VASOVAGAL SYNCOPE / SYNDROME • SYNCOPE is defined as temporary loss of consciousness with loss of postural tone but with spontaneous recovery. • VASOVAGAL SYNCOPE referred commonly as fainting which is a self limiting process if not managed correctly can be life threatening. • A most common emergency in dental office associated with all forms of dental care like tooth extraction, injections, venipuncture. PREDISPOSING FACTORS FOR VASODEPRESSOR SYNCOPE PSYCHOGENIC 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) • • • • • NON-PSYCHOGENIC FACTORS Erect sitting or standing posture Hunger from dieting or a missed meal Exhaustion Poor physical condition Hot, humid, crowded environment CLINICAL MENIFESTATIONS The clinical manifestations of vasodepressor syncope can be grouped into three definite phases: pre-syncope, syncope, & post-syncope (recovery period). Pre-syncopal signs and symptoms: EARLY SYMPTOMS • Feeling of warmth • Pale or ashen-gray skin tone • Heavy perspiration • Reports of "feeling faint" • Nausea • BP at baseline level/slightly lower • Tachycardia LATE SYMPTOMS • • • • • • • • • Pupillary dilation Yawning Hyperapnea Cold hands and feet Hypotension Bradycardia Visual disturbances Dizziness Loss of consciousness PATHOPHYSIOLOGY • Vasodepressor syncope is most commonly precipitated by a decrease in cerebral blood flow below a critical level and usually is characterized by a sudden drop in blood pressure and a slowing of the heart rate. Management of vasodepressor Assess consciousness (lack of response to sensory stimulation) Activate office emergency system Position patient supine with feet elevated slightly 1 A B —> C—Assess and open airway; assess airway patency , assess circulation and breathing D—Definitive care: Administer O2 Monitor vital signs Perform additional procedures: Administer aromatic ammonia (vaporole) Administer atropine if bradycardia persists Do not panic! ( postsyncopal recovery) Postpone further dental treatment Delayed recovery activate emergency medical service HYPERVENTILATION • Hyperventilation or over-breathing is the state of breathing faster and/or deeper than necessary. Results from a psychological state such as a panic attack from a physiological condition like metabolic acidosis or can be brought about voluntarily. SYMPTOMS • Hyperventilation cause symptoms such as numbness or tingling in the hands, feet and lips, light-headedness, dizziness, headache, chest pain, slurred speech, nervous laughter, and sometimes fainting. • Such effects are not precipitated by the sufferer's lack of oxygen or air. Rather, hyperventilation itself reduces the carbon dioxide concentration of the blood to below its normal level because one is expiring more carbon dioxide than being produced in the body, thereby raising the blood's pH value (making it more alkaline), initiating constriction of the blood vessels which supply the brain, and preventing the transport of oxygen and other molecules necessary for the function of the nervous system. CAUSES • Stress or anxiety commonly are causes of hyperventilation; this is known as hyperventilation syndrome. So dental treatment is one of the causes. • Hyperventilation can also be brought about voluntarily, by taking many deep breaths in rapid succession. • Hyperventilation can also occur as a consequence of various lung diseases, head injury, or stroke. • In case of metabolic acidosis, the body uses hyperventilation as a compensatory mechanism to decrease acidity of the blood. • In the setting of diabetic ketoacidosis, this is known as Kussmaul’s breathing -characterized by long, deep breaths. (increase in both rate and depth of respiration) HYPERPNEA VS HYPERVENTILATION • Hyperventilation is an increase in both rate and depth of respiration while as hyperpnea is increase in depth only. MANAGEMENT The management of hyperventilation is directed at correcting the respiratory problem and reducing the patient's anxiety