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)
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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
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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)
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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]
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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
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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
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Epinephrine
Oxygen
Airway maintenance
Histamine blocker
Corticosteroid (HYDROCORTIZONE SODIUM SUCCINATE)
Cricothyrotomy