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Loss of Conciousness

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Loss of Conciousness

  1. 1. EPISODIC IMPAIRMENT OF CONSCIOUSNESS Dr Saumya Mittal 21 April 2015
  2. 2. WHAT IS CONCIOUSNESS? Consciousness may be defined as a state of awareness of self and surroundings . Sleep, the only normal form of altered consciousness .
  3. 3.  Temporary loss of consciousness may be caused by  impaired cerebral perfusion (syncope, fainting)  cerebral ischemia,  migraine,  epileptic seizures,  metabolic disturbances,  sudden increases in intracranial pressure (ICP) or  sleep disorders.  Anxiety attacks, psychogenic seizures, panic disorder, and malingering may be difficult to distinguish from these conditions.
  4. 4. SYNCOPE Syncope refers to a symptom complex characterized by lightheadedness, generalized muscle weakness, giddiness, visual blurring, tinnitus, and gastrointestinal (GI) symptoms. The patient may appear pale and feel cold and “sweaty.” Presyncope- the sensation of an impending faint. The final common pathophysiological basis of syncope is always gradual failure of cerebral perfusion, with a reduction in cerebral oxygen availability
  5. 5. CAUSES OF SYNCOPE  Decreased cardiac output secondary to cardiac arrhythmias,  Outflow obstruction,  Hypovolemia,  Orthostatic hypotension, or  Decreased venous return  Neurological Causes  Cerebrovascular disturbances  Transient ischemic attacks (ACA/PCA)  cerebral vasospasm from migraine,  subarachnoid hemorrhage, or  hypertensive encephalopathy.  Situational syncope  cough,  micturition,  defecation,  swallowing,  Valsalva maneuver, or  diving.  Metabolic disturbances  hypoxia,  drugs,  anemia, and  Hypoglycemia. Cardiac Causes Non Cardiac Causes Sometimes no cause is found.
  7. 7.  History-  The onset of loss of consciousness is gradual or rapid e.g. cardiac arrhythmia.  Factors precipitating a simple faint are emotional stress, unpleasant visual stimuli, prolonged standing, or pain.  Position of head and neck  Duration of unconsciousness is brief (seconds to minutes).  Patient may be motionless or display myoclonic jerks,  NEVER TONIC-CLONIC MOVEMENTS.  Urinary incontinence is uncommon.  Frequency of attacks  Similar episodes- more than one type of attack.
  8. 8. AGE AND SEX DIFFERENCES  Syncope in children and young adults  frequently due to hyperventilation or  vasovagal (vasodepressor) attacks  less frequently due to congenital heart disease  benign tachycardias without underlying organic heart disease  Young females  basilar migraine  In later life  organic disease of the cerebral or cardiovascular circulation
  9. 9. HISTORY SUGGESTIVE OF CARDIAC SYNCOPE  History of palpitations or a fluttering sensation in the chest before loss of consciousness.  Generally are briefer. Syncopal episodes secondary to cardiac arrhythmias may be more prolonged.  Occur independently of position- arrhythmic.  May be precipitated by exertion*-  Arrhythmic- AV block, SA block, SVT, VT  decreased cardiac output secondary to blood flow obstruction  aortic arch disease  congenital heart disease,  Family history of sudden cardiac death-long QT-interval syndrome.
  10. 10. EXERTION INDUCED SYNCOPE  May be of cardiac etiology.  may be due to cerebrovascular disease  Pulseless disease (Takayasu disease),  Pulmonary hypertension,  Anemia,  Hypoxia,  Hypoglycemia  Situational syncope or autonomic dysfunction.
  11. 11. EXAMINATION IN SYNCOPE Examination during the episode is very informative but frequently impossible unless syncope is reproducible by a Valsalva maneuver or by recreating the circumstances of the attack, such as by position change.
