which patients should NOT be reffered to falls clinic
Those with cognitive impairment and falls (medical clinic for geriatrician review, direct to community therapists ideally for home visits) RH and NH patients (community PT, CMHT, geriatrician DV) Single falls with no gait or balance problems Definite/suspect syncope - syncope clinic Balance problems - balance clinic Falls with underlying medical predisposition e.g. alcoholism
86
Vestibular vs non vestibular causes of dizziness
Vestibular: BPPV Neuritis/labryinthitis Vertiginous migraine Ménière’s Persistent postural perceptive dizziness (3PD) SOLs Non vestibular: Light headedness - pre syncope/syncope, postural intolerance Drug S/Es Anxiety SOLs Allergies
87
How can subclavian steel syndrome cause syncope
Retrograde arterial flow in diastole Reduced perfusion to brain
88
What are the features for transient loss of conciousness?
Short duration Abnormal motor control Loss of responsiveness Amnesia for the TLOC
89
What features must be present to consider a fall syncopal?
TLOC Loss of voluntary muscle tone Rapid onset, spontaneous and prompt recovery (if resuscitation required Full recovery Results from transient global cerebral hypoperfusion
90
Grand mal seizure vs hypoxic seizure (epilepsy vs syncope)
Grand mal seizure: fit then fall Hypoxic seizures: fall then fit
91
Aetiology of syncope (3 main causes)
1. Reflex syncopal syndromes: situation (suggestive hx), vasovagal (suggestive hx), carotid sinus syndrome (autonomic evaluation) 2. Orthostatic hypotension (bed side evaluation LSBP) 3. Cardiac syncope - (must not miss, obligatory cardiac evaluation if suspected)
92
Family history relevant to syncope
Sudden cardiac death or other heart problems Recurrent falls/syncopal episodes
93
What causes TLOC most often caused by and when should this be considered?
Syncope: reflex, OH, cardiac Consider in absence of signs and symptoms specific for - head trauma - epilepsy - psychogenic TLOC - rare causes
94
Approach to a diagnosis of syncope:
Initial evaluation: History, physical examination, L&S BP and HR, ECG Certain or suspected dx -> +/- evaluate/confirm -> dx made -> manage/treat (OH, situational, vasovagal) If diagnosis unclear: ?cardiac hx, ?structural heart disease, ?abnormal ECG, ?FHx SCD - if any presents cardiac evaluation required. If cardiac evaluation NAD: Frequent or serve: autonomic evaluation
95
Red flags/high risk for cardiac syncope
New onset chest pain or SOB Sudden onset palpitations immediately prior Collapse during exercise or whilst supine or seated Personal PMH - significant arrhythmias - HF/LVSD - Ischemic heart disease - Valvular heart disease Family history SCD <50 years
96
?Cardiac syncope - indications for echo
Murmurs Heart failure Significant LVH
97
?cardiac syncope indications for cardiac monitors
Quench if events Abnormal 12 lead Patient on rate limiting treatments In AF Atrythomgrnic cardiac history
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Not all patients with syncope need cardiac evaluation but it is required for symptom rhythm evaluation if cardiac disease is suspected - how is it detected?
Rhythm: - ECG - Prolonged ECG monitoring (24/48hr tales, SPIDER, ILR) - EP study (?malignant arrhythmia including WPW) Structural : - ECG - Echocardiogram - MRI - CT Reversible ischemia - ECG - ETT - Echo - MRI - Isotope scans - Angio
99
Syncopal evaluation in non cardiac syncope
NM evaluation 1) Tilt table testing 2) Carotid sinus massage 3) ?ILR
100
Driving and presyncope/syncope considerations
TLOC: Trigger/provocation Posture Prodrome High risk syncope (seated/standing) if: Abnormal ECG Clinical evidence of structural disease Typical vasovagal/ prodrome identified or unexplained no prodrome Avoidable triggers CVS Cough syncope
101
When should seizures be considered as a cause of collapse?
Vagueness absences Abnormal movements Stereotyped movements Tonic clinic jerks Myoclonus LOC > transient Tongue biting Incontinence Post octal phase Grunting/snore
102
Vestibular related syncope - associated symptoms
Postural change association Association with rolling in bed Diplopia Tinnitus N&V Room spinning Motion like sickness Episodic No relationship to sit to stand No TLOC but falls
103
Early VS late orthostatic hyootension
Systolic BP fall > 20 mmHg or diastolic > 10 mmHg or <90mmHg from baseline In first 3 min of standing - early In first 10 min of standing - late
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Prevention of orthostatic hypotension
Recognise and avoid predisposing factors (warmth, alcohol/food, drugs, speed of position change, prolonged recumbent position) Elastic support stockings Increase intravascular volume (fluid &salt intake) Postoperative anti HTN/vasodilators esp. diuretics Fludrocortisone Midodrine (improves venous return)
105
Orthostatic hypotension pathophysiology
Normal physiology: Upon standing blood pressure decreases which is detected by carotid barorecptors which cause vasoconstriction and increased heart rate, causing blood pressure to increase In orthostatic hypotension instead hear rate decreases and peripheral vascular resistance decreases so BP decreases
106
Tilt table test
Pt strapped to table standing up with ECG and beat to beat BO monitor and tilted to try and induce blood pressure drops Gravitation shift of blood to venous capacitance symptom, decreased venous return and cardiac filling pressure, decreased SV, compensatory increase in heart rate is insufficient so SNS mediated increased TPR Indications: Confirm suspected diagnosis in VVS in recurrent unexplained syncope, high risk pts with single unexplained syncope, elderly with unexplained recurrent falls, postural orthostatic tachycardiaturn and cardiac filling pressure, decreased stroke volum syndrome (POTE) and part of autonomic function testing Consider in unexplained TIA like symptoms or recurrent ‘epilepsy’ Can help patients recognise early symptoms/prodrome
107
If a patient had a bone mineral density suggestive of severe osteoporosis, not just explained by being post menopausal, what other tests might you order?
TFTs Calcium PTH Bone turnover markers myeloma screen, to include urine and plasma electrophoresis, immunoglobulins and liver function tests