Syncope

Assessment and Management of Syncope

1. SYNCOPE By, Sreelekshmi J Intern KVG Dental College

2. CONTENTS Definition Classification Predisposing factors Prevention Dental Consideration Clinical manifestations Pathophysiology Investigations Management References

3. DEFINITION Syncope is defined as sudden and transient loss of consciousness which is secondary to period of cerebral ischemia. The term “syncope” is derived from the Greek word which means “to cut short” or “interrupt.”

4. Syncope and faintness occurs in upright posture except ‘Stokes-Adams’ attack in which syncope occurs in sitting and standing position . A syncopal prodrome ( presyncope ) is common, although loss of consciousness may occur without any warning symptoms. Typical presyncopal symptoms include dizziness, lightheadedness or faintness, weakness, fatigue and visual and auditory disturbances.

5. CLASSIFICATION Neurally mediated reflex syncope Vasovagal syncope Carotid sinus syndrome Situational faints (e.g., cough, defecation, excessive heat, micturition, pain , prolonged upright posture, sneeze, swallow, venipuncture , volume depletion) Other (e.g ., weightlifting , post-prandial)

6. Orthostatic syncope Secondary autonomic failure syndromes (e.g., diabetic neuropathy, amyloid neuropathy , drugs and alcohol) Volume depletion (e.g., hemorrhage , diarrhea , Addison’s disease) Primary autonomic failure syndromes (e.g., pure autonomic failure, multiple system atrophy, Parkinson’s disease with autonomic failure) Postural intolerance syndromes (e.g., postural orthostatic tachycardia syndrome ) in which syncope occurs occasionally, probably of reflex origin

7. Cardiac arrhythmias as primary cause Implanted device ( pacemaker) malfunction Structural cardiac or cardiopulmonary disease Acute myocardial infarction/ischemia Cardiac valvular disease Pulmonary embolus/pulmonary hypertension Pericardial disease/tamponade Cerebrovascular

8. PREDISPOSING FACTORS In the dental setting, stress is the primary cause in most cases of unconsciousness . The sudden loss of consciousness (syncope) that occurs during venipuncture or the intraoral injection of a local anesthetic is a classic example of vasodepressor syncope.

9. Impaired physical status is another factor working to increase the likelihood of syncope. When patients with impaired physical status are exposed to undue stress, whether physiologic or psychological, the chances are even greater that they may react adversely to the situation. For example, persons with underlying cardiovascular disease may respond with sudden cardiac arrest secondary to acute cardiac dysrhythmias, which are precipitated by the same physiologic stress that may cause vasodepressor syncope in a healthy individual.

10. A third factor associated with loss of consciousness is the administration or ingestion of drugs. The three major categories of drugs used in dentistry are analgesics ( nonopioids , including nonsteroidal antiinflammatory drugs; opioid analgesics; and local anesthetics ), antianxiety agents (anxiolytics and sedative-hypnotics), and antibiotics.

11. Drugs in the first two categories are CNS depressants and therefore produce alterations in the level of consciousness (e.g., sedation) or the loss of consciousness. Some of these drugs, primarily the opioid agonists, predispose the ambulatory dental patient to orthostatic (postural) hypotension. Opioids and other CNS-depressant drugs, if administered in larger doses, can induce the loss of consciousness as the CNS is progressively depressed to the point at which consciousness is lost.

12. PREDISPOSING FACTORS FOR VASOVAGAL SYNCOPE PSYCHOGENIC FACTORS NONPSYCHOGENIC FACTORS Fright Anxiety Emotional stress Receipt of unwelcome news Pain, especially sudden and unexpected Sight of blood or surgical or other dental instruments (e.g., local anesthetic syringe) Erect sitting or standing posture Hunger from dieting or a missed meal Exhaustion Poor physical condition Hot, humid, crowded environment Male gender(Age between 16 and 35 years)

13. PREDISPOSING FACTORS FOR POSTURAL HYPOTENSION Drug administration and ingestion Antihypertensives especially sodium-depleting diuretics, calcium channel blockers. Sedatives and tranquilizers Antiparkinsonism drugs like levodopa. Phenothiazines like chlorpromazine, thioridazine . Positional changes should be made slowly and carefully in patients receiving these drugs

14. Prolonged recumbency and convalescence Patients may remain recumbent in the dental chair for treatment lasting as long as 2 or 3 hours. In these circumstances, postural hypotension may develop when the dental chair is returned quickly to the upright position or the patient stands.

15. Inadequate postural reflex Healthy young people may faint when forced to stand motionless for prolonged periods, such as during school assemblies, religious services, or parades. Syncope also can develop when a patient is seated upright in the dental chair for a prolonged period. This situation is more likely to occur in a hot and humid environment, which produces concomitant peripheral vasodilation.

