Medical Emergencies

Medical Emergencies
“When you prepare for an emergency, the emergency ceases to exist.”
–GOLDBERGER
1
Medical Emergencies
CONTENTS:
1 Introduction 3
2 Definition 4
3 Classification 5
4 Prevention 7
5 Preparation 17
6 Unconsciousness 49
7 Respiratory distress 63
8 Altered consciousness 74
9 Seizures 92
10 Drug-related emergencies 97
11 Chest pain 108
12 Public health significance 115
13 Conclusion 115
14 References 115
2
Introduction
INTRODUCTION:
Life threatening emergencies can and do occur in the practice
dentistry. They can happen to anyone - a patient, a doctor, a member of the
office staff, or a person who is merely accompanying a patient. Although the
occurrence of life threatening emergencies in dental offices is infrequent, many
factors can increase the likelihood of such incidents. These include:
(1) the increasing number of older persons seeking dental care,
(2) the therapeutic advances in the medical profession,
(3) the growing trend toward longer dental appointments, and
(4) the increasing use and administration of drugs in dentistry.
Fortunately, other factors minimise the development of life-
threatening situations. This include a pretreatment physical evaluation of each
patient, consisting of a medical history questionnaire, dialogue history, and
physical examination and possible modifications in dental care to minimise
medical risks.
Inspite of most meticulous protocols designed to prevent the
development of life threatening situations, emergencies will still occur. However,
one should understand that no medical emergency is unique to dentistry. For
instance, even local anaesthetic overdose is seen outside dentistry in cocaine
abuse.
Although any medical emergency can developing dental office,
some are seen more frequently than the others. Many such situations are stress
3
Introduction
related (e.g., pain, fear, and anxiety) or involve pre-existing conditions the are
exacerbated when patients are placed in stressful environments. Stress-
induced situations include vasodepressor syncope and hyperventilation,
whereas pre-existing medical conditions that are exacerbated by stress include
most acute cardiovascular emergencies, bronchospasm (asthma), and
seizures. The effective management of pain and anxiety in the dental office is
therefore essential in the prevention and minimization of potentially catastrophic
situations.
Drug-related adverse reactions make up another category of life-
threatening situations that occur more often than dentists expect. The most
frequent are associated with local anaesthetics, the most commonly used drugs
in dentistry. Psychogenic reactions, drug overdose, and drug allergy are just a
few of the problems associated with the administration of local anesthetics. The
overwhelming majority of ‘drug-related’ emergencies are stress related;
however, other reactions like allergy, overdose represent responses to the drug
themselves. Most adverse drug responses are preventable. Therefore, thorough
knowledge of drug pharmacology and proper drug administration are critical in
the prevention of drug-related complications.
DEFINITION:
A medical emergency is an acute injury or illness that poses an
immediate risk to a person's life or long-term health1. Medical emergencies can
happen in any environment. The occurrence of such happenings in the dental
office is not a surprising event, given the stress many patients associate with
dental care.
4
Classification
CLASSIFICATION:
Medical emergencies can be classified based on many methods. The
traditional approach has been the systems-oriented classification, which lists
major organ systems and discusses life-threatening situations associated with
those systems.
A second classification method divides the emergency situations into two
broad categories- cardiovascular and non-cardiovascular emergencies, which is
broken down further into stress-related and non-stress related emergencies.
This system offers a very general breakdown of life-threatening emergencies
that is useful to the doctors.
A. Systems-oriented Classification:
• Infectious Diseases:
Immune system
- Allergies
- Angioneurotic edema
- Contact dermatitis
- Anaphylaxis
• Skin And Appendages
• Eyes
• Ears, Nose And Throat
• Respiratory Tract
Asthma
Hyperventilation
5
Classification
• Cardiovascular System
Ateriosclerotic heart diseases
Angina pectoris
Myocardial infarction
Heart failure
• Blood
• Gastrointestinal Tract And Liver
• Obstretrics And Gynecology
• Nervous System
Unconsciousness
- Vasodepressor syncope
- Orthostatic hypotension
Convulsive disorders
- epilepsy
Drug overdose reactions
Cerebrovascular accident
- Endocrine disorders
Diabetes mellitus
- Hyperglycemia
- Hypoglycemia
Thyroid gland
- Hyperthyroidism
- Hypothyroidism
Adrenal gland
- Acute adrenal insufficiency

6
Classification
B. Cardiac-oriented Classification:
NON-CARDIOVASCULAR CARDIOVASCULAR
Vasodepressor syncope
Angina pectoris
Hyperventilation
Acute myocardial infarction
Seizure
Acute heart failure
STRESS-RELATED Acute adrenal (pulmonary edema)
insuﬃciency
Cerebral ischemia and
Thyroid storm
infarction
Asthma Sudden cardiac arrest

Orthostatic hypotension
Acute myocardial infarction
Overdose reaction
Sudden cardiac arrest
NON-STRESS RELATED Hypoglycemia
Hyperglycaemia
Allergy
PREVENTION:
McCarthy stated that implementation of a complete system of
physical evaluation for all prospective dental patients could prevent upto 90% of
life-threatening situations. The remaining 10% would occur inspite of all
preventive efforts. Goldberger wrote, “When you prepare for an emergency, the
emergency ceases to exist.” This is accurate to the extent that adequate
preparation for emergency situations diminishes the likelihood of their resulting
in significant morbidity or death. Prior knowledge of a patient’s physical
condition permits the doctor to incorporate modifications into the dental
treatment plan. In other words, “To be forewarned is to be forearmed.”
GOALS OF PHYSICAL EVALUATION:
1. Determine the patient’s ability to physically tolerate the stress involved in
the planned treatment.
7
Prevention
2. Determine the patient’s ability to psychologically tolerate stress involved in
the planned treatment.
3. Determine whether treatment modifications are required to enable the
patient to better tolerate the stress involved in the planned treatment.
4. Determine whether the use of psychosedation is warranted.
a. Determine which sedation techniques is most appropriate.
b. Determine whether contraindications exist to any of the drugs to be used
in the planned treatment.
The first two goals involve the patient’s ability to tolerate the
stress involved in the dental treatment. The stress may be physiologic or
psychological. Many, if not most, patients with preexisting medical conditions
are less able to tolerate the normal levels of stress associated with dental
treatment. These patients are more likely to undergo acute exacerbation of
their pre-existing medical conditions when exposed to such stress. Examples of
such pre-existing conditions include angina pectoris, epilepsy, asthma and
sickle cell anaemia. Although most patients are able to tolerate dental
treatment, the doctor must determine before commencing treatment (1) the
potential problem, (2) the level of severity of the problem, and the potential
effect of the problem planned dental treatment.
Excessive stress may also be detrimental to a person who is not medically
compromised. Fear, anxiety and pain-especially sudden, unexpected pain-lead
to acute changes in the body’s homoeostasis. Many dental patients experience
8
Prevention
fear-related emergencies including hyperventilation and vasodepressor
syncope.
The third goal and physical evaluation is the determine whether the
planned dental treatment requires modification to better enable the patient to
terminate the stress. In some instances a healthy patient can handle the
treatment physically but is unable to cope up with it psychologically. When the
patient requires assistance in coping with the dental treatment, the doctor may
consider sedation. Determining the need for these techniques, selecting the
most appropriate technique, and choosing the most appropriate drug or drugs
for the patient are part of the final goal of the physical evaluation.
I. PHYSICAL EVALUATION:
Physical examination consists of medical history
questionnaire, physical examination and dialogue history. Armed with this
information, the doctor can better (1) determine the physical and psychological
status of the patient, allowing the doctor to (2) assign a risk factor classification
to that patient; (3) seek medical consultation and (4) institute appropriate
treatment modifications.
• MEDICAL HISTORY QUESTIONNAIRE:
The use of a written, patient-completed medical history
questionnaire is a moral and legal necessity in the health care professions. In
addition, the medical history questionnaire provides the doctor with valuable
information concerning the physical and psychological condition of the patient.
9
Prevention
There are two basic types - the short form medical history and
the long form medical history. The short form, usually one page, provides basic
information about a patients medical history and ideally is suited for a doctor
who has a considerable clinical experience in physical evaluation. The long
form, usually two or more pages, provides a more detailed summary of the
patient’s past and present physical condition. It is used most often in teaching
institutions.
Any medical history questionnaire can be extremely valuable or
entirely worthless. The ultimate value of the questionnaire resides in the
answers provided and to elicit additional information through dialogue history
and physical examination. The medical history questionnaire must be updated
on a regular basis, approximately every 3-6 months or after any prolonged
lapse in treatment. For example, a patient may answer that no change has
occurred in general health but may want to notify the doctor of a minor change
in condition, such as the end of a pregnancy or the recent diagnosis of type 2
diabetes or asthma.
• PHYSICAL EXAMINATION:
As important as the patient-completed medical history questionnaire
is in the overall assessment of a patient’s physical and psychological status, it
does have limitations. For the health history to be of value, patients must have
(1) be aware of their state of health and of any existing medical conditions,
and (2) be willing to share this information with their dentist. The doctor must
seek additional sources of information concerning the patient’s physical status.
The physical examination provides much of this information.

10
Prevention
Physical examination in dentistry consists of the following steps:
• Monitoring of vital signs
• Visual inspection of the patient
• Function tests as indicated
• Auscultation, monitoring (via ECG), and laboratory tests of the heart and
lungs as indicated.
Minimum physical evaluation of prospective patients should consist of
measurement of their vital signs and a visual inspection of a patient. The
primary value of this examination is that it provides the doctor with important
current information about patient’s physical status, whereas the questionnaire
provides historical, anecdotal information.
Ideally, physical examination should be completed at an initial visit
before the actual start of dental treatment. Vital signs obtained at this
preliminary appointment known as baseline vital signs, serve two functions.
First, they help to determine a patient’s ability to tolerate the stress involved in
the planned dental treatment. Second, baseline vital signs are used as a
standard during the management of emergency situations in comparison with
readings obtained during the emergency.
VITAL SIGNS:
The vital signs are as follows:
1. Blood pressure
2. Heart rate and rhythm
11
Prevention
3. Respiratory rate
4. Temperature
5. Height
6. Weight
VISUAL INSPECTION:
Visual inspection of the patient provides the doctor with additional
information about their physical status and degree of anxiety. Observation of a
person’s posture, body movements, speech, and skin may help the doctor
detect disorders that may previously have gone unnoticed.
Involuntary body movements occurring in conscious patients may
indicate significant disorders. Tremor may be noted in disorders such as fatigue,
multiple sclerosis, parkinsonism, and hyperthyroidism, as well as hysteria and
nervous tension.
The character of a patient’s speech may also be significant. A CVA
can cause muscle paralysis leading to speech difficulties. Epileptic patients
receiving long-term anti epileptic drug therapy may demonstrate sluggish
speech patterns. Anxiety about impending dental treatment can also be
detected in speech.
Additional risk factors revealed through visual examination include (1)
the presence of prominent jugular veins in a patient seated upright, an
indication of possible right ventricular failure; (2) clubbing of the fingers, which
may indicate chronic cardiopulmonary disease; (3) swelling of the ankles, seen
12
Prevention
in cases of right ventricular failure, varicose veins, renal disease, and
occasionally near-term pregnancy; and (4) exophthalmos, which can indicate
hyperthyroidism.
• DIALOGUE HISTORY:
Following the medical history and visual inspection regarding the
patient’s physical condition, the doctor must determine what significance, if
any, these disorders present to the planned dental treatment by dialogue
history, in which the doctor must use all the available knowledge of the
pathologic process to which the patient is at risk.
II. RECOGNITION OF DENTAL FEAR AND ANXIETY:
Heightened anxiety and fear of dentistry can lead to an acute
exacerbation of medical problems such as angina pectoris, seizures, and
asthma, as well as to other stress-related problems such as hyperventilation
and vasodepressor syncope. One of the goals of patient evaluation is to
determine whether a patient is psychologically capable of tolerating the stress
associated with the planned dental treatment. Three methods are available to
enable the doctor to recognise the presence of anxiety. The first is the medical
history questionnaire; second, the anxiety questionnaire; and third, the art of
observation.
ASA PHYSICAL STATUS CLASSIFICATION SYSTEM:
In 1963 the American Society of Anesthesiologists adopted what is now
referred to as the ASA Physical Status Classification System. The classification

13
Prevention
represents the method by which the doctor can estimate the medical risk to a
patient who is scheduled to receive anaesthesia for a surgical procedure. The
system has remained essentially unchanged and in continuous use since its
introduction and has proven a valuable method in determination of surgical and
aesthetic risk before medical and dental procedures.
ASA 1: A normal, healthy patient without systemic disease.
ASA 2: A patient with mild systemic disease.
ASA 3: A patient with severe systemic disease.
ASA 4: A patient with incapacitating systemic disease that is a constant threat to
life.
ASA 5: A moribund patient not expected to survive without the operation.
ASA 6: A declared brain-dead patient whose organs are being removed for
donor purposes.
ASA E: Emergency operation of any variety, with E preceding the number to
indicate the patient’s physical status (for example, ASA E-3).
14
Prevention
STRESS REDUCTION PROTOCOL:
NORMAL, HEALTHY, ANXIOUS MEDICAL RISK PATIENT (ASA 2,3,4)
PATIENT (ASA 1) • Recognise the patient’s degree of

• Recognise the patient’s level of medical risk.
anxiety. • Complete medical consultation before

• Pre-medicate the evening before the dental therapy as needed.
dental appointment, as needed. • Schedule the patient’s appointment in

• Pre-medicate immediately before the the morning.
appointment, as needed. • Monitor and record preoperative and

• Schedule the appointment in the postoperative vital signs.
morning. • Consider sedation during therapy.