level. Step 1: Termination of the dental procedure. The presumed cause of the episode (e.g., a syringe, dental hand piece, or pair of forceps) should be removed from the patient's line of vision. Step 2: P Position. The hyperventilating patient is conscious and will exhibit varying degrees of difficulty in breathing. The preferred position for this patient is usually upright. The supine position is normally uncomfortable for such patients because of the diminished ventilatory volume caused by the impingement of the abdominal viscera on the diaphragm. Step 3: A-B-C (airway – breathing - circulation) Basic life support as needed. Hyperventilating individuals rarely require basic life support. Such victims are conscious and breathing efficiently (indeed, they are over-ventilating), and the heart is quite functional. Step 4: D Definitive care Step 4a: Removal of materials from the mouth. All foreign objects such as a rubber dam, clamps and partial dentures should be removed from the patient's mouth and any tight bindings {e.g., a tight collar or tie} which may restrict breathing should be loosened. Step 4b: Calming of the patient. • Reassure the patient that all is well in a calm and relaxed manner. • Attempt to help the patient regain control of their breathing by speaking calmly. • Have the patient breathe slowly and regularly at a rate of about 4 to 6 breaths per minute, if possible. This will allow the PaCO2 to increase, reducing the pH of the blood to near normal and eliminating (slowly) any symptoms produced by respiratory alkalosis. Step 4c: Correction of respiratory alkalosis. • When the preceding steps are ineffective, helping the patient to increase their blood's PaCO2 level is our next concern. The patient may be instructed to breathe gaseous mixture of 7% CO2 and 93% O2, which is supplied in compressed gas cylinders but is highly unlikely to be available in a dental office. So the patient will be told to rebreathe exhaled air, which contains an increased concentration of CO2. • In addition to elevating PaCO2 levels, the warm exhaled air against their cold hands will warm the patient, alleviating one of the more frightening symptoms of hyperventilation. Step 4d: Drug management • Parenteral drug administration may be necessary to relieve the patient's anxiety and slow the rate of breathing. The drugs of choice in this situation are the benzodiazepines, diazepam, or midazolam. If possible, the drug is administered intravenously, in which case it is titrated (at 1 mL per minute) until the patient's anxiety is visibly reduced & the patient is able to control breathing. • When the intravenous route is unavailable, 10 mg diazepam or 3—5 mg midazolam may be administered intramuscularly. Midazolam is preferred because diazepam is not water soluble and burns when injected intramuscularly. It must be emphasized that drug therapy for the termination of hyperventilation is rarely required. Step 5: Subsequent dental treatment. • Once the episode of hyperventilation is ended, with all clinical signs and symptoms resolved, dental treatment may continue at this time if both the doctor and the patient are comfortable in doing so. However, subsequent dental treatment should be modified and the stress reduction protocol consulted to prevent a recurrence of hyperventilation. ALLERGY • Allergy is a hypersensitive state acquired through exposure to a particular allergen. • Allergic reactions can be mild to severe life threatening. • Allergic reactions can be immediate within seconds and delayed as long as 48 hours. • Allergy to local anesthetics does occur, but its incidence has decreased dramatically since the introduction of amide anesthetics. • Hypersensitivity to the ester-type local anesthetics is much more frequent: Procaine, Propoxycaine, benzocaine, tetracaine and procaine penicillin G and procainamide. • Allergy to one amide local anesthetic does not preclude the use of other amides, because