16. Pregnancy S upine hypotensive syndrome of pregnancy occurs late in the third trimester if the woman remains in the supine position for more than 3 to 7 minutes. Age The incidence of postural hypotension shows a very definite increase with increasing age and proves to be a major problem in the aged population. Chronic postural hypotension (Shy- Drager syndrome )

17. Venous defects in the legs Postural hypotension also occurs in patients with varicose veins and other vascular disorders of the legs. These disorders permit excessive pooling of blood in these patients’ legs . Addison’s disease Postural hypotension frequently occurs in patients with chronic adrenocortical insufficiency. The doctor may manage this condition through the administration of corticosteroids.

18. PREVENTION Prevention of vasodepressor syncope is directed at eliminating factors that predispose an individual to faint. Adequate air conditioning in the dental office eliminates the heat factor. Patient hunger, a result of dieting or a missed meal before the dental appointment, also should be considered. All patients, but especially those who are anxious, should be requested to eat a light snack or meal before their dental appointment to minimize the risk of developing hypoglycemia in addition to a psychogenic response.

19. Positioning: The risk of vasodepressor syncope is greatly increased in an apprehensive patient who is either standing or seated upright during treatment. Today, patients will be placed in a supine or semisupine (30- to 45-degree) position, a practice that has minimized the occurrence of vasodepressor syncope during dental treatment.

20. Anxiety Relief Each potential patient must be recognised and evaluated for the presence of dental anxiety. If the patient is overly anxious, dental treatment should be modified to minimize or to eliminate it . The inclusion of written anxiety questionnaire in the medical history questionnaire is worthwhile.

21. DENTAL CONSIDERATION Follow anxiety reduction protocol. Premedicate the patient with hypnotics for a relaxed sleep the night before the surgery. Premedicate the patient with sedatives on the day of surgery. Schedule the surgery in the morning. Minimise the patient waiting time. Consider psychosedation during surgery.

22. Administer adequate pain control measures during surgery. Reduce the length of the appointment. Avoid any anxiety during surgery. Follow-up postoperative pain and anxiety control. Effective postoperative analgesics.

23. CLINICAL MANIFESTATIONS The clinical manifestations of vasodepressor syncope c an be grouped into 3 definite phases: Presyncope Syncope Postsyncope (recovery period)

24. Presyncope EARLY SYMPTOMS LATE SYMPTOMS Feeling of warmth Loss of color ; pale or ashen- gray skin tone Heavy perspiration (diaphoresis) Reports of “feeling bad” or “feeling faint” Nausea Blood pressure at baseline level or slightly lower Tachycardia Pupillary dilation Yawning Hyperpnea Cold hands and feet Hypotension Bradycardia Visual disturbances Dizziness Loss of consciousness

25. Syncope Breathing may become irregular, jerky, and gasping; become quiet, shallow, and scarcely perceptible; or cease entirely (respiratory arrest or apnea ). The pupils dilate, and the patient takes on a deathlike appearance. Bradycardia, which develops at the end of the presyncopal phase, continues. Decreased blood pressure.

26. The pulse becomes weak and thready . Convulsive movements and muscular twitching of the hands, legs, or facial muscles are common when patients lose consciousness and become hypoxic (a result of cerebral hypoxia/anoxia), even for periods as short as 10 seconds.

27. Postsyncope In the postsyncopal phase the patient may demonstrate pallor, nausea, weakness, and sweating, all of which can last from a few minutes to several hours. Occasionally, symptoms persist for 24 hours . During the immediate postsyncopal phase, the patient may experience a short period of confusion or disorientation.

28. The heart rate, which is depressed, also returns slowly toward the baseline level, and the pulse becomes stronger . In addition, a point worth stressing is that once a patient loses consciousness, the tendency for that patient to faint again may persist for many hours if the patient assumes a sitting position or stands too soon or quickly.

29. PATHOPHYSIOLOGY Mechanism Clinical example Inadequate delivery of blood or O 2 to the brain Acute adrenal insufficiency Hypotension Orthostatic hypotension Vasodepressor syncope Systemic or local metabolic deficiencies Acute allergic reaction Drug ingestion and administration Nitrites and nitrates Diuretics Sedatives, opioids Local anaesthetics Direct or reflex effects on nervous system Cerebrovascular accident Convulsive episodes Psychic mechanisms Emotional disturbances Hyperventilation Vasodepressor syncope In his classic test on fainting, Engle divided the mechanisms that produce syncope into four categories:

30. PATHOPHYSIOLOGY OF VASOVAGAL SYNCOPE Anxiety Increased release of Catecholamines Decreased Peripheral Vascular Resistance Pooling of Blood in the peripheries and fall in arterial blood pressure Compensatory mechanisms

31. Increased heart rate, rapid breathing, pallor & perspiration Decompensation Hypotension, Reduced cerebral blood flow Syncope

32. INVESTIGATIONS Echocardiography is likely the most useful test to help risk stratify patients as it can identify those that have structural heart disease including valvular abnormalities, wall motion abnormalities and pericardial effusions. Hematologic studies or advanced imaging, including computed tomography scans, can be ordered based on the history and exam . Electrolytes and hematocrit can be assessed in a patient with a history of diarrhoea and vomiting or gastrointestinal hemorrhage respectively . Tilt table testing in unexplained syncope in high-risk settings or with recurrent faints in the absence of heart disease.