• Minimise the patient’s waiting time. • Administer adequate pain control
• Consider sedation during therapy. during therapy.
• Administer adequate pain control • Length of appointment variable; do not

during therapy. exceed patient’s limits of tolerance.
• Length of appointment variable. • Follow-up with the postoperative pain

• Follow-up with the postoperative pain and anxiety control.
and anxiety control. • Telephone the higher medical risk

• Telephone the highly anxious or fearful patient later on the same day that
patient later the same day the treatment was delivered.
treatment was delivered. • Arrange the appointment for highly

anxious or fearful, moderate-to-high
risk patient during first few days of the
week when the office is open for
emergency care and the treating
doctor is available.
15
Prevention
• Premedication: Oral sedative-hypnotics:
Administration of oral sedative drugs is one technique to help the
patient achieve restful sleep, which in turn helps to reduce his anxiety and
stress during the dental appointment. An anti anxiety or sedative-hypnotic drug,
such as triazolam, flurazepam, zolpidem, or zaleplon to be taken 1 hour before
sleep. The appropriate use of oral anti anxiety or sedative-hypnotic drugs is an
excellent means of minimising preoperative stress. Other drugs such as
diazepam, oxazepam, hydroxyzine, and promethazine, have proved effective in
adults and children.
DRUG ADULT DOSE PEDIATRIC
Alprazolam 4 mg/day NE
Diazepam 2-10 mg NE
Flurazepam 15-30 mg NE
Midazolam Rarely used ≥6 months NE
≥6 months 0.25-0.5 mg/kg

Oxazepam 10-30 mg 30-45 mi before surgery
Triazolam 125-250 µg NE
Eszopiclone 2-3 mg NE
Zalepon 5-10 mg NE
Zolpidem 10 mg NE
Oral sedative-hypnotics
Administration of CNS depressant to drug approximately one
hour prior to the schedule to treatment should decrease the patients anxiety
level to a degree such that the thought of dental treatment is no longer
frightening. It is recommended that orally administered CNS depressant drugs
16
Preparation
be administered to the patient in the dental office to avoid dosing errors. If the
drug was taken at home, the doctor must advise the patient against driving a
car or operating other potentially hazardous machinery.
PREPARATION:
In spite of efforts to prevent them, life-threatening emergencies can, and
do occur in the practice of dentistry. Prevention, as successful as it may be, is
not always enough. The entire dental office staff must be prepared to help
recognise and manage any potential emergency situation.
EMERGENCY DRUG KITS
The dental office emergency kit need not and, indeed, should not be
completed. It should be as simple as possible to use. The “KISS” principal is
important at this time: “Keep It Simple, Stupid.” The doctor should remember
three things in preparing and using emergency drug kits:
1. Drug administration is not necessary for the immediate management of
medical emergencies. (BLS is always implemented, as needed, first).
2. Primary management of all emergency situations involves BLS.
3. When in doubt, don’t medicate.
First and foremost in the management of emergency situations are
the steps of BLS (P→C→A→B→D). Only after these steps have been
implemented should the doctor consider drug administration. Even in
anaphylaxis, the acute multi system allergic reaction in which the patient
17
Preparation
experiences immediate
respiratory distress,
circulatory collapse, or
both, BLS remains the
immediate response,
followed as quickly as
possible by the
administration of
e p i n e p h r i n e .
Management of all
emergency situations
follows the
(P→C→A→B→D)
protocol. (D = definitive management: diagnosis, drugs, and defibrillation).
Components of emergency kit:
The emergency drugs and equipment are presented in four levels, or
modules. The design of each module is based on the training and experience in
emergency medicine:
• Module one: Basic emergency kit (critical drugs and equipment)
• Module two: Noncritical drugs and equipment
• Module three: ACLS drugs
• Module four: Antidotal drugs
18
Preparation
Two categories are described for each module - injectable, and non-
injectable drugs, as well as emergency equipment. Most injectable drugs are
prepared in 1-mL glass ampule or vial. The number of milligrams of drug
present in 1 mL of solution differs from drug to drug. For example, diazepam is
5 mg/mL and diphenhydramine is 50 mg/mL and ephedrine 10 mg/mL. The 1-
mL form of the drug is commonly known as its therapeutic dose, or unit dose.
Thus, 1 mL of drug is the usual dose administered to the adult patient. Body
weight is used as a point of distinction between paediatric and adult doses.
Patients weighing 30 kg or greater received adult doses, while those
weighing 15 kg up to 30 kg receive paediatric doses in an emergency situation.
For infants, the therapeutic dose is usually 0.25 mL of one quarter the adult
dose.
Module One: Critical Emergency Drugs and Equipment
Category Generic drug Alternative Quantity Availability
INJECTABLE
1 preloaded
Allergy- 1: 1000
Epinephrine none syringe + 3 ✕ 1
anaphylaxis (1 mg/mL)
mL ampules
Allergy-
Diphenhydramin Chlorphenir- 3 ✕ 1 mL
histamine 50 mg/mL
e amine ampules
blocker
NON-INJECTABLE
Oxygen Oxygen 1 E cylinder
NitroStat
1 metered spray 0.4 mg/
Vasodilator Nitroglycerin sublingual
bottle metered dose
tablets
Metered-dose
Meteprotere- 1 metered-dose
Bronchodilator Albuterol aerosol
nol inhaler
inhaler
19
Preparation
Antihypo- Insta-glucose
Sugar 1 bottle
glycemic gel
Inhibitor of 2 packets of
platelet Aspirin Clopidogrel powdered 325mg/dose
aggregation aspirin
Equipment Recommend Alternative Quantity
Oxygen delivery Positive pressure O2 delivery system Minimum: 1 large

system and demand valve with bag-valve-mask adult, 1 child
device
Automated Many AED 1

electronic
defibrillator (AED)
Syringes for drug Plastic disposable 3x2 mL syringes

administration syringes with needles for
parenteral drug
administration
Suction and suction High-volume Nonelectrical Oﬃce suction

tips suction suction system system
Tourniquets Rubber or velcro Sphygmomanometer 3 tourniquets and 1

tourniquet; rubber sphygmomanometer
tubing
Magill intubation Magill intubation 1 paediatric Magill

forceps forceps intubation forceps
CRITICAL INJECTABLE DRUGS:
The following two categories of injectable drugs are considered critical in
any emergency kit:
1. Epinephrine
2. Histamine blocker
Both are used in the management of anaphylaxis, the acute life-threatening
multi system allergic reaction.

20
Preparation
• PRIMARY INJECTABLE: DRUG FOR ACUTE ALLERGIC REACTION
(ANAPHYLAXIS):
Drug of choice - Epinephrine
Drug class - Catecholamine
Alternative drug - None
Epinephrine is the drug of choice in the management of the acute (life-
threatening) multi system allergic reaction, anaphylaxis. Epinephrine is valuable
in managing both the respiratory and cardiovascular manifestations of acute
allergic reactions, as well as providing a degree of vasoconstriction that can be
helpful in the presence of edema. Desirable properties of epinephrine include -
(1) a rapid onset of action; (2) potent action as a bronchial smooth muscle
dilator (ß2 properties); (3) histamine blocking properties; (4) vasodepressor
actions; and (5) cardiac effects, which include an increase in heart rate (21%),
increased systolic pressure (5%), decreased diastolic pressure (14%),
increased cardiac output (51%), and increased coronary blood flow.
Undesirable actions include epinephrine’s tendency to predispose the heart to
dysrhythmias and a relatively short duration of action.
Therapeutic indications:
Epinephrine in a 1:1000 ( ≥ 30 kg body weight) or 1:2000 ( < 30 kg)
concentration is used to treat cases of acute allergic reaction and
bronchospasm.
21
Preparation
Side effects, contraindications, and precautions:
Tachydysrhythmias, both supraventicular and ventricular, may develop.
Epinephrine should be administered with caution to pregnant women because
it decreases placental blood flow and can induce premature labor. When used,
all vital signs should be monitored frequently.
In the setting of dental office, epinephrine administration will be considered in
situations felt to be acutely life threatening such as anaphylaxis and cardiac
arrest. In such situations, the advantages of epinephrine administration clearly
outweigh any risks. Epinephrine is light sensitive and should be stored in the
carrying case provided, and should be stored at room temperatures. It should
not be refrigerated and the syringes and ampules should be protected from
freezing. The solution should be checked periodically for any discolouration or
precipitates. If the solution is discoloured (pale yellow, yellow, brown) or
contains a precipitate, the syringe should be replaced immediately.
• PRIMARY INJECTABLE: DRUG FOR NON LIFE-THREATENING ALLERGIC
REACTION:
Drug of choice - Diphenhydramine
Drug class - Histamine blocker (nonselective anti-histamine)
Alternative drug - Chlorpheniramine
Histamine blockers, commonly known as antihistamines, are valuable in the
management of the more common delayed allergic response and in the
definitive management of acute allergic reaction(administered after epinephrine
22
Preparation
has resolved the life-threatening phase of the reaction). Histamine blockers are
competitive antagonists of histamine; they do not prevent the release of
histamine from cells in response to drugs, injury or antigens but do prevent
histamine’s access to its receptor site on the cell, blocking the response of the
effector cell to histamine. Therefore, histamine blockers are more potent in
preventing the actions of histamine than in reversing these actions once they
occur. Histamine blockers also act as potent local anesthetics, especially
diphenhydramine and tripelennamine. Histamine blockers may also produce a
degree of CNS depression.
Histamine blockers are recommended in management of delayed-onset allergic
reactions and in definitive management of acute life-threatening allergic
reactions.
Side effects of histamine blockers include CNS depression, decreased blood
pressure, and thickening of bronchial secretions as a result of the drug’s drying
action. Because of this drying effect, histamine blockers are contraindicated in
the management of acute asthmatic episodes.
• PRIMARY NON-INJECTABLE: OXYGEN (O2):
Drug of choice: Oxygen
Drug class - none
Alternative drug - none

23
Preparation
The most useful drug in the entire emergency kit is oxygen, which is supplied in
variety of sizes of compressed gas cylinders.
O2 administration is indicated in any emergency situation in which respiratory
distress is evident.
None with the emergency use of O2, although O2 administration is not
indicated in the management of hyperventilation.
• PRIMARY NON-INJECTABLE: VASODILATOR
Drug of choice - Nitroglycerin
Drug class - vasodilator
Alternative drug - Amyl nitrite
Vasodilators are used for the immediate management of chest pain as may
occur with angina pectoris or acute myocardial infarction. Two varieties of
vasodilators are available: (1) nitroglycerin in a tablet and as spray and (2) an
inhalant, amyl nitrite. A patient with history of angina pectoris usually carries a
supply of nitroglycerin at all times. The sublingual tablets remain the most used
form of the drug by patients. Once exposed to air, nitroglycerin tablets begin to
degrade. Nitroglycerin tablets placed sublingually commonly produce a bitter
taste and impart a sting. If the bitter taste is absent, the doctor should suspect
the drug has become ineffective.
Amyl nitrite, another vasodilator, is available in inhalant form. It is supplied in a