  12. 12. EXAMINATION  Examination  Pulse- weak and often slow.  Breathing- shallow  Blood pressure- low.  Fainting episode corrects itself by the patient becoming horizontal  normal colour returns,  breathing becomes more regular,  pulse and blood pressure return to normal  patient experiences some residual weakness  UNLIKE THE POSTICTAL STATE, CONFUSION, HEADACHES, AND DROWSINESS ARE UNCOMMON  nausea when the patient regains consciousness.
  13. 13.  Normally, with standing, the systolic blood pressure and the pulse rate may increase.  An orthostatic drop in blood pressure greater than 15 mm Hg may suggest autonomic dysfunction.  Cardiac murmurs and abnormalities of the heart sounds.  Murmurs- AS, subaortic stenosis, or mitral valve origin.  Posture-related murmur- atrial myxoma.  Systolic click- MVP.  A pericardial rub- pericarditis  Heart rate  HR> 140 bpm- ectopic cardiac rhythm  HR< 40 bpm- complete atrioventricular (AV) block.  Heart disease as a cause of syncope is more common in the elderly patient
  14. 14.  Assess blood pressure in both arms when suspecting  cerebrovascular disease,  subclavian steal, or  Takayasu arteritis.  Carotid pulse and auscultation of the neck  AS may cause delayed carotid upstroke.  Carotid, ophthalmic, and supraclavicular bruits suggest underlying cerebrovascular disease.
  15. 15. CAROTID SINUS MASSAGE If performed, do in properly controlled conditions with ECG and BP monitoring. The response to carotid massage is either vasodepressor, cardioinhibitory, or mixed.
  16. 16. WHEN CAROTID SINUS MASSAGE  Carotid sinus massage sometimes terminates a supraventricular tachycardia (but not VT)- not advisable because of the risk of cerebral embolism from atheroma in the carotid artery wall.  Carotid massage should be avoided in patients with suspected cerebrovascular disease.  Carotid sinus massage may be useful in older patients suspected of having carotid sinus syncope- 25% of asymptomatic persons may have some degree of carotid sinus hypersensitivity.  Syncope in certain patients can be induced by unilateral carotid massage or compression or by partial occlusion (usually atherosclerotic) of the contralateral carotid artery or a vertebral artery or by the release of atheromatous emboli. Because of these risks, carotid artery massage is contraindicated.
  18. 18. AV BLOCK  The most common cause of arrhythmic cardiac syncope.  Complete AV block occurs primarily in elderly patients.  Heart sounds related to atrial contractions may be audible.  CF  slow-collapsing pulse  elevation of JVP, sometimes with cannon waves.  first heart sound is of variable intensity  ECG  independence of atrial P waves and  ventricular QRS complexes..
  19. 19. STOKES-ADAMS ATTACK  Disturbances of consciousness occurring in association with a complete AV block.  Onset is sudden,  Visual, sensory, and perceptual premonitory symptoms may be experienced.  Pulse disappears and no heart sounds are audible.  The patient is pale  If standing, falls down, often with resultant injury.  If the attack is sufficiently prolonged, respiration may become labored, and urinary incontinence and clonic muscle jerks may occur.  Prolonged confusion and neurological signs of cerebral ischemia may be present.  Regaining of consciousness generally is rapid.  ECG-  ventricular standstill  ventricular fibrillation or tachycardia
  20. 20. SINOATRIAL BLOCK  CF- dizziness, lightheadedness, and syncope.  Most frequent in the elderly.  O/E- Palpitations, pale.  Pulse may be regular between attacks. During an attack, the pulse may be slow or irregular, and any of a number of rhythm disturbances may be present  Other conduction disturbances, and certain drugs (e.g., verapamil, digoxin, beta-blockers) may further impair SA node function.
  21. 21. PAROXYSMAL TACHYCARDIA  Supraventricular tachycardias include  atrial fibrillation with a rapid ventricular response,  atrial flutter, and  the Wolff- Parkinson-White syndrome.  Suddenly reduce cardiac output.  Ventricular tachycardia or ventricular fibrillation may result in syncope if the heart rate is sufficiently fast and if the arrhythmia lasts longer than a few seconds.  Patients generally are elderly.  Evidence of underlying cardiac disease.
