Transcript Management of collapses ?causes in the elderly

Management of collapses
?causes in the elderly
Dr S Samadian
Collapse ?cause
• Blackout
• Transient loss of consciousness (T-LOC)
Blackout
• Widely understood
• No implied aetiology
• No implied stigma
Collapse ?cause
Blackout
T-LOC
• Seizure
• Fit
• Syncope
• Faint
• Psychogenic
• Feint
‘A syncope is when the action of the heart, and along with it that of the arteries,
is suddenly and very much lessened; whence the animal powers, the
senses and voluntary motions, immediately cease. Various kinds of
nervous diseases… every kind of debility… especially great loss of blood,
and many kinds of poisons produce fainting. Whatever weakens the motion
of the blood through the brain tends to produce fainting. The mere posture
of the body may either bring on or keep off fainting, or remove it after it has
already come on. This disorder may sometimes be of little consequence
and easily removed; at others, very dangerous, not only as a symptom, but
even in itself, as sometimes terminating in death’
(Edinburgh Practice of Physic Surgery and Midwifery 1803)
Transient Loss of Consciousness
(T-LOC)
• ‘spontaneous transient loss of
consciousness with complete recovery’
NICE TLOC scoping document 2008
Impact of Syncope
• 40% population, syncope at least once
• 1.6% of hospital admissions
• 1% of ED visits per year
• 10% of falls by elderly are due to syncope
• Injuries:
- 6% major morbidity
- minor injury in 29%
Syncope/Collapse:
UK 2005-2006
• Approximately 83,000 hospital admissions
- 94% emergency admissions
-average LOS, 3.9 days
• Average cost of hospital stay
- approx £836 per patient
- 83,000 admissions
- £70 million per annum
UK 2005-2006
Syncope/Collapse Economics
Age of patients admitted, average 67 years
• 3% were <15 years
• 26% aged 15-59 years
• 22% aged 50-74 years and
• 50% were >75 years
Cost of fractures adds to burden
• About 17% of falls secondary to
syncope/collapse
• Annual NHS burden for fractures >£1 billion
Syncope classification
• Neurocardiogenic
- vasovagal
-other: cough, micturition, carotid sinus
• Orthostatic hypotension
- dysautonomia, eg diabetes
-drugs, Parkinson’s
• Cardiac syncope
- arrhythmias (electrical)
- structural (plumbing)
Causes of Syncope
Structural cardiac or cardiopulmonary disease:
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Cardiac valvular disease
Acute myocardial infarction/ischaemia
Obstructive cardiomyopathy
Atrial myxoma
Acute aortic dissection
Pericardial disease tamponade
Pulmonary embolus/pulmonary hypertension
Cerebrovascular:
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Vascular steal syndrome
Causes of Syncope
Neurally mediated reflex syncopal syndrome:
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Vasovagal faint (common faint)
Carotid sinus syncope
- situational faint
- acute haemorrhage
- cough/sneeze
-gastrointestinal stimulation (swallow, defaecation, visceral pain)
- micturition (post-micturition)
- post-exercise
-others (eg weightlifting, post-prandial
- Glossopharyngeal and trigeminal neuralgia
CAROTID SINUS HYPERSENSITIVITY
Carotid sinus hypersensitivity is an exaggerated response to carotid sinus
baroreceptor stimulation. Syncope may occur with or without accompanying
bradycardia. Carotid sinus hypersensitivity is defined by the response to
gentle carotid sinus massage applied just below the angle of the jaw, near the
carotid bifurcation for between 5 and 10 seconds:
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At least 3 sec asystole (cardioinhibition – the commonest form;70-75% of
cases).
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Lowering of blood pressure by at least 50mmHg (vasodepression;5-10% of
cases) without slowing of the heart.
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A combination of cardioinhibition and vasodepression (20-25% of cases)
Epidemiology
• Rare before the age of 50.
• Prevalence estimated at about 25% in fallers.
• Men are affected more often than women.
• Hypersensitivity occurs more often on the right
carotid sinus than the left.