24
Preparation
yellow vaporole, or a gray cardboard vaporole with yellow printing in doses of
0.3 mL. When crushed between the fingers and held under the victim’s nose, it
produces profound vasodilation in about 10 seconds. The duration of action of
amyl nitrite is shorter than nitroglycerin, but its shelf life is considerably longer.
Side effects occur with all vasodilators but are more significant with amyl nitrite.
With onset of first-time chest pain, nitroglycerin is used as an aid in differential
diagnosis and for the definitive management of angina pectoris, the early
management of acute myocardial infarction and the management of acute
hypertensive episodes.
Side effects of nitroglycerin include a transient, pulsating head ache; facial
flushing; and a degree of hypotension, especially if the patient is in an upright
position. Because of its mild hypotensive actions, nitroglycerine is
contraindicated in patients who exhibit signs and symptoms of hypotension.
Nitroglycerin may be used in an exception of effectiveness in the management
of acute hypertensive episodes.
The side effects of amyl nitrite are similar to, but more intense than, those of
nitroglycerin. These include facial flushing, pounding pulse, dizziness, intense
headache, and hypotension. Amyl nitrite should not be administered to patients
seated in upright position because significant postural changes develop.
25
Preparation
• Primary non-injectable: bronchodilator:
Drug of choice - Albuterol, Salbutamol
Drug class - Bronchodilator (short acting ß2-adrenergic receptor agonist)
Alternative drug - Metaproterenol
Asthmatic patients and patients with allergic reactions manifested primarily by
respiratory difficulty require the use of bronchodilators. Although epinephrine
remains the most effective drug for management of bronchospasm, its wide-
ranging effects on systems other than respiratory have led to the
introduction of newer, more specific drugs known as ß2 - adrenergic receptor
agonists. These drugs, e.g., albuterol, have specific bronchial smooth
muscle - relaxing properties (ß2) with little or no stimulatory action on the
cardiovascular and gastrointestinal systems (ß1).
Before dental treatment begins, asthmatic patient who are at
greater risk of bronchospasm (e.g., patients with dental phobia or history of
frequent status asthmaticus) should be asked to make their bronchodilators
available.
Bronchodilators are used to treat bronchospasm and allergic reactions in which
bronchospasm is a component.
Albuterol, like other ß2 agonists, can have clinically significant effects in some
cardiac patients. This response is less likely to occur with albuterol than with
26
Preparation
other bronchodilators, hence its selection for the emergency kit. Metaproteronol,
epinephrine, and isoproterenol mistometers are more likely to produce
cardiovascular side effects, including tachycardia, and ventricular dysrhythmias.
Administration of these latter drugs is contraindicated in patients with
preexisting tachydysrhythmias from prior use of the drug.
• Primary non-injectable: antihypoglycemic
Drug of choice - orange juice
Drug class - Antihypoglycemic
Alternative drug - Glucose gel
Anti-hypoglycemics are useful in the management of hypoglycemia in
patients with diabetes mellitus or in non-diabetic patients with anti-
hypoglycemia. Diabetic patients normally carry a sugar source, such as sucking
candy, with them at all times.
Hypoglycemic states secondary to diabetes mellitus or fasting hypoglycemia in
the conscious patient.
Liquid or viscous carbohydrates should not be administered to a patient who
does not have an active gag reflex or is unable to drink without assistance.
Parenteral administration of anti-hypoglycemics is recommended in these
situations.
27
Preparation
• Primary non-injectable: anti-platelet:
Drug of choice - Aspirin
Drug class - Anti-platelet
Alternative drug - Clopidogrel
Aspirin is the recommended anti-thrombotic drug in the prehospital phase of
suspected myocardial infarction. Considered to be the standard anti-platelet
agent, aspirin represents the most cost-effective treatment available for patients
with acute ischemic coronary syndromes. Aspirin irreversibly acetylates platelet
cyclooxygenase, removing all cyclooxyrgenase active for the life span of the
platelet (8 to 10 days). Aspirin stops production of proaggregatory
thromboxane A2 and is also an indirect anti-thrombotic agent. Aspirin also
has important non-platelet effects because it likewise inactivates
cyclooxygenase in the vascular endothelium and thereby diminishes the
formation of anti-aggregatory prostacyclin. Administration of aspirin is
recommended for all patients with suspected acute MI or unstable angina.
Standard doses range from 160 to 324 mg given orally. Minimal side effects are
noted, particularly with 160 mg.
Aspirin is recommended in the management of patients with suspected
myocardial infarction or unstable angina.
Definite contraindications to aspirin therapy include ongoing major or life-
28
Preparation
threatening haemorrhage; significant predisposition to such haemorrhage, such
as a recent bleeding peptic ulcer; or a history of aspirin allergy.
Module Two: Secondary (Noncritical) Emergency Drugs and
Equipment
INJECTABLE
1x5 mL or 10
Anticonvulsant Midazolam Diazepam 5 mg/mL
mL vial
Morphine
Analgesic N2O-O2 3x1 mL ampules 10 mg/mL
sulfate
Vasopressor Ephredine 3x1 mL ampules 50 mg/mL
Antihypoglycemi 50 mL
50% dextrose Glucagon 1 vial
c ampule
Hydrocortisone 2x2 mL
Corticosteroid sodium Dexamethasone 50 mg/mL
succinate mix-o-vial
2x100 mg/mL
Antihypertensive Esmolol Labetalol 100 mg/mL
vial
Anticholinergic Atropine Scopolamine 3x1 mL ampules 0.5 mg/mL
NONINJECTABLE
Respiratory Aromatic 0.3 mL/

2 boxes
stimulant ammonia vaporole
25 mg
Antihypertensive Hydrazine Nitroglycerinin 1 bottle
tablets
29
Preparation
Drugs and equipment included in this module, though important and valuable in
the management of emergency situations, are not considered to be as critical
as those in basic office emergency kit.
SECONDARY INJECTABLE DRUGS:
Seven drug categories are included in this level:
1. Anticonvulsant
2. Analgesic
3. Vasopressor
4. Antihypoglycemic
5. Corticosteroid
6. Antihypertensive
7. Anticholinergic
• Secondary injectable: anticonvulsant
Drug of choice - Midazolam
Drug class - Benzodiazepine
Alternative drug - Diazepam
Seizure disorders may occur in the dental office under several circumstances,
including epileptic seizures, overdose reactions to local anesthetics, syncope in
which the airway is obstructed or the patient is not properly positioned,
hypoglycemia and febrile convulsions. Only rarely will administration of
anticonvulsant be required to terminate seizure activity.
30
Preparation
When barbiturates are administered to terminate seizure activity, the patient’s
post seizure depression is more profound and prolonged because of the
pharmacologic actions of the barbiturates. Barbiturates depress breathing, at
the same levels at which they depress the brain, terminating seizures. When
seizure activity is intense, the ensuing postictal period of depression usually is
more profound, with compromised respiration and a period of hypotension.
When barbiturates are used to terminate seizures, the ensuing depression will
likely be intensified, more likely than not leading to respiratory arrest and a
profound cardiovascular depression or collapse.
Unlike barbiturates, benzodiapines usually terminate seizure activity with
minimal depression of respiratory and cardiovascular systems. For many years,
diazepam was the anti-convulsant drug of choice because of its ability to
terminate seizures without profound postictal depression of the cardiovascular
and respiratory systems. Its lack of water solubility, however, limited its use to IV
administration. With the introduction of midazolam, a water soluble
benzodiazepine that is effective as anticonvulsant in the IV, IM, and IN routes
became available. IM or IN midazolam provides clinical action within 10 to 15
minutes.
Midazolam is used to treat prolonged seizures, local anesthesia-induces
seizures, hyperventilation and thyroid storm.
The major clinical side effect noted with benzodiazepines when used as
31
Preparation
anticonvulsants is respiratory obstruction, respiratory depression, or respiratory
arrest.
• Secondary injectable: analgesic
Drug of choice - Morphine sulfate
Drug class - Opioid agonist
Alternative drug - Nitrous oxide and oxygen
Analgesics are used in emergency situations in which acute pain or anxiety is
present. In most instances, pain or anxiety increases the myocardial workload,
which may prove detrimental to the patient’s well-being. Two such
circumstances include acute myocardial infarction (AMI) and heart failure (HF).
The analgesic drug of choice is the opioid agonist morphine sulfate. Nitrous
oxide and oxygen is and acceptable and, in the dental environment, more
readily available alternative.
Intense, prolonged pain or anxiety; acute myocardial infarction and congestive
heart failure.
Opioid agonists are potent central nervous and respiratory system depressants.
Vigilant monitoring of vital signs is mandatory whenever these drugs are used.
• Secondary injectable: vasopressor
Drug of choice - Ephredine

32
Preparation
Drug class - Vasopressor
Alternate drug - None
Ephredine releases endogenous norepinephrine from its storage sites. This
represents an indirect sympathomimetic effect. Norepinephrine, in turn,
stimulates various alpha and beta receptors. Ephredine may also stimulate ß-
receptors directly, particularly in bronchodilator smooth muscle. ß-adrenergic
effects result from the production of cyclic AMP by activation of the enzyme
adenylate cyclase. Ephredine relaxes bronchial smooth muscle by the
stimulation of ß2 receptors relieving mild bronchospasm, improving air
exchange and increasing vital capacity.
Vasopressors are used to manage clinically significant hypotension. Possible
uses include the following:
• Syncopal reactions
• Drug overdose reactions
• Post seizure states
• Acute adrenal insufficiency
• Allergy
Parenteral administration of most vasopressors is contraindicated in patients
with high blood pressure or ventricular tachycardia. The drugs must be used
with extreme caution in patients with hyperthyroidism, bradycardia, partial heart
block, myocardial disease or severe atherosclerosis.

33
Preparation
• Secondary injectable: antihypoglycemic
Drug of choice - Dextrose, 50% solution
Drug class - Antihypoglycemic
Alternative drug - Glucagon
In the management of low blood sugar, the mode of treatment depends largely
on the patient’s level of consciousness. In the conscious patient carbohydrate
administration is preferred, but when a patient is severely obtunded or
unconscious, 30 mL of a 50% dextrose solution should be administered IV.
Where the IV route is not available, glucagon is administered by IM route.
Glucagon, normally produced in the pancreas elevates the blood glucose level
by mobilising hepatic glycogen and converting it to glucose. Glucagon is
effective only when hepatic glycogen is available; it is ineffective in the
treatment of starvation or chronic hypoglycaemic states. As soon as the patient
begins to respond, oral carbohydrates should be administered.
Antihypoglycemics are used in the treatment of hypoglycemia and as a
diagnostic aid in unconsciousness or seizures of unknown origin.
50% dextrose solution, administered solely by IV route, may produce tissue
necrosis if extravascular infiltration occurs. There are no specific
contraindications to the use of 50% dextrose. Administration of bolus dose of
50% dextrose to an already hyperglycaemic patient does not significantly

34
Preparation
elevate blood glucose levels. Glucagon administered IV or IM is contraindicated
in patients in starvation states or in chronic hypoglycemia.
• Secondary injectable: corticosteroid
Drug of choice - Hydrocorisone sodium succinate
Drug class - Adrenal glucocorticosteroid
Corticosteroids are indicated for management of acute allergic reactions, but
only after the rescuer has brought the acute, life-threatening phase under
control through the use of epinephrine, oxygen, BLS and histamine blockers.
Corticosteroids are valuable primaryily in the prevention of recurrent
anaphylactic episodes. Corticosteroids also are used manage acute adrenal
insufficiency.
The onset of action of corticosteroids it slow, even following IV administration.
The antiallergic effects of corticosteroids are probably simple manifestations of
the non-specific anti-inflammatory action of the adrenal glucocorticoids
(hydrocortisone and cortisone). The use of dexamethasone is contraindicated in
patients with acute adrenal insufficiency. therefore, hydrocortisone sodium
succinate is the corticosteroid of choice for the dental emergency kit.
Corticosteroids are considered second-line drugs primarily because of their
slow onset of action.
Corticosteroids are used in the definitive management of acute allergy and in
the treatment of acute adrenal insufficiency.
35
Preparation
There are no contraindications to the administration of corticosteroids in the
management of life threatening medical emergencies. When corticosteroids are
administered for non-emergency treatment, many factors must be considered,
such as the presence of a pre-existing infection, peptic ulcer or hypoglycaemia.
• Secondary injectable: Antihypertensive
Drug of choice - Esmolol
Drug class - ß-adrenergic blocker
Alternative drug - Labetalol
The need to administer drugs to manage a hypertensive crisis is extremely
uncommon. First, the incidence of extreme acute blood pressure elevation is
rare; second, there are ways other than the parental administration of
antihypertensive drugs to decrease a patient’s blood pressure.
Esmolol is a ß1-selective adrenergic receptor blocking agent with a very short
duration of action. Esmolol is indicated for use as an antidysrhythmic agent in
patients with paraoxysmal supraventricular tachycardia and for the
management of intraoperative and postoperative tachycardia and hypertension.
Acute hypertensive episodes.
Esmolol is contraindicated in patients with sinus bradycardia, heart block
36
Preparation
greater than first degree, cardiogenic shock, or overt heart failure. Potentially
significant hypotension can develop with any dose of esmolol, but is more likely
to be seen with doses beyond 200 µg/kg per minute. Labetalol is
contraindicated in patients with asthma, a prime reason for it not being the
antihypertensive drug of choice.
• Secondary injectable: parasympathetic blocking agent
Drug of choice - Atropine
Drug Class - Anticholinergic
Atropine, a parasympathetic blocking agent, is recommended for the
management of clinically symptomatic bradycardia (adult heart rate <60 beats
per minute). By enhancing discharge from the sinoatrial node, atropine can
provoke tachycardia. Atropine is beneficial in situations in which the patient’s
heart has an overload of parasympathetic activity. Extremely fearful patients are
most likely to develop this response. With stimulation, vagus node decreases
SA node activity, decreasing the heart rate. When the heart rate becomes overly
slow, cerebral blood flow is decreased and clinical signs and symptoms of
cerebral ischemia develop. By blocking this vagal effect, atropine cats to
maintain adequate cardiac output and cerebral circulation. Atropine also is an
essential component of ACLS, in which it is used to manage hemodynamically
significant bradydysrhythmias.
Atropine is used to treat bradycardia and hemodynamically significant brady-
dysrhythmias.
37
Preparation
Large doses of atropine ( ≥ 2 mg) may produce clinical signs of overdose,
including hot, dry skin, headache, blurred nearsightedness, dry mouth and
throat; disorientation and hallucinations. Administration of atropine’s
contraindicated in patients with glaucoma or prostrate hypertrophy. Atropine
can increase the degree of partial urinary obstruction associated with
prostates; the drug is also contraindicated in older patients with narrow-angle
glaucoma.
SECONDARY NON INJECTABLE DRUGS:
Two non injectable drugs are considered at this level:
1. Respiratory stimulant
2. Antihypertensive
• Secondary non-injectable: respiratory stimulant
Drug of choice - Aromatic ammonia
Drug class - Respiratory stimulant
Alternative drug - none
Aromatic ammonia is the agent of choice for inclusion in the emergency kit as a
respiratory stimulant. It is available in silver-grey vaporale, which is crushed and
placed under the breathing victim’s nose until respiratory stimulation is effected.
Aromatic ammonia has noxious odour and irritates the mucous membrane of
the upper respiratory tract, stimulating the respiratory and vasomotor centres
of the medulla. This action in turn increases respiration and blood pressure.
Movement of the arms and legs often occurs in response to ammonia
38
Preparation
inhalation; these movements further increase blood flow and raise blood
pressure; especially in the patient who has been positioned properly.
Aromatic ammonia is used to treat vasodepressor syncope as well as
respiratory depression not induced by opioid analgesics.
Ammonia should be used in action in persons with chronic obstructive
pulmonary disease or asthma; its irritating effects on the mucous membrane of
the upper respiratory tract may precipitate bronchospasm.
• Secondary non-injectable antihypertensive:
Drug of choice - Hydralazine
Drug class - Antihypertensive
Alternative drug - Nitroglycerin
Hydralazine, used in the management of high blood pressure, is a peripheral
vasodilator , causing relaxation of the arteriolar smooth muscle via a direct
effect. The peripheral vasodilating effects of hydralazine result in
decreased arterial blood pressure and peripheral vascular resistance. In
addition, hydralazine induced reflex autonomic response increases the heart
rate, stroke volume, cardiac output and left ventricular ejection fraction. The
antihypertensive effects of oral hydralazine lasts about 2 to 4 hours.
Hypertensive urgencies. Although an initial dose of 10 mg is recommended, due