  22. 22. LONG QT SYNDROME  May have cardiac-only phenotype or may be associated with congenital sensorineural deafness in children. Manifests in adults as epilepsy.  Episodes begin in the first decade of life, but onset may be much later.  Exercise may precipitate an episode of cardiac syncope.  Long QT syndrome may be congenital or acquired  cardiac ischemia,  mitral valve prolapse,  myocarditis,  electrolyte disturbances  as well as many drugs.
  23. 23. SHORT QT SYNDROME  CF- highly variable (asymptomatic- to recurrent syncope to sudden death).  The age at onset often is young, and affected persons frequently are otherwise healthy.  A family history of sudden death indicates a familial short QT syndrome inherited as an autosomal dominant mutation.  The ECG demonstrates a short QT interval and a tall and peaked T wave, and electrophysiological studies may induce ventricular fibrillation.
  24. 24. BRUGADA SYNDROME  Syncope as a result of ventricular tachycardia or ventricular fibrillation.  The ECG demonstrates an  incomplete RBBB- leads V1 and V2,  ST-segment elevation in the right precordial leads.
  25. 25. DECREASED CARDIAC OUTPUT  Syncope may occur as a result of a sudden and marked decrease in cardiac output.  Congenital Causes-  Tetralogy of Fallot  cyanotic heart disease  Acquired Causes-  Ischemic heart disease and myocardial infarction (MI),  aortic stenosis,  idiopathic hypertrophic subaortic stenosis,  pulmonary hypertension and other causes of obstruction of pulmonary outflow,  atrial myxoma, and  cardiac tamponade  Exercise-induced or effort syncope e.g. aortic or subaortic stenosis  Exercise induced syncope and exercise-induced cardiac arrhythmias may be related.
  26. 26.  Secondary to conditions causing in inflow obstruction or reduced venous return  Superior and inferior vena cava obstruction,  tension pneumothorax,  constrictive cardiomyopathies,  constrictive pericarditis,  cardiac tamponade,  aortic dissection,  hypovolemia  Acute blood loss- GI tract bleeding  Dehydration may cause faintness and weakness, but true syncope is uncommon except when combining dehydration and exercise.
  27. 27. THE COMMON FAINT-VASOVAGAL/ VASODEPRESSOR SYNCOPE  Recurrent  Affect 20% to 25% of young people  Occur in relation to emotional stimuli  Certain circumstances  hot crowded room,  tired or hungry person  upright or sitting posture.  Venipuncture,  sight of blood,  sudden painful or traumatic experience  Presyncopal symptoms  lethargy and fatigue,  nausea,  weakness,  sensation of an impending faint,  yawning, and  blurred vision.  Transitory fall in BP  Bradycardia  LoC+Loss of postural tone  Signs of autonomic hyperactivity  pallor,  diaphoresis,  nausea, and  dilated pupils.
  28. 28.  After recovery, patients may have persistent pallor, sweating, and nausea; usually is no confusion or headache, although weakness is frequent.  If they get up too quickly, they may black out again.  If the period of cerebral hypoperfusion is prolonged  urinary incontinence and a few clonic movements may occur (convulsive syncope).
  29. 29. REFLEX CARDIAC ARRHYTHMIAS  A hypersensitive carotid sinus- syncope in elderly men. Syncope may result from a reflex sinus bradycardia, sinus arrest, or AV block; peripheral vasodilatation with a fall in arterial pressure; or a combination of both.  Carotid sinus syncope-  initiated by wearing a tight collar or by carotid sinus massage on clinical examination.  Patient usually is upright  Duration of the loss of consciousness- few minutes.  On regaining consciousness, the patient is mentally clear.