Risk factors
• Carotid sinus hypersensitivity is associated with:
• Hypertension
• Coronary artery disease
• Other causes of syncope
• Dementia with Lewy bodies
• Medication, eg digitalis, beta-blockers and methyldopa
Management
• Lifestyle modification
• Cardiac pacing with a permanent cardiac pacemaker
• Surgical denervation of the carotid sinus
Causes of Syncope
Orthostatic:
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Autonomic failure
- Primary autonomic failure syndrome (eg pure autonomic failure, multi system
atrophy, Parkinson’s Disease with autonomic failure
- Secondary autonomic failure syndrome (eg diabetic neuropathy, amyloid neuropathy
- Drugs and alcohol
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Volume depletion
- Haemorrhage, diarrhoea, Addison’s Disease
Orthostatic Hypotension
• Systolic ↓ >20 mmHg
• Diastolic ↓ >10 mmHg
• Prevalence 10 – 20% over 65
• Increased incidence in institutions
• Measurement
- supine 20”
-standing 2”, 5”
Mechanism
• Normal autonomic function
• Rapid rise in concentration of noradrenaline
• Alpha receptors depressed
Possible explanation:
- Increased rigidity of blood vessel
Treatment of orthostatic hypotension
General advice:
• Chronic expansion of intravascular volume
- higher salt and fluid intake
• Reduction of gravitational induced pooling
- support stockings
• Small frequent meals
• Induce physical counter measures such as leg crossing
Treatment of orthostatic hypotension
• Appropriate leg and abdominal muscle exercise
swimming
• Pharmacological
-Fludrocortisone
-Vaso-constrictor – Midodrine
-Desmopressin for nocturia
-EPO for anaemia
Causes of Syncope
Cardiac arrhythmias as primary cause:
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Sinus node dysfunction (including bradycardia/tachycardia syndrome)
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Atrioventricular conduction system disease
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Paroxysmal supraventricular and ventricular tachycardia
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Inherited syndrome (eg long QT syndrome, Brugada sybndrome
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Implanted device (pacemaker, ICD) malfunction, drug induced proarrhythmias
Initial Evaluation
True syncope from ‘non-syncopal’
disorders
Cardiac from non-cardiac syncope
Clinical features and basic investigations
suggesting a diagnosis or route of referral
for specialist advice
Why cardiac v neurally mediated?
Cardiac syncope is bad for you
• Cardiac syncope
- 25% excess 1-year mortality v unexplained, neurally
mediated
- Structural heart disease greatest predictor of increased
mortality
- Exclusion of heart disease excludes cardiac cause in
97% of patients
• Neurally mediated syncope
- Virtually 0% excess mortality
• Unexplained syncope
- 5% excess mortality
Features suggestive of neurally
mediated syncope
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No cardiac disease
Long history, teen fainter
After unpleasant sight, sound, smell, pain, blood
Situational (cough etc)
Prolonged standing, hot crowded places
Post-meal
Head rotation, pressure on carotid sinus (eg
tumours, shaving, tight collars)
• After exertion
• Post-syncopal exhaustion
Fits and Faints
• ‘Convulsive syncope’
- overlap of symptoms in fits and cardiovascular
(particularly neurally mediated) syncope
- lack of aura, short ictus, minor shaking, no
post-ictal confusion
- incontinence rare
- seen in lab conditions in vasovagals with
prolonged asystole during tilt testing
• ‘Treatment resistant epilepsy’
- 8-40% due to vasovagal syncope
Seizures
• Intermittent, stereotyped disturbances of consciousness,
behaviour, emotion, motor or sensory function , that are
judged on clinical grounds to result from cortical
neuronal discharge.
• They can produce an enormous range of symptoms and
behaviours during partial seizures.
• The more localised the cortical discharge the greater the
diagnostic uncertainty.
Chronic Seizures : Epilepsy
Incidence
Alz
Major causes:
Cerebrovascular disease
Dementia
Neoplasm
Infection
Trauma
No definite cause
134 per 100,000
124 per 100,000
33%
11.7%
4%
0.6%
1%
50%
The risk of epilepsy is highest in the first year
after the occurrence of the CNS insult
Types of Seizures
Type:
Partial seizures
• Simple partial
• Complex partial
• Secondarily generalised
Generalised seizures
• Absence
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Primary generalised tonic-clonic
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Myoclonic
Atonic
Tonic
Clonic
Characteristics:
No impairment of consciousness
Consciousness is altered
Begins as a simple or complex partial
seizure and then spreads to involve both
hemispheres.
Brief episodes of impaired consciousness
with a characteristic EEG type
Loss of consciousness with an initial tonic
phase followed by a clonic phase
Brief shocklike muscle contractions
Brief episodes of loss of tone or posture
Brief tonic episodes
Brief clonic episodes
Acute symptomatic seizures
• Are common, particularly in the elderly
- occur in 30% of medical ITU admissions with
neurological symptoms
• Are almost always tonic-clonic seizures
• Will be accompanied by encephalopathy
- often with tremor, asterixis or myoclonus
Causes of Acute Symptomatic Seizures
• Systemic disturbance
- drugs
- withdrawal syndromes
- electrolyte imbalance
- endocrine abnormalities
- organ failure
- porphyria
• CNS disorders
- vascular events
- head injury
- infection
- cerebral hypoxia
Fits versus faints
Seizure likely
Syncope likely
Findings during LOC
Prolonged tonic-clonic movements, onset
coincides with LOC
Hemilateral clonic movements
Automatisms (chewing, lip-smack etc)
Tongue biting, blue face
5 mins or more
Tonic-clonic movements short
duration (<15 s), start after LOC
Symptoms pre-LOC
Aura
Nausea, vomiting, cold, sweaty
(neurally mediated)
Light-headedness
Blurred vision
Symptoms post-LOC
Prolonged confusion
Aching muscles
Short duration
Nausea, vomiting, pallor
Other findings to suggest
fits
FH, nocturnal, ‘pins & needles’, incontinence,
injury, headache
CASE STUDY
 82 year old man from Sri Lanka, retired accountant, presented with episodic
loss of consciousness which happened both indoors and outdoors. The
loss of consciousness was brief and on occasions associated with short
jerking movements of the limbs and happened seated or standing.