39
Preparation
to significant first pass effect of hydralazine, initial doses of 25 mg are usually
safe. Maximum recommended dosage is 300 mg/day PO.
Administration of hydralazine is contraindicated in patients with mitral valve
rheumatic heart disease. Caution is indicated in the presence of cardiovascular
disease, cerebrovascular disease and severe renal impairment.
Module Three: Advanced Cardiovascular Life Support (ACLS):
A third category of injectable drugs that should be included in the emergency kit
are those classified as essential in the perforce of ACLS.
• ACLS essential: cardiac arrest
Drug of choice - Epinephrine
Drug class - Vasopressor
Three items form the essentials of ACLS - epinephrine, O2 and defibrillation.
Epinephrine’s importance lies in the fact that no other drug can maintain
coronary artery blood flow while CPR is in progress, which is essential for
preserving the blood flow. Epinephrine also preserves blood flow to the brain,
helping to minimise neurologic damage. In the ascent of drug therapy, cerebral
blood flow during CPR is minimal, with most blood entering into the common
carotid artery and flowing into the external carotid branch, not into the internal
carotid artery. After the administration of a drug such as epinephrine, with alpha-
40
Preparation
adrenergic properties, cerebral blood flow increases significantly.
Cardiac arrest, ventricular fibrillation, pulseless ventricular tachycardia,
asystole, and pulseless electrical activity.
Alternative
Category Generic drug Quantity Availability
drug
INJECTABLE
3x10 mL 1:10000
Cardiac arrest Epinephrine preloaded (1 mg/10 mL
syringes syringe)
Antidysrhythmic Amiodarone Lidocaine 1x3 mL vial 50 mg/mL
Symptomatic
Atropine Isoproterenol 2x10 mL syringes 1 mg/10 mL
bradycardia
Paroxysmal
supraventicular Verapamil 2x4 mL ampules 2.5 mg/mL
tachycardia
NONINJECTABLE
Oxygen Oxygen 1 E cylinder 1 E cylinder
In those situations requiring epinephrine, no contraindications to its
administration exist. Epinephrine may induce or exacerbate ventricular ectopy,
especially in patients receiving digitalis.
• ACLS essential: O2
• ACLS essential: anti-dysrhythmic
Drug of choice - Amiodarone
Drug class - Anti-dysrhythmic
41
Preparation
Alternative drug - Lidocaine
Amiodarone is both an anti-dysrhythmic and a potent vasodilator. Amiodarone is
the first line management of VF and pulseless VT that is unresponsive to CPR,
defibrillation and vasodepressor therapy.
Amiodarone is indicated for treatment of refractory life-threatening ventricular
dysrhythmias. Lidocaine is administered in the management of hemo-
dynamically stable monomorphic VT. Administered parentally, lidocaine is used
in the management of acute life-threatening ventricular dysrhythmias.
Amiodarone is absolutely contraindicated in the following situations:
atrioventricular (AV) block, bradycardia, cardiogenic shock, iodine
hypersensitivity, sick sinus syndrome.
Excessive doses of lidocaine produce myocardial, circulatory and CNS
depression. Clinical signs and symptoms of lidocaine overdose include
drowsiness, paresthesias, and muscle twitching. More severe overdoses may
produce tonic-clonic seizure activity.
• ACLS essential: symptomatic bradycardia - Atropine
• ACLS essential: paraoxysmal supraventriular tachycardia (PSVT)
Drug of choice - Verapamil
Drug class - Calcium channel blockers
42
Preparation
Verapemil is a calcium channel blocker indicated for management of ischemic
heart disease including variant angina (Prinzmetal’s angina), unstable angina,
chronic stable angina, supraventricular tachydysrhythmias and hypertension.
In emergency cardiac care, verapamil is used to treat primarily PSVT that
doesnot require cardioversion. When verapamil is ineffective in the
management of PSVT, synchronised cardioversion is recommended.
A transient decrease in arterial pressure may be noted because of peripheral
vasodilation in response to verapamil.
Module Four: Anti-dotal Drugs
ANTIDOTAL DRUGS:
Categories of anti-dotal drugs include the following:
1. Opioid antagonist
2. Benzodiazepine antagonist
3. Antiemergence delirium drug
4. Vasodilator
43
Preparation
INJECTABLE
2x1 mL
Opiod antagonist Naloxone Nalbuphine 0.4 mg/mL
ampules
Benzodiazepine
Flumazenil 1x10 mL vial 0.1 mg/mL
antagonist
Anticholinergic
toxicity 3x2 mL
Physostigmine 1 mg/mL
Antiemergence ampules
delirium
2x1 mL
Vasodilator Phenotalamine Procaine 5 mg/mL
ampules
• Antidotal drug: opioid antagonist
Drug of choice - Naloxone
Drug class - Thebaine derivative
Alternative drug - Nalbuphine
The most significantly side effect of parenterally administered opioid agonist is
there ability to produce respiratory depression by diminishing the
responsiveness of the brain’s respiratory centres to arterial carbon dioxide.
Thus, the patient’s breathing rate is decreased.
Naloxone is the only opioid antagonist free of a any agonist properties, which
also reverses other properties of opioids, such as analgesia and sedation.
Naloxone may be administered as an IV route or endotracheally, improved
respiratory function is noted within 2 minutes.
Nalbuphine, an opioid agonist - antagonist, has been successfully used to
44
Preparation
reverse respiratory distress induced by opioid agonists. Because nalbuphine
has its own agonist properties, it provides excellent reversal of opioid induced
respiratory depression but does not remove post surgical analgesia or sedation
because of its own analgesia-inducing properties.
Naloxone is indicated for use in opioid-induced depression, including respiratory
depression.
When administered via IV route or endotracheal tube, naloxone’s effects last
only 30 minutes. Respiratory depression may recur if the opioid previously
administered is of longer duration (e.g., morphine). The IM administration of a
second dose of naloxone after the IV dose is common. Although this dose is
slower in onset, its duration is considerably longer than that of the IV dose. This
regimen minimises a possible recurrence of respiratory depression.
• Antidotal drug: benzodiazepine antagonist
Drug of choice - Flumazenil
Drug class - Benzodiazepine antagonist
Flumazenil has been demonstrated to produce a rapid reversal of sedation and
to improve the patient’s ability to comprehend and obey commands. The
duration of anterograde amnesia associated with midazolam was reduced from
45
Preparation
121 minutes without flumazenil to 91 minutes with flumazenil. Flumazenil also
decreased the recovery time from midazolam sedation, increased alertness,
and provided a decreased amnesic effect in the geriatric population. The
availability of flumazenil is recommended whenever benzodiazepines such as
diazepam, midazolam, or lorazepam are administered parenterally. Reversal
with flumazenal is not effective following the oral administration of
benzodiazepines (e.g., triazolam)
Flumazenil is used to reverse the clinical actions of parenterally
administered benzodiazepines.
Flumazenil administration can be associated with the onset of seizures in
patients using benzodiazepines to control seizures and in persons who have
become dependent on benzodiazepines.
• Antidotal drug: anti emergence delirium drug
Drug of choice - Physostigmine
Drug class - Cholinesterase inhibitor
Several drugs that are commonly employed parenterally to induce sedation can
produce what is known as emergence delirium (anticholinergic syndrome).
Scopolamine and the benzodiazepines, diazepam and midazolam, are most
likely to produce this phenomenon in which the patient appears to lose contact
46
Preparation
with the reality. There may also be increased muscular moment, and the patient
may seem to speak but makes unintelligible sounds. Physostigmine, a
reversible cholinesterase with the ability to cross the blood brain barrier, has
become the drug of choice in the management of emergence delirium.
Physostigmine is recommended for inclusion in the emergency kit if
scopolamine, benzodiazepines, or other drugs that may produce emergency
delirium are administered parenterally.
Physostigmine is used to reverse emergence delirium.
Side effects noted with physostigmine administration are increased salivation,
possible emesis, and involuntary urination and defecation. If administered to
rapidly, physostigmine can reduce the preceding fracture effects as well as
bradycardia and hypersalivation, leading to respiratory difficulties. Atropine
should always be available whenever physostigmine is administered because it
is an antagonist and antidote for physostigmine. Physostigmine should not be
administered to patients with asthma, diabetes, cardiovascular disease, or
mechanical obstruction of the gastrointestinal or genitourinary tracts.
47
Preparation
• Antidotal drugs: Vasodilator
Drug of choice - Phentolamine mesylate
Drug class - alpha-adrenergic receptor antagonist
Alternative drug - Procaine
A drug with significant vasodilating effects is recommended for inclusion in the
emergency kit whenever IM or IV are employed. Indications for administration of
phentolamine mesylate include extravascular injection of an irritating chemical
and accidental intra-arterial administration of a drug. In both instances the
problems of those of localised irritation tissue irritation and compromised
circulation in either localised area or a limb.
Procaine HCL drug is an alternative bag possessing drug possessing excellent
vasodilating properties along with its anaesthetic actions, both of which make it
ideal for administration in the aforementioned situations.
Management of vasospasm and compromised circulation following intraarterial
injection of a drug. Management of pain and vascular compromise following
extravascular administration of irritating drugs.
Phentolamine mesylate administration is contraindicated in patients with known
hypersensitivity to phentolamine because of the risk of an allergic reaction,
including anaphylaxis.
48
Unconsciousness
UNCONSCIOUSNESS:
The terms syncope and faint commonly are used interchangeably to describe
the transient loss of consciousness caused by reversible disturbances in
cerebral function.
PREDISPOSING FACTORS:
Three factors when present increase the likelihood that a patient may
experience an alteration in, or loss of, consciousness:
1) Stress,
2) Impaired physical status, and
3) Administration or ingestion of drugs.
In the dental setting, stress is the primary cause in most cases of
unconsciousness. Vasodepressor syncope, the most common cause of
unconsciousness in dentistry, commonly occurs as a result of unusually high
levels of stress. The sudden loss of consciousness that occurs during
venipuncture or the intraoral injection of a local anaesthetic is a classic example
of vasodepressor syncope.
Impaired physical status (American Society of
Anesthesiologists PS 3 or 4) is another factor working to increase the likelihood
of syncope. When patients with impaired physical status are exposed to undue
stress, whether physiological or psychological, the chances are even greater
that they may react adversely to the situation.
49
Unconsciousness
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 (non-opioids, including NSAIDs; opioid analgesics;
and local anesthetics), anti anxiety drugs (anxiolytics and sedative-hypnotics)
and antibiotics. Drugs in the first two categories are central nervous system
d e p r e s s a n ts a n d th e r e fo r e p r o d u c e a l te r a ti o n s i n th e l e v e l o f
consciousness(e.g., sedation) or the loss of consciousness.
Local anesthetics represent the most commonly used drugs
in dentistry, and because injection is required for them to be effective, local
anesthetics play a major role in the development of syncope. Life-threatening
situations associated with the administration of local anesthesia can and do
occur. By far the overwhelming majority of these adverse reactions are stress
induced (fear and anxiety), however adverse reactions directly related to the
local anaesthetic drug are rarely observed. These include overdose reactions
and allergy.
PREVENTION:
Loss of consciousness can be prevented in many, if not most,
instances by thorough pre-treatment medical and dental evaluation of the
prospective patient. Important elements of this evaluation include a
determination of the patient’s ability to tolerate the stresses - both physiologic
and psychological - associated with their planned treatment. Use of a medical
history questionnaire and physical history of the patient, followed by dialogue
history, may uncover medical or psychological disabilities that predispose the
patient toward syncope. Detection of these factors permits the doctor to permit
the doctor to modify the planned treatment to better accommodate the patient’s
physical or psychological status.