  30. 30.  Glossopharyngeal neuralgia-  Rare syndrome  Intense paroxysmal pain in the throat and neck  Initiated by swallowing, chewing, speaking, laughing, coughing, shouting, sneezing, yawning, or talking.  Bradycardia or asystole, severe hypotension  If prolonged, seizures.  Pain always precedes the loss of consciousness.  Rarely, cardiac syncope may be due to bradyarrhythmias consequent to vagus nerve irritation caused by esophageal diverticula, tumors, and aneurysms in the region of the carotid sinus or by mediastinal masses or gallbladder disease.
  31. 31. ORTHOSTATIC HYPOTENSION  Failure of autonomic factors compensating upright posture.  Drugs that impair SNS.  Diuretics,  Antihypertensive  nitrates,  vasodilators,  sildenafil,  CCBs,  l-dopa,  alcohol,  TCAs  Rarely  subacute combined degeneration,  syringomyelia,  spinal cord lesions may damage the descending sympathetic pathways.  Primary autonomic failure  Shy-Drager syndrome  Riley-Day syndrome.  ANS Neuropathies  diabetes mellitus,  amyloidosis,  Guillain-Barré syndrome,  AIDS,  chronic alcoholism,  hepatic porphyria,  beriberi, and  autoimmune subacute autonomic neuropathy and small fiber neuropathies.
  32. 32. CEREBROVASCULAR ISCHEMIA  Syncope may result from reduction of cerebral blood flow in either the  carotid system- loss of consciousness, lightheadedness, giddiness, and a sensation of an impending faint.  vertebrobasilar system- loss of consciousness (dizziness, lightheadedness, drop attacks without loss of consciousness). Certain head movements can cause syncope secondary to vertebrobasilar arterial ischemia.  Underlying condition  Atherosclerosis  reduction of cerebral blood flow due to cerebral embolism,  mechanical factors in the neck (e.g., severe osteoarthritis), and  arteritis (e.g., Takayasu disease or cranial arteritis).
  33. 33.  Subclavian steal syndrome- upper extremity exercise resulting in diversion of cerebral blood flow to the peripheral circulation.  Basilar artery migraine/SAH- vasospasm causes syncope.  Takayasu disease-  major occlusion of carotid and vertebrobasilar systems.  Pulsations and BP are not recordable.  Occur with mild or moderate exercise and with certain head movements.
  34. 34. METABOLIC DISORDERS  The abruptness of onset of loss of consciousness depends on the acuteness and reversibility of the metabolic disturbances e.g. hypoglycemia comes slowly.  Symptoms are unrelated to posture but may increase with exercise.  May be unrelated to any significant change in BP or PR.  Susceptibility factors are present e.g. cardiac or pulmonary disease in anoxia.  Psychogenic origin- e.g. hyperventilation-induced syncope  Metabolic disturbances include  hypoglycemia,  anoxia,  hyperventilation-induced alkalosis,  hypoadrenalism,  calcium, magnesium, potassium metabolism,  chronic anemia or certain hemoglobinopathies
  35. 35. SITUATIONAL SYNCOPE  Cough (tussive syncope)- blockage of venous return by raised intrathoracic pressure.  Micturition syncope- peripheral vasodilatation caused by the release of intravesicular pressure and bradycardia. The relative peripheral vasodilatation from recent alcohol use and a supine sleeping position may contribute  Weight-lifting syncope.  Diving and the postprandial state syncope  CONVULSIVE SYNCOPE is an episode of syncope of any cause that is sufficiently prolonged to result in a few clonic jerks; the other features typically are syncopal and should not be confused with epileptic seizures.
  36. 36. INVESTIGATION The diagnostic tests depend on initial DD
  37. 37. SEIZURES Epileptic seizures cause sudden, unexplained loss of consciousness in a child or an adult.
  38. 38. HISTORY AND PHYSICAL EXAMINATION The most definitive way to diagnose epilepsy and the type of seizure is clinical observation of the seizure.