cross allergenicity does not occur. But with ester type local anesthetic allergy, cross allergenicity does occur, thus all ester type local anesthetics are contraindicated with a documented history of ester allergy. • Methylparaben (BACTERIOSTATIC), Sodium metabisulfite (ANTIOXIDANT for vasoconstrictor), latex, topical anesthetics of esters benzocaine, tetracaine cause allergy. CLASSIFICATION OF ALLERGIC DISEASES TYPE MECHANISM ANTIBODY REACTION CLINICAL EXAMPLE CELL TYPE TIME • TYPE-I Anaphylactic (Immediate) IgE Seconds – Minutes Anaphylaxis Drugs, Insect venom Atopic bronchial asthma Allergic rhinitis, Urticaria Angioedema • TYPE-II Cytotoxic IgG, IgM (Antimembrane) ---- Transfusion reactions Autoimmune hemolysis Hemolytic anemia Certain drug reactions CLASSIFICATION OF ALLERGIC DISEASES TYPE MECHANISM ANTIBODY REACTION CLINICAL EXAMPLE CELL TYPE TIME • TYPE-III Immune complex (Serum sickness) IgG 6 – 8 hr • TYPE-IV Cell mediated (Delayed) IgG 48 hr Serum sickness Lupus nephritis Acute viral hepatitis Allergic contact dermatitis, Infectious granulomas Tissue graft rejection Chronic hepatitis TYPE I, TYPE II, TYPE III = Immediate reactions TYPE IV = Delayed reaction GENERAL ANAPHYLAXIS PROGRESSION & ITS SIGNS SYMPTOMS 1. Early Phase: Skin reactions 2. Gastrointestinal and Genitourinary disturbances (related to smooth muscle spasm) 3. Respiratory system symptoms 4. Cardiovascular system symptoms SKIN REACTION [early phase] • • • • • • • • • Patient complains of feeling sick. Intense itching (pruritus). Flushing (erythema). Hives (Urticaria) over the face and upper chest. Nausea and vomiting. Conjunctivitis. Rhinitis Increased nasal mucous secretion. Pilomotor erection (feeling of hair standing on end) Gastrointestinal & Genitourinary disturbances (related to smooth muscle spasm) • Severe abdominal cramps. • Nausea and vomiting. • Diarrhea. • Fecal and urinary incontinence. RESPIRATORY SYMPTOMS • Sub-sternal tightness or pain in chest. • Cough may develop. • Wheezing (BRONCHOSPASM). • Dyspnea. • If the condition is severe, cyanosis of mucous membrane and nail beds. • Laryngeal edema. CARDIOVACULAR SYSTEM SYMPTOMS • • • • • • • • Pallor Lightheadedness Palpitations Tachycardia Hypotension Cardiac dysrhythmias Unconsciousness Cardiac arrest MANAGEMENT PATIENTS ALLERGIC TO LOCAL ANESTHESIA • Allergy testing. • For minor procedures like I&D of an abscess, inhalational sedation with nitrous oxide and oxygen. • Use general anesthesia in place of local anesthesia. • Avoid topical application or spray of LA in these patients. • Avoid infiltration of skin or mucous membrane with LA. • Histamine blockers as local anesthetic should be considered, DIPHENHYDRAMINE HYDROCHLORIDE. • Electronic dental anesthesia EDA. • Non-drug technique of pain control like HYPNOSIS. TREATMENT FOR PATIENT WITH ALLERGY • Basic management P A B C D Definitive care • Histamine blocker -- 50mg Diphenhydramine or q6 h 3days 10mg Chlorpheniramine. IMMEDIATE SKIN REACTION • Epinephrine 0.3mg - Adult IM/SC / 0.15mg - Child. • Histamine blocker - Diphenhydramine 50 mg IM Adult Diphenhydramine 25 mg IM Child RESPIRATORY REACTIONS • If bronchospasm Most patients in respiratory distress prefer to be seated upright. DEFINITIVE CARE • Oxygen = 5-6 liters/min • Epinephrine or other bronchodilator ADULT = 0.3mg IM/SC CHILD = 0.15mg • Histamine blocker LARYNGEAL EDEMA • Present when movement of air through the patients nose and mouth cannot be heard or felt in presence of spontaneous respiratory movements. • Impossible to carry out artificial ventilation with patent airway. • Partial obstruction of larynx produces stridor, wheezing and bronchospasm. • Partial obstruction may gradually or rapidly progress to total obstruction . • Patient rapidly loses consciousness from lack of oxygen. TREATMENT • • • • • • Epinephrine Oxygen Airway maintenance Histamine blocker Corticosteroid (HYDROCORTIZONE SODIUM SUCCINATE) Cricothyrotomy