50
Unconsciousness
CLINICAL MANIFESTATIONS:
The unconscious patient is described as one who does not
respond to sensory stimulation, has lost protective reflexes, and is unable to
maintain a patent airway. Primary management of unconsciousness is directed
at reversing these clinical manifestations. Clinical signs and symptoms
associated with the incipient loss of consciousness (presyncope) and the
actual state of unconsciousness (syncope) vary depending upon the primary
cause of situation.
PATHOPHYSIOLOGY:
In his classic test on fainting, Engle divided the mechanisms that
produce syncope into four categories:
Mechanism Clinical example

Acute adrenal insufficiency
Inadequate delivery of blood or O2 to the Hypotension
brain Orthostatic hypotension
Acute allergic reaction
Drug ingestion and
administration
Systemic or local metabolic deficiencies Nitrites and nitrates
Diuretics
Sedatives, opioids
Local anesthetics
Cerebrovascular accident
Direct or reflex effects on nervous system
Convulsive accidents
Emotional disturbances
Psychic movements Hyperventilation
51
Unconsciousness
MANAGEMENT:
Recognise Unconsciousness
(Lack of response to sensory stimulation)
↓
Discontinue dental treatment
↓
Activate office emergency team
↓
P - Place unconscious victim in supine position with
feet elevated
↓
C→A→B - Quickly assess for spontaneous breathing
and palpable pulse for not more than 10 seconds.
In absence of pulse, chest compression is immediately

started.
In presence of palpable pulse, airway and breathing are

performed as needed.
↓
Activate emergency medical services if recovery of
consciousness is not immediate
C, circulation; A, airway; B, breathing; D, definitive care; P, position.
VASODEPRESSOR SYNCOPE
An abrupt, transient loss of consciousness associated with inability to maintain
postural tone. The episode is usually due to hypo-perfusion to the cerebral
cortex and cerebral reticular activating system.
◆ Predisposing factors:
PSYCHOGENIC FACTORS:
• Fright
• Anxiety
52
Unconsciousness
• Emotional stress
• Receipt of unwelcome news
• Pain, especially sudden and unexpected
• Sight of blood or surgical or other instruments
NON-PSYCHOGENIC FACTORS:
• 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
Clinical manifestations:
A. Pre-syncope:
EARLY:
• Feeling of warmth
• Loss of colour; pale pr ashen-grey skin tone
• Heavy perspiration (diaphoresis)
• Reports of “feeling bad” or “feeling faint”
• Nausea
• Blood pressure at baseline level or slightly lower
• Tachycardia
LATE:
• Pupillary dilation
• Yawning
• Hyperpnea
53
Unconsciousness
• Cold hands and feet
• Hypotension
• Bradycardia
• Visual disturbances
• Dizziness
• Loss of consciousness
B. Syncope:
• With loss of consciousness breathing may
1. Become irregular, jerky and gasping;
2. Become quiet, shallow and scarcely perceptible; or
3. Cease entirely.
• Pupils dilate and patient takes on death like appearance
• Convulsive movements and muscular twitching
• Bradycardia, which develops at the end of pre syncope continues, with
≤ 50 bpm.
• Loss of consciousness is also associated with a generalised muscle
relaxation that commonly leads to partial/complete airway obstruction.
C. Postsyncope: (recovery)
• With proper positioning, recovery is rapid.
• BP and heart rate increases; short period of confusion or

disorientation.
54
Unconsciousness
Pathophysiology:
Stress
↓
Catecholamines release
↓
Decreased peripheral vascular release &↑ blood flow to peripheral muscles
↓
↓ venous return
↓
↓ circulatory blood volume & drop in arterial BP
↓
Activation of compensatory mechanisms
↓
Reflux bradycardia develops (<50 bpm)
↓
Significant drop in cardiac output associated with fall in BP below the critical
level
↓
Cerebral ischemia & loss of consciousness
Management:
Assess Unconsciousness
↓
↓
P - Position patient in supine position with feet elevated
↓
C→A→B - Assess circulation; assess and open airway;
assess airway patency and breathing
↓
D - Definitive care:
Administer O2
Monitor vital signs
Preform additional procedures:
Administer aromatic ammonia vaporole; Administer ‘sugar’
Administer atropine if bradycardia persists.
Do not panic!
↓ ↓
(Post-syncopal recovery) (Delayed recovery)
Postpone further dental Activate EMS
treatment ↓
Determine precipitating factors

55
Unconsciousness
POSTURAL HYPOTENSION
A drop in systolic BP of at least 20 mm Hg or of diastolic BP of at least 10 mm
Hg within 3 minutes of standing when compared with BP from sitting or standing
position.
Predisposing factors:
• Administration and ingestion of drugs, like antihypertensives, especially the
sodium-depleting diuretics, calcium channel blockers, and ganglionic-blocking
agents; psychotherapeutics; opioids; histamine blockers and levodopa.
• Prolonged period of recumbency or convalescence
• Inadequate postural reflex
• Late-stage pregnancy
• Advanced age
• Venous defects in the legs
• Recovery from sympathectomy for ‘essential’ hypertension
• Addison’s disease
• Physical exhaustion and starvation
• Chronic postural hypotension (Shy-Drager syndrome)
• Precipitous drops in blood pressure and lose consciousness whenever they
stand or sit upright.
• Do not exhibit any prodromal signs and symptoms
• May become lightheaded, or develop blurred vision
56
Unconsciousness
• Clinical signs and symptoms - precipitating drugs
• Blood pressure during syncopal period is quite low
• Unlike vasodepressor syncope , heart rate during postural hypotension
remain at the baseline level or somewhat higher
• Consciousness returns rapidly once the patient is returned to the supine
position.
Pathophysiology:
When patient moves into an upright position

↓
SBP drops and approaches 60 mm Hg in 1 minute
↓
DBP also drops
↓
Slight changes in heart rate and not at all
↓
Cerebral blood flow drops below the critical level
↓
May lose consciousness
↓
Once the patient is placed into supine position, reestablishment of cerebral
blood flow occurs
57
Unconsciousness
Management:
↓
↓
↓
C→A→B - Assess circulation; assess and open airway;
assess airway patency and breathing
↓
Administer O2
Monitor vital signs
Do not panic!
↓ ↓
(patient recovers (Delayed recovery)
consciousness) Activate EMS
Slowly reposition
chair ↓
Continue BLS as needed
↓
Discharge patient
ACUTE ADRENAL INSUFFICIENCY
• Cortisol deficiency can lead to a relatively rapid onset of clinical symptoms,
including loss of consciousness and possible death.
• First recognised by the British physician Thomas Addison in 1849.
• Addison’s disease - 1º adrenocortical insufficiency is an insidious and usually
progressive condition.
58
Unconsciousness
• Administration of exogenous glucocorticosteroids, to a patient with functional
adrenal cortices - 2nd form of adrenal hypofunction - 2º adrenal insufficiency.
• Exogenous glucocorticoid administration produces a disuse atrophy of the
adrenal cortex, decreasing its ability to ↑ corticosteroid levels in response to
stressful situations, which in turn leads to the development of signs and
symptoms associated with acute adrenal insufficiency.
• 2º adrenal insufficiency is 2-3 times more common than 1º.
Lack of glucocorticosteroid hormones is the major predisposing factor in all
cases of acute adrenal insufficiency.
• Mechanism 1: sudden withdrawal of steroid hormones in a parent who
suffers 1º adrenal insufficiency (Addison’s disease).
• Mechanism 2: sudden withdrawal of steroids from a patient with normal
adrenal cortices but with a temporary insufficiency resulting from cortical
suppression through prolonged glucocorticosteroid administration (2º
insufficiency).
• Mechanism 3: after stress, either physiologic or psychological.
• Mechanism 4: after bilateral adrenalectomy or removal of a functional
adrenal tumour that was suppressing the other adrenal gland.
• Mechanism 5: after sudden destruction of pituitary gland.
59
Unconsciousness
• Mechanism 6: after both adrenal glands are injured through trauma,
hemorrhage, infection, thrombosis, or tumour.
RULE OF TWOs:
Adrenocortical suppression should be suspected if a patient has received
glucocorticoid therapy via 2 of the following:
1. In a dose of 20 mg or more of cortisone or its equivalent.
2. Via the oral or parenteral route for a continuous period of 2 weeks or longer.
3. Within 2 years of dental therapy.
Symptoms Signs
• Weakness, fatigue • Hyperpigmentation
• Anorexia • Salt craving
• GI symptoms • Orthostasis, syncope
• Weight loss • Vitiligo
• BP ≤ 110/70 • Hyperkalemia
• Fever • Hypercholemia and acidosis
• Depression, apathy • Hypoglycemia
• Myalgia, arthralgia
• Articular calcifications
60
Unconsciousness
Pathophysiology:
61
Unconsciousness
Management:
Conscious
(Victim responds to sensory stimulation)
↓
Terminate dental treatment
↓
P - Position patient comfortably if symptomatic; supine with feet
slightly elevated, if symptomatic
↓
C→A→B - Provide BLS as needed
↓
Monitor vital signs
Summon medical assistance
Obtain emergency kit and O2
Administer glucocorticosteroid, if available, and if history of
adrenal insufficiency exists
↓
Consider additional management:
Provide BLS as needed
Provide O2 as needed
Provide glucocorticosteroid as needed
Unconscious
(Victim unresponsive to sensory stimulation)
↓
P - Position patient supine with feet elevated slightly
↓
C→A→B - Provide BLS as needed
↓
Summon medical assistance
Obtain emergency kit and O2
Evaluate medical history
Monitor vital signs
↓
Consider additional management:
Provide BLS as needed
Provide O2
Provide glucocorticosteroid as needed
Establish IV access if possible
↓
Transfer to hospital
62
Respiratory Distress
RESPIRATORY DISTRESS
• Hyperventilation
• Vasodepressor syncope
• Asthma
• Hypoglycaemia
• Overdose reaction
• Acute MI
• Anaphylaxis
• Angioneurotic edema
• Cerebrovascular accident
• Epilepsy
• Hyperglycemia
• Most cases, retain consciousness throughout acute episode, which is a + sign
that minimum amount of blood and O2 is available for normal cerebral
function, but leads to an additional problem, acute anxiety.
63
Management:
Recognise respiratory distress

(sounds: wheeze, cough, crackling, abnormal rate or
depth of breathing)
↓
↓
P - Position patient in supine, if unconscious
or comfortably (usually upright) if conscious
↓
C→A→B - Assess and provide basic life support, as
needed
↓
D - Monitor vital signs: blood pressure, heart rate,
respiratory rate
Manage patient’s anxiety
Provide definitive management of respiratory distress
Activate emergency medical services as needed
FOREIGN BODY AIRWAY OBSTRUCTION:
Prevention:
• Rubber dam
• Oral packing (4¨x4¨ gauze)
• Chair position
• Dental assistant
• Suction
• Magill intubation forceps
• Ligature - dental floss

64
Management:
VISIBLE OBJECTS
If assistant is present
Place the patient into supine or Trendelenburg
position
↓
Use magill intubation forceps or suction to remove
foreign body
If assistant is NOT present
Instruct the patient to bend over arm of chair with
their head down
↓
Encourage patient to cough
SWALLOWED OBJECTS
Consult radiologist
↓
Obtain appropriate radiographs to determine the
location of object
↓
Initiate medical consultation with appropriate
specialist
ASPIRATED FOREIGN BODIES

Place patient in left lateral decubitus position
↓
Encourage patient to cough
↓ ↓
Foreign body Consult with radiologist
is retrieved or emergency dept;
↓ obtain appropriate xrays
Initiate medical to determine the location
consultation of foreign body
before ↓
discharge Perform bronchoscopy
to visualise and
retrieve foreign body

65
HYPERVENTILATION
Ventilation in excess of that of required to maintain normal blood PaO2 and
PaCO2. It is produced by ↑ in frequency or depth of reparation or both.
• Acute anxiety
• Apprehensive patient who hide their fear
System Signs & symptoms
Cardiovascular Palpitations; Tachycardia; Precordial “pain”
Dizziness; lightheadedness; disturbance of

Neurologic consciousness; disturbance of vision;
numbness and tingling of extremities; tetany
(rare)
Shortness of breath; chest “pain”; dryness of
Respiratory
mouth
Gastrointestinal Globus hystericus; epigastric pain
Muscle pain and cramps; tremor; stiffness;

Musculoskeletal
carpopedal tetany
Psychological Tension; anxiety; nightmares
66
Management:
Recognise problem
(rapid, deep, uncontrolled breathing)
↓
P - Position patient comfortably
↓
C→A→B - Basic life support, as needed
↓
Remove dental materials from patient’s mouth
Calm patient
Correct respiratory alkalosis
Initiate drug management as needed
↓
Dental care may continue if BOTH doctor and patient agree
↓
Discharge patient
ASTHMA
A Philadelphia physician, Eberle in 1830, described asthma as, “Paroxysmal
affection of the respiratory organs, characterised by great difficulty of breathing,
tightness across the chest, and a sense of impending suffocation, without fever
or local inflammation”.
Today asthma is defined as, “A chronic inflammatory disorder that is
characterised by reversible obstruction of the airways.”
• Allergy - extrinsic asthma
• Respiratory infection
67
• Physical exertion
• Environmental and air pollution
• Occupational stimuli
• Pharmacologic stimuli
• Psychological factors
• Status asthmaticus - most severe; wheezing, dyspnea, hypoxia; true medical
emergency - patient may die due to respiratory changes that develop
secondary to respiratory distress.
Commonly prescribed drugs for management of obstructive airway
disease:
BRONCHODILATORS:
• Albuterol, salmeterol, metaproterenol, levalbuterol, pirbuterol, terbutaline,
isoetharine, isoproterenol, epinephrine, tiotripium, formoterol -
sympathomimetic.
• Ipatropium - anticholinergic.
• Theophylline, aminophylline - theophylline.
CORTICOSTEROID:
• Beclomethasone, triamcinolone acetonide, flunisolide, mometasone,
fluticasone, budesonide.
ANTIMEDIATOR:
• Cromolyn sodium, nedocromil sodium