  39. 39.  Family history, birth history, H/O CNS infection, head trauma, and previous febrile seizures.  Complete description of the episode.  Inquire about any  warning before the event,  possible precipitating factors, and  other neurological symptoms.  Important considerations are the  age at onset- GTCS and CPS may begin at any age,  frequency, and  diurnal variation of the events.  Postictal confusion suggests CPS, GTCS.
  40. 40.  The neurological examination may reveal an underlying structural disturbance responsible for the seizure disorder.  Birth-related trauma- asymmetry of physical development  Cranial bruits may indicate an AVM  SOLs- papilledema, focal motor, sensory, or reflexes.  In the pediatric age group, mental retardation occurs in association with birth injury or metabolic defects.  The skin should be examined for abnormal pigment changes and other dysmorphic features characteristic of some of the neurodegenerative disorders.
  41. 41. ABSENCE SEIZURES  Onset-ages of 5 and 15 years.  Family history of seizures is present in 20% to 40%.  Abrupt, brief episode of decreased awareness without any warning, aura, or postictal symptoms.  A simple absence seizure is characterized clinically only by an alteration of consciousness. Lasts 10 to 15 seconds, but it may be shorter or as long as 40 seconds.Resumption of activity immediately.  Complex absence seizure- alteration of consciousness and other signs such as minor motor automatisms.  Hyperventilation for 3 to 4 minutes induces absence seizure.
  42. 42. TONIC-CLONIC SEIZURES  Characterized by motor activity and LoC.  Autonomic changes may be present.  Injury may result from a fall or tongue biting.  In the postictal period, consciousness returns slowly, and the patient may remain lethargic and confused for a variable period.  No warning or aura/few myoclonic jerks may occur.  The seizure begins with a tonic phase- sustained muscle contraction lasting 10 to 20 seconds.  Following this phase is a clonic phase that lasts approximately 30 seconds and is characterized by recurrent muscle contractions.
  43. 43. COMPLEX PARTIAL SEIZURES  First manifestation may be an alteration of consciousness  Frequently aura or warning symptom present.  Lasts 1 to 3 minutes but may be shorter or longer.  It may become generalized and evolve into a tonic- clonic convulsion.  Automatisms may occur-continuation of the patient’s activity, or they may be new motor acts.  Rarely, patients with complex partial seizures have drop attacks; in such cases, the term temporal lobe syncope often is used.
  44. 44. PSEUDOEPILEPTIC SEIZURES  Paroxysmal episodes of altered behavior that superficially resemble epileptic seizures (GTCS).  However, as many as 40% of patients with pseudo- or nonepileptic seizures also experience true epileptic seizures.  Generally abrupt onset  Do not occur during sleep.  Motor activity is uncoordinated  Urinary incontinence and physical injury are uncommon.  Pelvic thrusting is common.  Ictal eye closing is common in nonepileptic seizures, whereas the eyes tend to be open in true epileptic seizures.
  45. 45.  Seizure types that must be distinguished from syncope include  Orbito-frontal complex partial seizures, which can be associated with autonomic changes, and  Complex partial seizures that are associated with sudden falls and altered awareness, followed by confusion and gradual recovery (temporal lobe syncope).
  46. 46. BREATH-HOLDING SPELLS  Start at 6 to 28 months of age  Disappear by 5 or 6 years of age.  Breath-holding spells occur several times/day.  Cyanotic Breath Holding Spells-  Trigger -sudden injury or fright, anger, or frustration.  Provoked child cries vigorously.  Then stops breathing in expiration  Develops cyanosis rapidly.  Unconscious due to hypoxia.  Stiffening, a few clonic movements, and urinary incontinence occasionally.  History differentiates from seizures.  Neurological examination and the EEG are normal.  Pallid Breath Holding Spell  Provocation is mild painful injury or a startle.  Cries initially  Becomes pale  Then unconscious.  Stiffening, clonic movements, and urinary incontinence may rarely occur.  Loss of consciousness is secondary to  excessive vagal tone,  Resulting bradycardia  Subsequent cerebral ischemia.

Notas do Editor

  • Pathological reflexes may be elicitable