Management of collapses ?causes in the elderly

1. Management of collapses ?causes in the elderly Dr S Samadian

3. Collapse ?cause • Blackout • Transient loss of consciousness (T-LOC)

5. Blackout • Widely understood • No implied aetiology • No implied stigma

6. Seizure Syncope Psychogenic Fit Faint Feint Collapse ?causeBlackoutT-LOC

7. ‘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)

8. Transient Loss of Consciousness(T-LOC) • ‘spontaneous transient loss of consciousness with complete recovery’ NICE TLOC scoping document 2008

9. 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%

10. 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

11. UK 2005-2006Syncope/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

13. Syncope classification • Neurocardiogenic - vasovagal -other: cough, micturition, carotid sinus • Orthostatic hypotension - dysautonomia, eg diabetes -drugs, Parkinson’s • Cardiac syncope - arrhythmias (electrical) - structural (plumbing)

14. Causes of Syncope Structural cardiac or cardiopulmonary disease: • Cardiac valvular disease • Acute myocardial infarction/ischaemia • Obstructive cardiomyopathy • Atrial myxoma • Acute aortic dissection • Pericardial disease tamponade • Pulmonary embolus/pulmonary hypertension Cerebrovascular: • Vascular steal syndrome

15. Causes of Syncope Neurally mediated reflex syncopal syndrome: • 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

16. 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: • At least 3 sec asystole (cardioinhibition – the commonest form;70-75% of cases). • Lowering of blood pressure by at least 50mmHg (vasodepression;5-10% of cases) without slowing of the heart. • A combination of cardioinhibition and vasodepression (20-25% of cases)

17. 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.

18. 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

19. Management • Lifestyle modification • Cardiac pacing with a permanent cardiac pacemaker • Surgical denervation of the carotid sinus

20. Causes of Syncope Orthostatic: • 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 • Volume depletion - Haemorrhage, diarrhoea, Addison’s Disease

21. Orthostatic Hypotension • Systolic ↓ >20 mmHg • Diastolic ↓ >10 mmHg • Prevalence 10 – 20% over 65 • Increased incidence in institutions • Measurement - supine 20” -standing 2”, 5”

22. Mechanism • Normal autonomic function • Rapid rise in concentration of noradrenaline • Alpha receptors depressed Possible explanation: - Increased rigidity of blood vessel

24. 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

25. Treatment of orthostatic hypotension • Appropriate leg and abdominal muscle exercise swimming • Pharmacological -Fludrocortisone -Vaso-constrictor – Midodrine -Desmopressin for nocturia -EPO for anaemia

26. Causes of Syncope Cardiac arrhythmias as primary cause: • Sinus node dysfunction (including bradycardia/tachycardia syndrome) • Atrioventricular conduction system disease • Paroxysmal supraventricular and ventricular tachycardia • Inherited syndrome (eg long QT syndrome, Brugada sybndrome • Implanted device (pacemaker, ICD) malfunction, drug induced proarrhythmias

27. 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

28. 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

29. Features suggestive of neurally mediated syncope • 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

30. 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

31. 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.

33. Chronic Seizures : Epilepsy Incidence 134 per 100,000 Alz 124 per 100,000 Major causes: Cerebrovascular disease 33% Dementia 11.7% Neoplasm 4% Infection 0.6% Trauma 1% No definite cause 50% The risk of epilepsy is highest in the first year after the occurrence of the CNS insult

34. Type: Partial seizures Simple partial Complex partial Secondarily generalised Generalised seizures Absence Primary generalised tonic-clonic 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 Types of Seizures

35. 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

36. Systemic disturbance - drugs - withdrawal syndromes - electrolyte imbalance - endocrine abnormalities - organ failure - porphyria CNS disorders - vascular events - head injury - infection - cerebral hypoxia Causes of Acute Symptomatic Seizures

39. Fits versus faints

40. 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

41. Symptom or finding: 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 Possible Cause: Vasovagal Vasovagal or autonomic failure Vasovagal Post-prandial Vasovagal or autonomic failure Neuralgia (glossopharyngeal or trigeminal neuralgia) Clinical features suggestive of specific causes of real or apparent loss of consciousness 1

42. Symptom or finding: 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 Possible cause: Spontaneous carotid sinus syncope Orthostatic hypotension Drug induced Cardiac syncope Tachyarrhythmia Cardiac/tachyarrhythmia Clinical features suggestive of specific causes of real or apparent loss of consciousness2

43. Symptom or finding: 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 Possible cause: Brainstem transient ischaemic attack (TIA) Subclavian steal Subclavian steal or aortic dissection Seizure Seizure Psychiatric illness Clinical features suggestive of specific causes of real or apparent loss of consciousness3

44. Important Historical Features Questions about circumstances just prior to attack: • 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: • Nausea, vomiting, abdominal discomfort, feeling of cold, sweating, aura, pain in neck or shoulders, blurred vision

45. Important Historical Features Questions about attack (eye witness) • 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: • Nausea, vomiting, sweating, feeling of cold, confusion, muscle aches, skin colour, injury, chest pain, palpitations urinary or faecal incontinence

46. Important Historical Features Questions about background: • 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

47. 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

48. ECG abnormalities suggesting arrhythmic syncope • 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

49. Psychogenic faints • Bizarre presentation • Prolonged ictus • Lack of injury despite unheralded ‘syncope’ • Frequent attacks • Hyperventilation/panic symptoms • Social circumstances/context

50. Where to refer? • Local syncope/T-LOC service • Cardiology services • Anybody with an interest!