68
• Feeling of chest congestion
• Cough, with or without sputum production
• Wheezing
• Dyspnea
• Patient wants to sit or stand up
• Use of accessory muscles of respiration
• Increased anxiety and apprehension
• Tachypnea (>20 to >40 beats pm in severe cases)
• Rise in BP
• Increase in heart rate (>120 bpm in severe episodes)
• Diaphoresis
• Agitation
• Somnolence
• Confusion
• Cyanosis
• Supraclavicular and intercostal injection
• Nasal flaring
69
Management:
Recognise problem
(respiratory distress, wheezing)
↓
↓
↓
(usually upright)
↓
C→A→B - Assess and perform basic life support, as needed
↓
D - Provide Definitive management:
↓
Administer O2
Administer bronchodilator via inhalation
(episode terminates) (episode terminates)
↓ ↓
Dental care may activate EMS
continue ↓
↓ administer parenteral drugs
Discharge patient ↓
Hospitalise or discharge patient,
per EMS recommendation
HEART FAILURE AND ACUTE PULMONARY EDEMA
Heart failure is defined as, the inability of the heart to supply sufficient
oxygenated blood for the body’s metabolic needs.
Acute pulmonary edema is a life-threatening condition marked by an excess of
serous fluid in the alveolar spaces or intestinal tissues of the lungs
accompanied by extreme difficulty in breathing.
70
• Increasing the workload of the heart.
• Damaging the muscular walls through MI.
• Cardiac valvular deficiencies
• increase in body’s requirement for O2 & nutrients.
• Hypertension
Prevention:
• Medical history questionnaire
• Dialogue history
• Physical evaluation
• Physical inspection - cyanosis - skin and mucous membrane; prominent

jugular veins; pitting edema in ankles.
Dental therapy considerations:
ASA physical status classification for heart failure:
• ASA 1 - no dyspnea and fatigue with normal exertion. No special
dental modifications.
• ASA 2 - mild dyspnea and fatigue during exertion. Stress reduction
protocol should be considered.
• ASA 3 - dyspnea and fatigue with normal activities. Medical
consultation, stress reduction, other treatment modifications.
71
• ASA 4 - dyspnea, undue fatigue and orthopnea at all times. Only
elective procedures - dental emergencies managed with medication -
physical intervention only in hospital dental clinics.
Heart failure:
Signs:
• Pallor, cool skin Symptoms:
• Weakness and undue

• Sweating (diaphoresis)
fatigue
• LVH
• Dyspnea on exertion
• Dependent edema
• Hepatomegaly and
• Nocturia
splenomegaly
• Paraoxysmal nocturnal
• Narrow pulse pressure
dyspnea
• Pluses alterans
• Wheezing (cardiac
asthma)
• Ascites
Acute pulmonary edema:
• All the signs and symptoms of heart failure.
• Moist rales of lungs
• Tachypnea
• Cyanosis
• Frothy pink sputum
• Increased anxiety, dyspnea at rest

72
Pathophysiology:
Structural and functional cardiac disorder

↓
Impairs left ventricular ability to fill with or eject blood
↓
Limit exercise tolerance and fluid retention
↓
Pulmonary congestion and peripheral edema
↓
right ventricular failure signs and symptoms related to systemic venous and
capillary congestion
↓
acute pulmonary edema - drastic symptom of heart failure
↓
Excess fluid in alveolar spaces and interstitial tissues
↓
Suffocation and oppression of the heart
↓
Elevates heart rate and BP
↓
Increases additional load to the heart
↓
Further increase in cardiac function due to hypoxia
↓
If this vicious circle is not interrupted, it may lead rapidly to death
73
Altered consciousness
Management:
Recognise problem
(conscious patient exhibiting difficulty in breathing)
↓
↓
P - Position conscious patient comfortably, usually upright
↓
Activate office emergency system
↓
Calm the patient
↓
C→A→B - Assess and do basic life support, as needed
↓
Administer O2
Monitor vital signs
Alleviate symptoms of respiratory distress:
Perform bloodless phlebotomy
Administer vasodilator e.g., Nitroglycerine
Alleviate apprehension e.g., Morphine
↓
Discharge patient
↓
Modify subsequent dental treatment
C, Circulation; A, Airway; B, Breathing; D, Definitive Care; P, Position.
ALTERED CONSCIOUSNESS
• A state of altered consciousness may represent a clinical manifestation of any
number of systemic medical conditions.
• Altered consciousness may be the 1st clinical sign of a serious medical
problem requiring immediate and intensive therapy.
74
• Ingestion or administration of drugs - alcohol, sedatives, benzodiazepines,
local anesthetics.
• Diabetes mellitus
• Cerebrovascular ischemia
• Thyroid gland dysfunction
Management:
Recognise problem
(alteration in the level of consciousness)
↓
↓
↓
P - Position patient appropriately
↓
C→A→B - Assess pulse, airway and breathing.
Administer basic life support as needed.
↓
Activate EMS if indicated
↓
Monitor vital signs
Manage signs and symptoms
Definitive management as needed
75
DIABETES MELLITUS - HYPERGLYCEMIA & HYPOGLYCEMIA
Most common endocrine disorder.
Group of diseases marked by high levels of blood glucose resulting from
defects in insulin production, insulin action or both.
Acute complications:
• Hypoglycemia
• Diabetes ketoacidosis
• Hyperglycemia.
Chronic complications:
• Vascular system, kidney, nervous system, eyes, skin, mouth and pregnancy
complications.
• Mouth - gingivitis, increased incidence of dental caries and periodontal
disease, alveolar bone loss.
Type I diabetes: factors that selectively destroy insulin producing beta cells.
• Genetic factors
• Environmental factors like drugs, toxins and viruses (mumps, rubella,

coxsackie)
• Autoimmune factors
76
Type II diabetes: 3 cardinal abnormalities - resistance to action of insulin in
peripheral tissues; defective insulin secretion, particularly in response to a
glucose stimulus; increased glucose production by liver.
• Genetic factors
• Insulin secretion
• Insulin resistance
• Obesity
• Adipocyte derived hormones and cytokines
Other specific types of diabetes mellitus
• Gestational diabetes mellitus
• Impaired glucose tolerance
• Impaired fasting glucose
Precipitants of hypoglycemia in diabetic patients:
• Addison’s disease
• Anorexia nervosa
• Decrease in usual food intake
• Ethanol
• Factitious hypoglycemia
• Hepatic impairment
• Hyper and hypothyroidism
• Increase in usual exercise
• Insulin
• Islet cell tumours
77
• Incorrectly used insulin pump
• Malnutrition
• Old age
• Oral hypoglycemic agents
• Over aggressive treatment of ketoacidosis
• Pentamidine, Phenylbutazone, Propranolol
• Recent change in dose
• Salicylates
• Sepsis
ASA physical status - Treatment considerations
II
• Eat normal breakfast and take usual insulin dose in the morning
• Avoid missing meals before and after surgery
• If missing meal is unavoidable, consult physician or reduce insulin dose by

half.
III
• Monitor blood glucose levels more frequently for several days following
surgery and modify insulin accordingly
• Consider medical consultation
78
IV
• Consult physician before treatment
• Antibiotic coverage in the postsurgical period is appropriate
• Stress reduction protocol to be followed
Clinical manifestations of hypoglycemia:
Early stage – mild reaction
• Diminished cerebral function
• Changes in mood
• Decreased spontaneity
• Hunger
• Nausea
More severe stage
• Sweating
• Tachycardia
• Piloerection
• Increased anxiety
• Bizarre behavioral patterns
• Belligerence
• Poor judgment
• Uncooperativeness
79
Later severe stage
• Unconsciousness
• Seizure activity
• Hypotension
• Hypothermia
Pathophysiology:
Hyperglycemia:
• Prolonged lack of insulin (type I) or prolonged lack of tissue response (type II)
• Blood glucose levels remains elevated for longer time coz of glycogenolysis
and ↓ uptake by peripheral tissues
• Glucose exceeds 180mg/100 ml – glucosuria
• Because of its large molecular size, glucose in urine carries away large
+ +
volumes of water and electrolytes (Na & K ) – polyuria
• Dehydrated state – skin dry and flushing - polydipsia
• Weight loss due to depletion of water, glycogen, triglyceride(TGA) stores
• Loss of muscle mass due to aminoacids → glucose and ketone bodies
• TGA → free fatty acids (FFA) in the liver
• FFA – acetoacetate and β – hydroxybutyrate (BHA) – diabetic

ketoacidosis
• Decreased cardiac contractility, catecholamine response, respiratory alkalosis
• Diabetic coma
Hypoglycemia:
• Hypoglycemia in adults – blood sugar < 50 mg/dl, in children - < 40 mg/dl
• Alters normal functioning of the cerebral cortex
80
• Mental confusion and lethargy
• Lack of glucose → ↑ activities of sympathetic and parasympathetic nervous

systems
• With the mediation of epinephrine,↑ systolic and mean blood pressures
• ↑ sweating and tachycardia
• When the blood sugar level drops even further
• Hypoglycemic coma and insulin shock
Patients may experience tonic – clonic convulsions.
Management of hyperglycemia - unconscious patient:
Recognise problem
(lack of response to sensory stimulation)
↓
↓
↓
↓
C→A→B - Assess and perform basic life support as needed.
↓
D - Provide definitive management as needed
Summon EMS
Establish IV - 5% dextrose and water, if possible
Administer O2
Transport to hospital for definitive management
81
Management of hypoglycemia - conscious patient and unconscious
patient:
Recognise problem
↓
↓
↓
↓
↓
D - Definitive management:
Summon EMS
Administer carbohydrates
Establish IV - 5% dextrose solution
1 mg glucagon via IV or IM route
Trans mucosal sugar, or rectal honey or syrup
Monitor vital signs every 5 minutes
Administer O2
↓
Allow patient to recover and discharge per medical recommendations
Recognise problem
(altered consciousness )
↓
↓
↓
↓
↓
Administer oral carbohydrates
If successful If unsuccessful
↓ ↓
Permit patient to recover activate EMS
↓ ↓
Discharge patient Administer parenteral
Carbohydrates
↓
Monitor patient
↓
Discharge patient
82
THYROID GLAND DYSFUNCTION
The thyroid gland secretes 3 hormones (T3,T4 and calcitonin)that are vital in
the regulation of the level of biochemical activity of most of the body’s tissues.
• Thyroid gland dysfunction may occur either through overproduction
(thyrotoxicosis) and underproduction (hypothyroidism) of thyroid hormone.
Causes of hypothyroidism:
PRIMARY HYPOTHYROIDISM:
• Autoimmune - Hashimoto’s and graves’
• Iatrogenic - radioactive I2 therapy, thyroidectomy
• Iodine related - iodine deficiency/excess
• Drug related - lithium, amiodarone, interferon-alpha, iodine excess,

propylthiouracil, methamizole.
• Thyroiditis - subacute, silent, postpartum, amiodarone
• Congenital defect in thyroid hormone synthesis
CENTRAL HYPOTHYROIDISM:
• Euthyroid sick syndrome
• Pituitary disease - pituitary adenoma, hemorrhage, infiltrative
• Hypothalamic disease
83
Causes of hyperthyroidism:
• Graves’ disease
• Toxic multinodular goitre
• Toxic adenoma
• Factitious thyrotoxicosis
• Thyrotoxicosis associated with thyroiditis
• Hashimoto’s thyroiditis
• Subacute (de Quervain’s) thyroiditis
• Postpartum thyroiditis
• Sporadic thyroiditis
• Amiodarone thyroiditis
• Iodine-induced hyperthyroidism
• Amiodarone
• Radiocontrast media
• Metastatic follicular thyroid carcinoma
• hCG-mediated thyrotoxicosis
• Hydatiform mole
• Metastatic choriocarcinoma
• Hyperemesis gravidarum
• TSH-producing pituitary tumors
• Struma ovarli
84
Prevention:
• Medical history questionnaire
• Dialogue history
Dental therapy considerations
• Euthyroid patient with normal hormone levels can be managed
normally.
• Hypothyroid – avoidance of CNS depressants (opioids, sedative
hypnotics).
• Hyperthyroid – avoidance of atropine and vasoconstrictors, least
concentrated solution is preferred 1:200,000, smallest effective volume
of anesthetic and vasodepressor, aspiration prior to every injection.
• Evaluation of cardio vascular disease.
Hypothyroidism:
Signs Symptoms
Pseudomyotonic reflexes
Paresthesias 
Change in menstrual pattern
Loss of energy
Hypothermia 
Intolerance to cold
Dry, scaly skin
Muscular weakness 
Puffy eyelids 
Pain in muscles and joints
Hoarse voice 
Inability to concentrate
Weight gain 
Drowsiness 
Dependent edema 
Constipation
Sparse axillary and pubic hair Pallor
Forgetfulness 
Thinning eyebrows
Depressed auditory acuity
Yellow skin 
Emotional instability
Loss of scalp hair
Headaches 
Abdominal distension
Dysarthria
Goitre
Decreased sweating
85
Thyrotoxicosis:
Signs Symptoms
Common
Fever 
Tachycardia 
Weight loss
Sinus tachycardia
Palpitations
Dysrhythmias 
Nervousness
Wide pulse pressure
Tremor 
Tremor 
Less common
Thyrotoxic stare and eyelid retraction 
Hyperkinesis 
Chest pain
Heart failure 
Dyspnea
Weakness 
Edema
Coma 
Psychosis
Tender liver 
Disorientation
Infiltrative ophthalmopathy Somnolence
Diarrhea
or obtundence Jaundice
Abdominal pain
Pathophysiology:
Hypothyroidism:
Insufficient levels of thyroid hormones