 He has a past medical history of hypertensive ischaemic heart disease.
 Drugs – ACE, diuretic, aspirin, statin
 Clinical findings – normotensive with no postural drop, loud left carotid bruit
 Investigations – several 24 & 72 hour ECGs – short SVEs but asymptomic
throughout recordings
 CT brain scan – extensive small vessel disease
 Carotid doppler – 50% stenosis
Clinical features suggestive of specific causes of real or apparent loss of
consciousness
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Symptom or finding:
Possible Cause:
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Vasovagal
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Vasovagal or autonomic failure
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Vasovagal
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Post-prandial
Vasovagal or autonomic failure
Neuralgia (glossopharyngeal or
trigeminal neuralgia)
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After sudden unexpected
unpleasant sight, sound, smell
Prolonged standing, crowded,
warm places
Nausea, vomiting associated
with syncope
Within 1 hour of a meal
After exertion
Syncope with throat or face
pain
Clinical features suggestive of specific causes of real or apparent loss of
consciousness
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Symptom or finding:
Possible cause:
• With head rotation, pressure
on carotid sinus (tumours,
shaving tight collars)
• Within seconds to minutes
upon active standing
• Temporal relationship with
start or change of
medication
• During exertion or supine
• Preceded by palpitations
• Family history of sudden
death
• Spontaneous carotid sinus
syncope
• Orthostatic hypotension
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Drug induced
Cardiac syncope
Tachyarrhythmia
Cardiac/tachyarrhythmia
Clinical features suggestive of specific causes of real or apparent loss of
consciousness
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Symptom or finding:
Possible cause:
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Associated with vertigo,
dysarthria, diplopia
With arm exercise
Differences in blood pressure
or pulse in two arms
Confusion after attack >5 min
Tonic-clonic movements,
automatism, tongue biting, blue
face, epileptic aura
Frequent attacks with somatic
complaints, no organic heart
disease
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Brainstem transient ischaemic
attack (TIA)
Subclavian steal
Subclavian steal or aortic
dissection
Seizure
Seizure
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Psychiatric illness
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Important Historical Features
Questions about circumstances just prior to attack:
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Position (supine, sitting or standing)
Activity (rest, change in posture, during/after exercise, during or immediately after
urination, defaecation, cough or swallowing
Predisposing factors (eg crowded or warm places, prolonged standing, post-prandial
period) and of precipitating events (eg fear, intense pain, neck movements).
Questions about onset of attack:
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Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck
or shoulders, blurred vision
Important Historical Features
Questions about attack (eye witness)
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Way of falling (slumping or keeling over), skin colour (pallor, cyanosis, flushing),
duration of loss of consciousness, breathing pattern (snoring), movements (tonic,
clonic, tonic-clonic or minimal myoclonus, automatism) and their duration, onset of
movement in relation to fall, tongue-biting.
Questions about end of attack:
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Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin colour,
injury, chest pain, palpitations urinary or faecal incontinence
Important Historical Features
Questions about background:
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Family history of sudden death, congenital arrhythmogenic heart disease or fainting
Previous cardiac disease
Neurological history (Parkinsonism, epilepsy, narcolepsy)
Metabolic disorders (diabetes etc)
Medication (antihypertensive, antianginal, antidepressant agent, antiarrhythmic,
diuretics and QT prolonging agent(s)
Information on recurrence such as the time from the first syncopal episode and on the
number of spells
Initial Evaluation:
Cardiac v non-cardiac syncope
• Examination
- Cardiovascular, neurological
- Structural heart disease
• 12 lead ECG
- Normal: low risk of cardiac syncope
- Abnormal: independent predictor of increased
mortality.
• Lying/standing blood pressure measurement
ECG abnormalities suggesting
arrhythmic syncope
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Bifascicular block (LBBB or RBBB with LA/PFB)
Trifasicular block (RBBB, 1st degree AVB, LAD)
RBBB, LBBB
Mobitz l 2nd degree AVB
Asymptomatic sinus bradycardia <50 bpm
Pre-excited QRS complexes
Prolonged QT interval
Q waves suggesting MI
Psychogenic faints
• Bizarre presentation
• Prolonged ictus
• Lack of injury despite unheralded
‘syncope’
• Frequent attacks
• Hyperventilation/panic symptoms
• Social circumstances/context
Where to refer?
• Local syncope/T-LOC service
• Cardiology services
• Anybody with an interest!