Falls Flashcards
Key facts to ascertain in a falls history?
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?
What should examination of a patient who has had a fall focus on?
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
What falls risk assesmement tools may be used?
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
Osteoporosis risk factors?
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
When might a patient over 75 be automatically commenced on osteoporosis treatment?
When they have fractured a large bone with minimal trauma
What condition should all falls patients be assessed for risk of?
Osteoperosis
What are osteoporosis and osteopenia?
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.
Why are post-menopausal women at higher risk of osteoporosis?
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.
Which cells increase bone synthesis?
osteoBLASTS
Which cells increase bone resorption?
osteoCLASTS
What is the FRAX score?
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
How is bone mineral density measured and where is the reading key for classification and management of osteoporosis?
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.
How can BMD be represented, what do the scores mean and which is most clinically important?
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.
What T score (at the hip) indicates normal BMD?
More than -1
What T score (at the hip) indicates osteopenia (less severe reduction in bone density than osteoporosis)?
-1 to -2.5
What T score (at the hip) indicates osteoperosis?
Less than -2.5
What indicates severe osteoporosis in terms of T score and clinical picture?
Less than -2.5 AND a fracture
Which patients should have a FRAX score calculated?
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.
What are the possible outcomes of a FRAX score without BMD measurement?
Low risk – reassure
Intermediate risk – offer DEXA scan and recalculate the risk with the results
High risk – offer treatment
What are the possible outcomes of a FRAX score with BMD measurement?
Treat
Lifestyle advice and reassure
Management of osteopetrosis?
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
What lifestyle changes are advised in patients with osteoperosis?
Activity and exercise
Maintain a healthy weight
Adequate calcium intake
Adequate vitamin D
Avoiding falls
Stop smoking
Reduce alcohol consumption
Vitamin D and Calcium role in treatment of osteoporosis?
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.
What are bisphosphonates, with examples?
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)
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
Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating - why?
Prevent reflux and oesophageal erosions
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.
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.
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.)
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
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.
Tests to assess a patient’s balance?
Timed Up and Go (TUG) test
180-degree turn
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
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
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)
Common medications that increase falls risk?
Beta-blockers (bradycardia)
Diabetic medications (hypoglycaemia)
Antihypertensives (hypotension)
Benzodiazepines (sedation)
Antibiotics (intercurrent infection)
Clinical examination of a patient presenting after a fall?
General: Alert and orientated, able to perform timed up and go test
- 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 - Resp
Inspection: increased work of breathing
Auscultation: coarse crackles (e.g. pneumonia)
Percussion: dullness (e.g. pleural effusion) - 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) - GI
Abdominal tenderness
Organomegaly - MSK
Check for injuries associated with falls and examine carefully the point of contact with the floor - ENT
Is there any evidence of ear wax?
Are the tympanic membranes intact?
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)
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)
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
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)
Potential causes of a fall: general
Mechanical: bad footwear, poor flooring, visual impairment
Polypharmacy
Potential fall causes: CVS
Arrhythmias
Orthostatic hypotension
Bradycardia
Valvular heart disease
Potential fall causes: neuro
Stroke
Peripheral neuropathy
Epilepsy
Potential fall causes: genitourinary
Incontinence
Urinary tract infection
Potential fall causes: endocrine
Hypoglycemia
Potential fall causes: MSK
Arthritis
Disuse atrophy
Potential fall causes: ENT
Benign paroxysmal positional vertigo
Ear wax
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
Syncopal vs non-syncopal transient LOC
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).
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
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.
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.
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.
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.
SDH risk factors
Advancing age (>65 years old)
Bleeding disorders or anticoagulant therapy
Chronic alcohol use, and
Recent trauma.
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!
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
Primary causes of syncope
Dehydration
Missed meals
Extended standing in a warm environment
Vasovagal response to a stimulie such as pain/suprise/blood
Secondary causes of syncope
Hypoglycemia
Dehydration
Anaemia
INfection
Anaphylaxis
Arrhythmias
Valvular heart diease
Hypertrophic obstructive cardiomyopathy
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
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
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)
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
Where do fragility fractures most commonly occur
Vertebra
Proximal Renee
Distal radius
Humerus
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)
Hypocalcemia
Muscle weakness
Tingling sensation
Spasam
Tetany
What treatment can be considered in lieu or oral bisohosphinates in patients with low eGFR
Denosumab
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)
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.
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
‘Unconscious’ causes of collapse
Trauma
Metabolic
Infection
Neurological: SAH, epilepsy, CVA
TLOC causes of collapse
Transient, self limited, no external trauma:
Syncope
Epilepsy
(TIA or subclavian steel syndrome)
Causes of collapse - apparent unconsciousness
Falls (dizziness, vestibular, accidental (externsic factor))
Psychogenic pseudo syncope (PPS)
Psychogenic non epileptic seizures (PNES)
Dissociative attacks
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
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
What to ask in collateral/witness history following a fall
Posture before
Appearance/colour
Any movement
Tongue biting/incontinence
Duration
Post event confusion
Focal
Common associated symptoms with falls
Weak legs
Fatigue
General unwellnes
Weight gain
Swollen ankles
SOB
Off balance
Trios
Falls whilst not using aids
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 )
Falls evaluation algorithm
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
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
OT and PT outcome measures
10m walk test
Timed up and go
180 turn (no. steps)
Tinetti gait and balance
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
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
How can subclavian steel syndrome cause syncope
Retrograde arterial flow in diastole
Reduced perfusion to brain
What are the features for transient loss of conciousness?
Short duration
Abnormal motor control
Loss of responsiveness
Amnesia for the TLOC
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
Grand mal seizure vs hypoxic seizure (epilepsy vs syncope)
Grand mal seizure: fit then fall
Hypoxic seizures: fall then fit
Aetiology of syncope (3 main causes)
- Reflex syncopal syndromes: situation (suggestive hx), vasovagal (suggestive hx), carotid sinus syndrome (autonomic evaluation)
- Orthostatic hypotension (bed side evaluation LSBP)
- Cardiac syncope - (must not miss, obligatory cardiac evaluation if suspected)
Family history relevant to syncope
Sudden cardiac death or other heart problems
Recurrent falls/syncopal episodes
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
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
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
?Cardiac syncope - indications for echo
Murmurs
Heart failure
Significant LVH
?cardiac syncope indications for cardiac monitors
Quench if events
Abnormal 12 lead
Patient on rate limiting treatments
In AF
Atrythomgrnic cardiac history
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
Syncopal evaluation in non cardiac syncope
NM evaluation
1) Tilt table testing
2) Carotid sinus massage
3) ?ILR
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
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
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
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
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)
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
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
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