↓
Body functions slow down
↓
Infiltration of mucopolysaccharides and mucoproteins in skin
↓
Hard nonpitting mucinous edema – myxedema
↓
Cardiac enlargement, pericardial and pleural effusions
↓
Cardiovascular and respiratory difficulties
↓
End point is myxedema coma- loss of consciousness due to hypothermia,
hypoglycemia and CO retention
2
86
Thyrotoxicosis:
Thyroid hormones ↑ body’s energy consumption and BMR

↓
Fatigue &weight loss
↓
Direct actions on myocardium - ↑ HR, ↑ myocardial irritability
↓
↑ cardiac work load
↓
Palpitations, dyspnea, chest pain
↓
↑ incidence of angina pectoris and heart failure
↓
↑ thyroid hormones also affects liver function
↓
End point – thyroid storm and crisis
Management:
HYPOTHYROID PATIENT (MYXEDEMA COMA)

HYPERTHYROID PATIENT (THYROID STORM)
RECOGNISE PROBLEM
↓
↓
↓
P - Position patient supine with feet elevated
↓
↓
D - Definitive management:
Activate EMS, if recovery not immediate
Establish IV access, if possible
Administer O2
↓
Discharge or hospitalisation of patient as per emergency medical
technicians
C, Circulation; A, Airway; B, Breathing; D, Definitive Care; P, Position. 
87
CEREBROVASCULAR ACCIDENT
Any vascular injury that reduces vascular injury that reduces cerebral blood flow
to a specific region of the brain, causing neurologic impairment.
• CVA is a focal neurologic disorder caused by destruction of brain substance
as a result of intracerebral hemorrhage, thrombosis, embolism or vascular
insufficiency, aka stroke, cerebral apoplexy and brain attack.
Classification:
• Cerebral ischemia and infarction - atherosclerosis & thrombosis, cerebral
embolism
• Intracranial hemorrhage - arterial aneurysms & hypertensive vascular disease
• Others – TIA – Transient ischemic attacks
TIA is a neurologic deficit that has complete clinical resolution within 24
hours.
• Consistently elevated blood pressure is a major risk factor
• Diabetes mellitus
• Cardiac enlargement
• Hypercholesterolemia
• Use of oral contraceptives
• Cigarette smoking
88
• Length of time elapsed since the CVA – should not undergo elective
dental care within 6 months of the episode
• Minimization of stress – morning appointments, effective pain control,
psychosedation during treatment
• Assessment of bleeding – most of CVA patients on antiplatelet or
anticoagulant therapy.
INFARCTION:
• Gradual onset of signs and symptoms
• TIA frequently preceding
• Headache, usually mild
• Neurologic signs and symptoms
• Transient monocular blindness - TIA
EMBOLISM:
• Abrupt onset of signs and symptoms
• Mild headache preceding neurologic signs and symptoms by several hours
HEMORRHAGE:
• Abrupt onset of signs and symptoms
• Sudden, violent headache
89
• Nausea and vomiting
• Chills and sweating
• Dizziness and vertigo
• Neurologic signs and symptoms
Pathophysiology
Cerebrovascular ischemia and Hemorrhagic CVA

infarction
• At cellular level, ischemia

• Anaerobic glycolysis with production of
lactate
• Mitochondrial dysfunction → disruption •Subarachnoid hemorrhage – ruptured
of membrane and vascular endothelium aneurysms
• BBB breaks down and edema forms  •Intracranial hemorrhage – hypertensive
• Edema ↑ tissue mass in cranium causes vascular disease •Once vessels rupture
mild headache •Arterial blood supply fills the cranium
• Severe edema may forces the portions •↑ in intracerebral blood pressure
of cerebral hemisphere into tentorium •Rapid displacement of brain stem into
cerebelli tentorium cerebelli •Ultimately death
• Ischemia and infarction of
upperbrain stem (medulla)
• Loss of consciousness and fatal
90
Management:
CONSCIOUS PATIENT
Recognise problem
(patient responds to sensory stimulation)
↓
↓
↓
↓
↓
Activate EMS
Monitor vital signs
Manage signs and symptoms
If BP elevated, place patient in semi-Fowler position
Administer O2
Do NOT administer CNS depressants
↓ ↓ ↓
Symptoms Symptoms Loss of
consciousness
resolve TIA(?) persist CVA/TIA hemorrhagic CVA (?)
↓ ↓ ↓
Follow-up Hospitalisation P - position supine
management with feet elevated
↓
C→A→B - BLS
↓
Monitor vital signs
↓
If BP ↑, reposition (semi-Fowler)
↓
D - Definitive care: Establish IV
91
Seizures
SEIZURES
Classification of epileptic seizures:
Partial seizures Generalised seizures
• Simple partial seizures • Absence seizures (true petit mal)

• Complex partial seizures • Myoclonic seizures
• Partial seizures evolving to • Tonic-clonic seizures (grand mal)
generalised tonic-clonic • Unclassified seizures
Causes:
• Congenital abnormalities
• Perinatal abnormalities
• Metabolic and toxic disorders
• Head trauma
• Tumours and other space-occupying lesions
• Vascular diseases
• Degenerative disorders
• Infectious diseases
• Hypoxia , hypoglycemia, hypocalcemia
• Flashing lights, fatigue, decreased physical health, a missed meal, alcohol
ingestion, physical or emotional stress, sleep and menstrual cycle.
Prevention:
• Care in selection of LA agent & use of proper technique
92
Seizures
• Medical history questionnaire about fainting spells, seizures
• Dialogue history about previous experience of seizures, onset,
duration, management
Conscious sedation – N2O – O2 & benzodiazepines
• Simple partial seizure – individual remains conscious while a limb jerks for
several seconds
• Complex partial seizures – altered consciousness with altered behavioral
patterns (automatisms) like some uncoordinated purposeless activities (lip
smacking, chewing or sucking)
• Absence seizure – sudden immobility and a blank stare and minor facial
clonic movements
• Tonic-clonic seizure – 3 phases: a prodromal phase, including preictal
phase; a convulsive, or ictal phase; and a postseizure or postictal phase.
- PREICTAL PHASE:
• Increase in anxiety and depression, appearance of aura and soon loses

consciousness, a series of myoclonic jerks occur (epileptic cry).
• Increase inherit rate, blood pressure, bladder pressure, piloerection,

glandular hypersecretion, mydriasis, apnea.
93
Seizures
- ICTAL PHASE:
• Series of generalized skeletal muscle contractions progresses to a

extensor rigidity of extremities and trunk – tonic component.
• Generalized clonic movements, heavy stertorous breathing, alternate

muscle relaxation and violent flexor contractions – clonic component.
- POSTICTAL PHASE:
• Tonic-clonic movements cease, breathing returns to normal,

consciousness gradually returns.
Pathophysiology:
Intrinsic intracellular and extracellular metabolic disturbances in neurons of

epileptic patients
Excessive and prolonged depolarisation
↑ in neuronal permeability to sodium and potassium ions
Ach. & GABA sustained membrane depolarization followed by local hyper

polarization
This abnormal discharge propagated through neuronal pathways and partial

seizure becomes generalized
94
Seizures
Management of petit mal and partial seizures:
Recognise problem
↓
↓
↓
P - position patient supine feet elevated
↓ ↓
Seizure ceases: Seizure continues (>5 min):
reassure patient Activate EMS
↓ ↓
Allow patient to recover C→A→B
before discharge perform bls
Management of tonic-clonic seizure (grand mal):
PRODROMAL PHASE
Recognise aura
↓
ICTAL PHASE
↓
↓
↓
Consider activation of EMS
↓
C→A→B - Assess and perform basic life support
↓
D - Definitive care
Protect patient from injury
POSTICTAL PHASE
↓
↓
↓
D - Definitive care
Administer O2
Monitor vital signs
Reassure patient and permit necessary
Discharge patient
↓ ↓ ↓
To hospital to home to physician
95
Seizures
Management Of Tonic-Clonic Status:
PRODROMAL PHASE
Recognise aura
↓
ICTAL PHASE
↓
↓
↓
↓
↓
D - Definitive care
Protect patient from injury
IF SEIZURE PERSISTS FOR MORE THAN 5 MINUTES
↓ ↓
C→A→B - Assess and if available
perform basic life support perform venipuncture
Protect patient from injury & administer IV
anticonvulsant
↓ ↓
D - Definitive care administer 50% IV
Protect the patient from injury dextrose solution
Until EMS arrives
96
Drug-related emergencies
DRUG RELATED EMERGENCIES
Classification of Adverse Drug Reactions:
1. TOXICITY RESULTING FROM DURECT EXTENSION OF
PHARMACOLOGIC EFFECTS
• Side effects
• Abnormal dose (overdose)
• Local effects
2. TOXICITY RESULTING FROM ALTERED RECIPIENT
• Presence of pathologic process
• Emotional disturbance
• Genetic aberrations (idiosyncrasy)
• Teratogenicity
• Drug-drug interactions
3. TOXICITY RESULTING FROM DRUG ALLERGY
DRUG OVERDOSE REACTIONS
Clinical signs and symptoms that result from overly high blood levels of a drug
in various target organs and tissues.
1. OVERDOSE REACTION FROM LOCAL ANESTHETICS:
Predisposing factors for local anesthesia overdose reactions:
97
PATIENT FACTORS:
• Age
• Body weight
• Pathalogic processes (liver, heart)
• Genetics (atypical plasma cholinesterase)
• Mental attitude
• Gender
DRUG FACTORS:
• Vasoactiviiy
• Dose
• Route of administration
• Rate of injection site
• Presence of vasoconstrictor.
Causes of high blood levels of LA:
• Biotransformation of the drug is unusually slow
• Drug is slowly eliminated from the body through the kidneys
• Total dose of LA administered is too large
• Absorption of LA from the site of injection is usually rapid
• LA is inadvertently administered intravenously
98
CLINICAL MANIFESTATIONS:
SIGNS
Low to moderate overdose levels:
• Confusion, talkativeness, apprehension, excitednesss, slurred speech,
generalised stutter, muscular twitching and tremor of the face and extremities,
nystagmus, increased blood pressure, heart rate and respiratory rate.
Moderate to high blood levels:
• Generalised tonic-clonic seizure followed by : generalised central nervous
system depression, decreased blood pressure , heart rate and respiratory
rate.
SYMPTOMS:
• Headaches, dizziness, light headedness, blurred vision, inability to focus,
ringing in ears, numbness of tongue and periodical tissues, flushed or chilled
feeling, drowsiness, disorientation and loss of consciousness.
Usual LA blood level for onset of clinical manifestations of overdose:
Usual threshold for CNS signs

Agent
and symptoms
Bupivacaine, etidocaine 1-2 µg/mL
Prilocaine 4 µg/mL
Lidocaine, mepivacaine 5 µg/mL
99
Management of mild LA overdose with rapid onset and mild overdose
with delayed onset(>10 min):
Recognise problem
(onset 5-10 minutes after LA administration, talkativeness, ↑
anxiety, facial muscle twitching, ↑ BP,HR,RR)
↓
↓
P - Position patient supine comfortably
↓
Reassure the patient
↓
C→A→B - Assess circulation, airway, breathing and perform
basic life support as needed
↓
Administer O2
Monitor vital signs
Administer anticonvulsant drug as needed
Activate EMS a needed
Permit patient to recover
Discharge patient
100
Management of severe LA overdose with slow or rapid onset:
Recognise problem
(onset seconds to 1 minute after LA administration, generalised
tonic-clonic seizures, loss of consciousness)
↓
P - Position patient supine with legs elevated slightly
↓
Activate EMS
↓
C→A→B - Assess circulation, airway, breathing and
perform basic life support as needed
↓
Administer O2
Protect the patient from injury
Monitor vital signs
Establish IV and administer anticonvulsant drug as needed
↓
Postictal management
C→A→B - Assess circulation, airway, breathing and perform basic
life support as needed
↓
Administer O2
Monitor vital signs
101
2. EPINEPHRINE OVERDOSE REACTION:
Precipitant factors:
• Vasoconstrictor in LA - epinephrine
• Racemic epinephrine cord to retract gingival tissue
SIGNS:
• Elevated BP
• Elevated heart rate
SYMPTOMS:
• Fear • Perspiration
• Anxiety • Weakness
• Tenseness • Dizziness
• Restlessness • Pallor
• Throbbing headache • Respiratory difficulty
• Tremor • Palpitations
102
Management of epinephrine overdose:
Recognise problem
(↑ anxiety after injection, tremor of limbs, diaphoresis, headache,
florid appearance, possible ↑/↓ HR,↑ BP)
↓
↓
↓
C→A→B - Assess circulation, airway, breathing and administer basic
life support as needed
↓
Reassure the patient
Monitor vital signs
Activate EMS as needed
Administer O2
Permit patient to recover
Administer vasodilator as needed
Discharge of patient
ALLERGY
Allergy is defined as the hypersensitive state acquired through exposure to a
particular allergen, re-exposure to which produces heightened capacity to react.
Drugs used in dentistry that may potentially cause allergy:
ANTIBIOTICS:
• Penicillins • Tetracylines
• Cephalosporins • Sulfonamides
103
ANALGESICS:
• Acetylsalicylic acid • NSAIDs
OPIOIDS:
• Fentanyl • Meperidine
• Morphine • Codeine
LOCAL ANESTHETICS:
• Esters • Antioxidant
• Procaine • Sodium (meta)bisulfite
• Propoxycaine • Parabens
• Benzoicaine • Methylparaben
• Tetracaine
OTHER AGENTS: ANTIANXIETY DRUGS:
• Acrylic monomer (methyl methacrylate) Barbiturates
Allergenic drugs and possible substitutes:
Category Drug Substitute
Antibiotics Penicillin Erythromycin
Acetaminophen
Analgesics Acetylsalicylic acid
NSAIDs
Flurazepam
Diazepam
Sedative- hypnotics Opioid
Triazolam
Hydroxyzine
Avoid use if possible,

Acrylic Methyl methacrylate otherwise use heat-cured
acrylic
Non-vasodepressor
Antioxidants Bisulfites containing local
anesthetic
104
Signs and Symptoms of an Allergic Reaction
• Cutaneous reactions are the most common occurrence and include
urticarial, exanthematous, and eczemoid reactions. Itching is common
and can also find exfoliative dermatitis and bullous dermatosis.
• Angioedema (Swelling) this varies from localized slight swelling of the
lips, eyelids, and face to more uncomfortable swelling of the mouth,
throat, and extremities.
• Respiratory (Tightness in chest, sneezing, bronchospasm)
bronchospasm is a generalized contraction of bronchial smooth
muscles resulting in the restriction of airflow. This may also be
accompanied by edema of the bronchiolar mucosa.
• Bronchospasm is more common with pre-existing pulmonary disease
such as asthma or infection but can also be caused by the inhalation of
a foreign substance.
• Ocular reactions include conjunctivitis and watering of eyes.
• Hypotension can occur with any allergic reaction.
Anaphylaxis:
Signs and symptoms include:
• Cardiovascular symptoms including; pallor, syncope, palpitations,
tachycardia, hypotension, arrythmias, and convulsions.
• Respiratory symptoms include; sneezing, cough, wheezing, tightness
in chest, bronchospasm, laryngospasm.