33. San Francisco Syncope Rule CHESS C – Congestive Heart Failure history H – Hematocrit < 30% E – ECG (Abnormal) S – Shortness of breath S – Systolic Blood pressure<90mm of Hg. Patients that meet any of these 5 criteria are predicted to be at higher risk for adverse outcomes at 7 or 30 days. Adverse outcomes include death, myocardial infarction, arrhythmia, pulmonary embolism, stroke, subarachnoid hemorrhage , or significant hemorrhage .

34. MANAGEMENT The main aim of treatment of syncope is to avoid fall or injury during an attack. Includes management of 4 separate stages of syncope: presyncope , syncope , delayed recovery, and post-syncope .

35. Presyncope STEP-1 (POSITION): - As soon as presyncopal signs and symptoms are noted, the dental procedure is terminated and the patient placed into the supine position with legs slightly elevated. - This position change usually halts the progression of symptoms. - Muscle movement also helps increase the return of blood from the periphery. - If patients can move their legs vigorously, they are less likely to experience significant peripheral pooling of blood, minimizing the severity of the reaction.

36. STEP-2 : C  A  B -CIRCULATION  AIRWAY  BREATHING - Because the victim is still conscious in the presyncopal period and can speak, C, A and B are assessed as being adequate . STEP-3 : D(DEFINITIVE CARE): - O 2 may be administered through use of a full-face mask, or an ammonia ampule may be crushed under the patient’s nose to help speed recovery

37. An aromatic ammonia vaporole is crushed between the rescuer’s fingers and held near the patient’s nose to stimulate movement.

38. Syncope Basic management recommended for all unconscious patients: P → C → A → B . Step 1: Assessment of consciousness. - The patient (victim) suffering vasodepressor syncope demonstrates a lack of response to sensory stimulation . Step 2: Activation of the dental office emergency system. - Office team members should perform their assigned duties.

39. Step 3: Position - The first and most important step in the management of syncope is the placement of the victim into the supine position. - A slight elevation of the legs helps increase the return of blood from the periphery. - Failure to place the victim in the supine position may result in death or permanent neurologic damage secondary to prolonged cerebral ischemia

40. Placement of unconscious patient in the supine position with feet elevated slightly.

41. Step 4: C → A → B (basic life support, as needed). -The victim must be assessed immediately and a patent airway ensured. - In most instances of vasodepressor syncope, the head tilt–chin lift procedure successfully establishes a patent airway. -To assess circulation, the carotid pulse is palpated.

42. Airway patency may be obtained through use of the head tilt–chin lift method.

43. Step 5: D (DEFINITIVE CARE). A dministration of O 2 . - O 2 may be administered to the syncopal or postsyncopal patient at any time during the episode . Monitoring of vital signs. - Vital signs, including blood pressure, heart rate, and respiratory rate, should be monitored.

44. Additional procedures . Loosening of binding clothes such as ties, collars and belts. Use of a respiratory stimulant, such as aromatic ammonia. If bradycardia persists, an anticholinergic, such as atropine, may be considered for administration either intravenously or intramuscularly . Administration of “sugar” in the form of orange juice or a nondiet soft drink may be beneficial in case of hypoglycemia .

45. Delayed Recovery If the victim does not regain consciousness after the previous steps have been performed or does not recover completely in 15 to 20 minutes, a different cause for the syncopal episode should be considered and the emergency medical services (EMS) system activated. Possible causes of delayed recovery from syncope include: seizure, cerebrovascular accident (stroke), transient ischemic attacks (TIA), cardiac dysrhythmias, and hypoglycemia .

46. Postsyncope After recovery, patients should not undergo additional dental treatment the remainder of that day. B ody may require up to 24 hours to return to its normal state. Prior to dismissal of the patient from the dental office, the doctor should determine the primary precipitating event and any other factors (e.g., hunger or fear) that might have contributed to it . Arrangements must be made for a responsible adult escort(e.g., family member) to take the patient home.

47. REFERENCES Medical Emergencies in the Dental Office – Stanley F. Malamed Textbook of Oral & Maxillofacial Surgery – S M Balaji Internet