105
• Skin is warm and flushed with itching, urticaria, and angioedema.
• Nausea, vomiting, abdominal cramps, and diarrhea also possible.
Evaluation of Allergic Reactions: Things to remember.
• Skin manifestations may precede more serious cardiorespiratory
problems.
• Recognition of skin reactions and early treatment may abort more
serious problems.
• Most important factor is assessing the seriousness of the condition is
the rate of onset.
• Reactions that occur greater than one hour after the administration of
the allergen will usually be of a non- emergent nature.
MANAGEMENT:
1. General Treatment:
• Airway, Breathing and Circulation should be evaluated.
• Maintain airway, administer oxygen, and determine possible need for

intubation or surgical airway.
• Monitor vital signs.
• If in shock put patient in a horizontal or slight Trendelenburg position.
2. Mild Reactions:
• Antihistamines usually effective. (Benadryl 50-100mg or

Cholpheniramine maleate 4-12 mg IV, or IM.)
106
• Identify and remove allergen.
• Follow up medications in 4-6 hours.
3. Severe Reactions:
• If available start IV Fluids
• Epinephrine is drug of choice. Usually prepackaged 1:1,000 in 1mg

vials or syringe
• If IV in place titrate 1:1,000 solution to effect.
• If drop in blood pressure is minimal, start with 0.5ml (0.5mg.)
• If drop in blood pressure is severe start with 2ml (2mg.)
• Repeat after 2 minutes if needed.
• If no IV use 1:1,000 (1mg/CC) IM 0.3 to 0.5mg (0.3-0.5CC.)
• For an adult repeat this dose in 10 to 20 minutes.
• If the patient is intubated can give epinephrine endotracheally
• If Asthma, edema, or pruritis are present can use Corticosteroids.

However these drugs are to slow acting to be used for an emergency
situation.
• Hydrocortisone sodium succinate 100-500mg IV or IM.

Dexamethasone 4-12mg IV or IM.
Repeat dose at 1, 3, 6, and 10 hours as indicated by severity of
symptoms.
4. Other Considerations
• Monitor and record vital signs.
• Seizures are possible as a result of circulatory or respiratory

insufficiency.
• Most severe allergic reactions require hospitalization and observation

for 24 hours.
107
Chest pain
CHEST PAIN
ANGINA PECTORIS
A characteristic thoracic pain, usually substernal, precipitated chiefly by
exercise, emotion, or a heavy meal; relieved by vasodilator drugs and a few
minutes rest; and a result of a moderate inadequacy of the coronary circulation.
Precipitating factors:
• Physical activity
• Hot, humid environment
• Cold whether
• Large meals
• Emotional stress
• Caffeine ingestion
• Fever, anemia, thyrotoxicosis
• Cigarette smoking
• Smog
• High altitudes
• Second – hand smoke
• Avoid overstressing the patient
• Supplemental oxygen via nasal cannula or nasal hood during the treatment –
3-5 L/min
• Pain control during therapy – appropriate use of local anesthesia – smaller
dose with maximum effect – slow administration
108
Chest pain
• Vasodepressor administration should be minimized in increased risk patients
• Psychosedation – N O – O is preferable
2 2
• Monitoring vital signs
• Nitroglycerine premedication 5 min before treatment
• Pain: sudden onset of chest pain, described as a sensation of squeezing,
burning, pressing, choking, aching, bursting, tightness or gas
• Dull aching heavy pain located substernally
• Radiation of pain: most commonly to left shoulder and arm (ulnar nerve
distribution)
• Less frequently to right shoulder, arm, left jaw, neck and epigastrium
Pathophysiology:
Imbalance between myocardial oxygen demand and supply

↓
Compensatory mechanism by coronary arteries
↓
If myocardial oxygen requirement reaches this critical level
↓
Myocardial ischemia
↓
Clinical manifestation of angina pain due to adenosine , bradykinin, histamine
and serotonin from ischemic cells
↓
If there is consistent high B.P and tachycardia → ↑work load of the heart
↓
Ventricular dysrhythmias and becomes fatal
109
Chest pain
Management of chest pain with history of angina pectoris:
Recognise problem
(chest pain, patient states he/she is having an anginal attack)
↓
↓
↓
↓
↓
C→A→B - Assess airway, breathing and circulation
↓
D - Provide definitive management:
↓ ↓
HISTORY OF NO HISTORY
ANGINA PRESENT ANGINA PRESENT
↓ ↓
Administer Activate EMS
Vasodilator & O2
(up to 3 doses)
↓ ↓ ↓
IF PAIN RESOLVES IF PAIN DOES Administer O2
NOT RESOLVE and consider
Nitroglycerin
↓ ↓ ↓
Consider future Activate EMS Monitor and record
dental treatment ↓ vital signs
modifications Administer
aspirin
↓
Monitor and record vital signs
110
Chest pain
ACUTE MYOCARDIAL INFARCTION
It is a clinical syndrome caused by a deficient coronary arterial blood supply to a
region of myocardium that results in cellular death and necrosis.
• Atherosclerosis and coronary artery disease
• Coronary thrombosis, occlusion and spasm
• Other risk factors are-
• Males
• 5th and 6th decades of life
• Undue stress
Prevention:
• Medical history questionnaire – chest pain, shortness of breath, history of
heart disease, stroke, high B.P, family history of diabetes & heart problems,
thyroid and diabetes, previous surgeries and medications
• Dialogue history – episodes of angina, last myocardial infarction and
currently taking medications
• Vital signs should be recorded before and immediately after dental
appointments
• Visual examination – peripheral cyanosis, coolness of extremities,
peripheral edema, possible orthopnea.
111
Chest pain
• Avoid overstressing the patient.
• Supplemental oxygen via nasal cannula or nasal hood during
the treatment – 3-5 L/min and 5 – 7 L/min
• Pain control during therapy – appropriate use of local anesthesia – smaller
dose with maximum effect – slow administration
• Vasodepressor administration is a relative contraindication
• Psychosedation – N2O – O2 is preferable.
• It is strongly recommended that elective dental care is avoided until at least
6months after MI.
• Medical consultation and anticoagulation and anti-platelet therapy need not
be altered.
• Inferior alveolar NB and Posterior superior alveolar NB – risk of hemorrhage –
should be avoided.
Clinical manifestations of acute MI:
SYMPTOMS:
• Pain
Severe to intolerable
Prolonged, 30 min
Crushing, choking
Retrosternal
Radiates: left arm, hand, epigastrium, shoulder, neck, jaw
• Nausea and vomiting
• Weakness
112
Chest pain
• Dizziness
• Palpitations
• Cold perspiration
• Sense of impending doom
SIGNS:
• Restlessness
• Acute diseases
• Skin - cool, pale, moist
• Heart rate - bradycardia to tachycardia; PVCs common.
Pathophysiology:
Infarction of myocardium
↓
Left ventricle is commonly involved in acute MI
↓
Blood supply leaving the heart may be diminished
↓
Signs and symptoms of acute MI
↓
Larger the infarct, greater the circulatory insuficiency
↓
Signs and symptoms of heart failure
↓
Increased left ventricular pressure
↓
Left ventricular failure → hypotension, ↓ cardiac output, cardiogenic shock
↓
Fatal
113
Chest pain
Management of chest pain:
Recognise problem
(chest pain, no history of angina)
↓
↓
↓
↓
C→A→B - Assess airway, breathing and circulation
↓
D - Provide definitive management:
↓ ↓
HISTORY OF NO HISTORY
ANGINA PRESENT ANGINA PRESENT
↓ ↓
Follow angina Activate EMS, STAT
management protocol ↓
Administer O2, consider
Nitroglcerin (1 dose only)(if
systolic >90 mm Hg)
↓
Administer aspirin
(powdered or chewable)
↓
Manage pain
(parenteral opioids, N2O-O2)
↓
Monitor and record vital signs
↓
Prepare to manage
complications (e.g., SCA)
↓
stabilise and transfer to
hospital
emergency department
114
Public Health Significance
PUBLIC HEALTH SIGNIFICANCE
• The knowledge and training in medical emergencies aids to be ready to face
any emergencies that occur in the dental practice.
• Proper knowledge in recognising the emergency and managing the same is
useful to manage patients in dental camps and other places where health
services are provided.
• This can be used anywhere, since no medical emergency is specific to dental
practice.
• It helps to be prepared to treat any patient with medical complications, should
any emergency occur.
CONCLUSION
• Prompt recognition and efficient management of medical emergencies by a
well-prepared dental team can increase the likelihood of a satisfactory
outcome.
• The basic algorithm for managing medical emergencies is designed to ensure
that the patient’s brain receives a constant supply of blood containing oxygen.
REFERENCES
1. Medical emergency. Wikipedia, The Free Encyclopedia. Available from :
en.wikipedia.org [Accessed 14th March, 2018].
2. S F. Malamed. Medical Emergencies in the Dental Office. 7th edition. New
Delhi: Elsevier. 2016.

115

Medical Emergencies

Uploaded by

Document Informationclick to expand document information

Copyright:

Available Formats

Medical Emergencies

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Medical Emergencies

Uploaded by

Copyright:

Available Formats

Medical Emergencies

“When you prepare for an emergency, the emergency ceases to exist.”

Life threatening emergencies can and do occur in the practice

dentistry. They can happen to anyone - a patient, a doctor, a member of the

office staff, or a person who is merely accompanying a patient. Although the

occurrence of life threatening emergencies in dental offices is infrequent, many

factors can increase the likelihood of such incidents. These include:

(1) the increasing number of older persons seeking dental care,

(2) the therapeutic advances in the medical profession,

(3) the growing trend toward longer dental appointments, and

(4) the increasing use and administration of drugs in dentistry.

Fortunately, other factors minimise the development of life-

threatening situations. This include a pretreatment physical evaluation of each

patient, consisting of a medical history questionnaire, dialogue history, and

physical examination and possible modifications in dental care to minimise

Inspite of most meticulous protocols designed to prevent the

development of life threatening situations, emergencies will still occur. However,

one should understand that no medical emergency is unique to dentistry. For

instance, even local anaesthetic overdose is seen outside dentistry in cocaine

Although any medical emergency can developing dental office,

exacerbated when patients are placed in stressful environments. Stress-

induced situations include vasodepressor syncope and hyperventilation,

whereas pre-existing medical conditions that are exacerbated by stress include

most acute cardiovascular emergencies, bronchospasm (asthma), and

therefore essential in the prevention and minimization of potentially catastrophic

Drug-related adverse reactions make up another category of life-

overwhelming majority of ‘drug-related’ emergencies are stress related;

themselves. Most adverse drug responses are preventable. Therefore, thorough

knowledge of drug pharmacology and proper drug administration are critical in

the prevention of drug-related complications.

A medical emergency is an acute injury or illness that poses an

immediate risk to a person's life or long-term health1. Medical emergencies can

happen in any environment. The occurrence of such happenings in the dental

Medical emergencies can be classified based on many methods. The

traditional approach has been the systems-oriented classification, which lists

major organ systems and discusses life-threatening situations associated with

A second classification method divides the emergency situations into two

broad categories- cardiovascular and non-cardiovascular emergencies, which is

broken down further into stress-related and non-stress related emergencies.

This system offers a very general breakdown of life-threatening emergencies

that is useful to the doctors.

• Skin And Appendages

• Ears, Nose And Throat

Ateriosclerotic heart diseases

• Gastrointestinal Tract And Liver

• Obstretrics And Gynecology

Drug overdose reactions

- Acute adrenal insufficiency

Asthma Sudden cardiac arrest

McCarthy stated that implementation of a complete system of

life-threatening situations. The remaining 10% would occur inspite of all

emergency ceases to exist.” This is accurate to the extent that adequate

preparation for emergency situations diminishes the likelihood of their resulting

in significant morbidity or death. Prior knowledge of a patient’s physical

condition permits the doctor to incorporate modifications into the dental

treatment plan. In other words, “To be forewarned is to be forearmed.”

GOALS OF PHYSICAL EVALUATION: