Medical emergencies dental office

 INTRODUCTION
 PREVENTION
 PREPARATION
 CLASSIFICATION OF LIFE THREATENING EMERGENCIES
 UNCONSCIOUSNESS
› Vasodepressor Syncope
› Postural Hypertension
› Acute Adrenal Insufficiency
 RESPIRATORY DISTRESS
› Foreign Body Airway Obstruction
› Hyperventilation
› Asthma
› Heart Failure and Acute Pulmonary Edema
 ALTERED CONSCIOUSNESS
› Diabetes Mellitus: Hyperglycemia and Hypoglycemia
› Thyroid Gland Dysfunction
› Cerebro vascular Accident
 SEIZURES
 DRUG RELATED EMERGENCIES
› Drug Overdose Reactions
› Allergy
 CHEST PAIN
› Angina Pectoris
› Acute Myocardial Infarction



Goldberger 1990, “When you prepare for
an emergency, the emergency ceases
to exist.”

Goals of physical evaluation
Physical evaluation –
 Medical history questionnaire,
 Physical examination
 Dialogue history.

 Class1: Healthy patient with no systemic disease.
 Class 2: Mild Systemic disease with no limits on activity.
 Class 3: Severe systemic disease that limits activity.
 Class 4: Incapacitating systemic disease that is life
threatening.
 Class 5: Moribund and E refers to emergency of any kind.

 Recognize patient‟s anxiety level.
 Consider using pre-medication or sedation
 Schedule morning appointments.
 Minimize waiting time and watch appointment length.
 Make sure to use adequate pain control. This will vary from
patient to patient.
 Monitor vital signs.
 Medical consult if required.

Drug Recommended dosage for adults
Alprazolam 4 mg / day
Diazepam 2-10 mg
Flurazepam 15-30 mg
Midazolam Rarely used
Oxazepam 10-30 mg
Triazolam 125-250µg
Eszopiclone 2-3 mg
Zaleplon 5-10 mg
Zolpidem 10 mg

Situation Agent Regimen
Standard general
prophylaxis
Amoxicillin Adults: 2g
Children: 50mg/kg
orally
1 hour before the procedure
Inability to take oral
medications
Ampicillin Adults: 2g
Children: 50 mg/kg
IM/IV
30 min before procedure
Allergy to penicillin Clindamycin or
Cephalexin/Cefadroxil or
Azithromycin/
Clarithromycin
Adults 600 mg
Children 20 mg /kg
Adults 2g
Children 50mg/kg
Adults 500 mg
Children 50 mg/kg
Orally
1 hour before the procedure
Allergy to penicillin and
inability to take oral
medications
Clindamycin or
Cefazolin
Adults 600mg
Children 20mg/kg
IV 30 min before
Adults 1g
Children 25 mg/kg
IM/IV 30 min before

 Endocarditis prophylaxis RECOMMENDED:
 High-risk category-
 Prosthetic cardiac valves- bioprosthetic and homograft
valves
 Previous bacterial endocarditis
 Cyanotic congenital heart disease- e.g., single ventricle
states, trans position of great arteries, tetralogy of fallot
 Surgically constructed systemic pulmonary shunts
 Moderate-risk category-
 Other congenital cardiac malformations
 Acquired valvular dysfunction- e.g., rheumatic heart
disease
 Hypertrophic cardiac myopathy
 Mitral valve prolapse with valvar regurgitation or
thickened leaflets

Endocarditis prophylaxis NOT RECOMMENDED:
 Negligible-risk category-
 Isolated atrial septal defect (ASD)
 Surgical repair of ASD, VSD or patent ductus arteriosus
(no residual effects in 6 months)
 Previous coronary artery bypass graft surgery
 Mitral valve prolapse with out valvular regurgitation
 Physiologic, functional or innocent heart murmurs
 Previous rheumatic fever without valvular dysfunction
 Cardiac pacemakers and implanted defibrillators

Module one – critical or essential emergency drugs
Category Generic drug alternative quantity Availability
Allergy –
anaphylaxis
Epinephrine None 1 preloaded
syringe +3x1
ml ampules
1:1000
(1mg/ml)
allergy –
histamine
blocker
Chlorphenira
mine
Diphenhydra
mine
(Benadryl)
3x1 ml
ampules
10 mg/ml
Oxygen Oxygen 1 “E” cylinder
Vasodilator Nitroglycerin Nitrostat
sublingual
tablets
1 metered spray
bottle
0.4 mg /metered
dose
Bronchodilator Albuterol Metaproterenol 1 metered dose
inhaler
Metered aerosol
inhaler
Antihypoglyce
mic
Sugar Insta – glucose
gel
1 bottle
Inhibitor of
platelet
aggregation
Asprin None 2 packets 325mg/tablet

Equipment Recommended Alternative Quantity
Oxygen delivery
system
Positive pressure and
demand valve
Pocket mask
Oxygen delivery
system with bag valve
mask device
Minimum: 1 large
adult, 1 child
1 per employee
Automated electronic
defibrillator(AED)
Many 1 AED
Syringes for drug
administration
Plastic disposable
syringes with needles
3x2 ml syringes with
needles for parenteral
drug administration
Suction and suction
tips
High volume suction
Large diameter, round
ended suction tips
Non electrical suction
system
Office suction system
Minimum 2
Tourniquets Robber and Velcro
tourniquet; rubber
tubing
spygmomanometer 3 torniquets and 1
spygmomanometer
Magill intubation
forceps
Magill intubation
forceps
1 pediatric Magill
intubation forceps

Module two – secondary/ noncritical drugs and equipment
Category Generic Drug Alternative Quantity Availability
Anticonvulsant Midazolam diazepam 1x5 ml vial 5 mg/ml
Analgesic Morphine
sulphate
Meperidine 3x1 ml ampules 10 mg/ml
Vasopressor Phenylephrine 3x1 ml ampules 10 mg/ml
Antihypoglycem
ic
50% dextrose Glucagon 1 vial 50 ml ampule
Corticosteroid Hydrocortisone
sodium succinate
Dexamethasone 2x2 ml mix- o –
vial
50 mg/ml
Antihypertensive Esmolol Propranolol 2x100 mg/ml
vial
100 mg/ml
Anticholinergic Atropine Scopolamine 3x1 ml ampules 0.5 mg/ml
Respiratory
stimulant
Aromatic
ammonia
2 boxes 0.3 ml/vaporole
Antihypertensive Nifedipine 1 bottle 10mg/capsule

Module three – Advanced Cardiac Life Support (ACLS) : essential
drugs
Cardiac Arrest epinephrine 3x10 ml
preloaded
syringes
1:10,000
(1mg/10ml
syringe)
Analgesic Morphine
sulphate
N2O – O2 3x1 ml ampules 10 mg/ml
Antidysrhythmic Lidocaine Procainamide 1 preloaded
syringe and 2x5
ml ampules
100 mg/ syringe
Symptomatic
Bradycardia
Atropine Isoproterenol 2x10 ml
syringes
1.0 mg/10 ml
Paroxysmal
Supraventricular
Tachycardia
verapamil 2x4 ml ampules 2.5 mg/ml

Module four – antidotal drugs
Opioid
antagonist
Naloxone nalbuphine 2x1 ml ampules 0.4 mg/ml
Benzodiazepine
antagonist
Flumazenil 1x 10 ml vial 0.1 mg/ml
Anticholinergic
toxicity
Antiemergence
delirium
Physostigmine 3x2 ml ampules 1 mg/ml

Syncope is a general term referring to a sudden, transient loss of
consciousness that usually occurs secondary to a period of
cerebral ischemia.
Predisposing factors:
Psychogenic factors
 Fright
 Anxiety
 Emotional stress
 Receipt of unwelcome news
 Pain especially sudden &unexpected
 Sight of blood/ surgical/ dental instruments
 (e.g. local anesthetic syringe)

Non psychogenic factors
 Erect sitting or standing posture
 Hunger from dieting or a missed meal
 Exhaustion
 Poor physical condition
 Hot, humid, crowded environment
 Male gender
 Age between 16 and 35 years

Prevention: Proper positioning and Anxiety relief
Pre-syncope
 Warm feeling in face and neck.
 Pale or ashen coloration.
 Sweating.
 Feels cold.
 Abdominal discomfort.
 Lightheaded or dizziness.
 Mydriasis (Pupillary dilatation.)
 Yawning.
 Increased heart rate.
 Steady or slight decrease in blood pressure.

Syncope
 Patient loses consciousness.
 Generalized muscle relaxation.
 Bradycardia (Weak thready pulse.)
 Seizure (Twitching of hands, legs, and face.)
 Eyes open (Out and up gaze.)
Post-syncope
 Variable period on mental confusion.
 Heart rate increases (Strong rate and rhythm.)
 Blood pressure back to normal levels.

Pathophysiology:
Stress
Catecholamines release
Decreased peripheral vascular resistance & ↑ blood flow to peripheral
muscles
↓ venous return
↓ circulatory blood vol. & drop in arterial B.P.
Activation of Compensatory mechanisms
Reflux bradycardia develops (< 50)
Significant drop in cardiac output associated with fall in B.P below the
critical level
Cerebral ischemia & loss of consciousness

Assess consciousness (loss of response to sensory stimulation)
Activate office emergency system
P- Position patient supine with feet elevated slightly
A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency&
breathing; assess circulation (palpation of carotid pulse)
D – Definitive care:
Administer O2
Monitor vital signs
Perform additional procedures:
Administer aromatic ammonia vaporole
Administer atropine if bradycardia persists
Do not panic!
Post syncopal recovery- delayed recovery-
Postpone dental treatment Activate EMS
Determine precipitating factors

 Administration and ingestion of drugs e.g. antihypertensives
like sodium depleting diuretics, calcium channel blockers
&ganglion blocking agents, sedatives and narcotics,
histamine blockers, levo dopa
 Prolonged period of recumbency or convalescence
 Inadequate postural reflex
 Late stage pregnancy
 Advanced age
 Venous defects in legs (e.g. varicose veins)
 Recovery from sympathectomy
 Addisson‟s disease
 Physical exhaustion and starvation
 Chronic postural hypotension (Shy – Drager syndrome)

Clinical manifestations:
 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
 Clinical signs and symptoms - precipitating drugs
 Blood pressure during syncopal period is quite low
 Un like 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 one 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

P- Position patient supine with feet elevated slightly
A→B→C – Assess & open airway (head tilt &chin lift); assess
airway patency& breathing; assess circulation (palpation of
carotid pulse)
Administer O2
Monitor vital signs
Patient recovers consciousness-
slowly reposition chair delayed recovery -
activate EMS
Continue BLS as needed and discharge patient

A third potentially life - threatening situation that may result in the
loss of consciousness. The condition is uncommon, is
potentially life – threatening, but is readily treatable.
 Lack of gluco-corticosteroid hormones
 Mechanism 1: sudden withdrawal of steroid hormones in the
patient who suffers primary adrenal insufficiency (Addison’s
disease)
 Mechanism 2: After the sudden withdrawal of steroid
hormones from a patient with normal adrenal cortices but
with a temporary insufficiency resulting from cortical
suppression through prolonged exogenous gluco-
corticosteroid administration (secondary insufficiency)
 Mechanism 3: Stress either physiologic or psychological.

If the adrenal gland cannot meet the increased demand, clinical
signs and symptoms of adrenal insufficiency develop.
 Mechanism 4: After bilateral adrenalectomy
 Mechanism 5: After sudden destruction of pituitary gland.
 Mechanism 6: Injury to the both adrenal glands (trauma,
infection, thrombosis, or tumor)
Prevention:
 History of rheumatic fever, asthma, TB, emphysema, other
lung diseases, arthritis and rheumatism
 Allergic history to drugs, food, medications, latex
Dialogue history
Rule of TWOs
 In a dose of 20 mg or more of cortisone or its equivalent
 Via oral or parenteral route for a continuous period of two
weeks or longer
 Within 2 years of dental therapy

Dental therapy considerations:
 Glucocorticosteroid coverage
 Stress reduction protocol
Symptom Sign Laboratory finding
1. Weakness, tiredness,
fatigue
2. Anorexia
3. GI symptoms like
nausea vomiting
constipation,
abdominal pain,
diarrhea
4. Salt craving
5. Postural dizziness
6. Muscle or joint pain
1. Weight loss
2. Hyperpigmentation
3. Hypotension (<110
mm Hg systolic
4. Vitiligo
5. Auricular
calcification
1. Electrolyte
disturbance:
 Hyponatremia
 Hyperkalemia
 Hypercalcemia
1. Azotemia
2. Anemia
3. Eosinophilia

Management :
Conscious
Terminate dental treatment
P – Position patient comfortably if asymptomatic;
Supine with legs elevated slightly, if symptomatic
A→B→C – Assess & open airway (head tilt &chin lift); assess airway
patency& breathing; assess circulation (palpation of carotid pulse)
Monitor vital signs
Summon medical assistance
Obtain emergency kit and O2
Administer glucocorticosteroid

General Signs and Symptoms
 Gasping for breath
 Patient grabs at throat
 Panic
 Suprasternal or supraclavicular retraction
 Inability to speak, breathe, cough
If Partial Obstruction
 Snoring
 Gurgling
 Wheezing
 „Crowing‟ sound on inspiration
 Forceful cough
 Wheezing between cough
 Absent or altered voice sounds
 Possible cyanosis, lethargy, disorientation
If Total Obstruction - No noise

Visible objects – if assistant is present
Place patient into supine or Trendelenburg position
Use Magill intubation forceps or suction
if assistant is not present
Instruct patient to bend over arm of chair with their head down
Encourage patient to cough
Aspirated foreign bodies
Place patient in left lateral decubitus position
Encourage patient to cough

CONSCIOUS victim with obstructed airway
Identify complete airway obstruction Ask – „Are you choking‟
Apply abdominal thrusts until foreign body is expelled
Have medical or paramedical personnel to evaluate the patient

CONSCIOUS victim with known obstructed airway who loses
consciousness
Place victim in supine position with head in neutral position
Maintain airway (head tilt – chin lift)
Look in mouth for foreign object prior to ventilation.
If INEFFECTIVE:
Perform abdominal thrust, repeating until the object is
expelled
Check for foreign body. If visible, perform finger swipe to
remove

Establishing an emergency airway –
Non invasive procedures
Invasive procedures

If foreign body is not retrieved
Consult radiologist
Obtain appropriate radiographs and initiate medical
consultation
Perform bronchoscopy to visualize and retrieve foreign body

 It is defined as ventilation in excess of that required to
maintain normal blood pa O2 (arterial oxygen tension) and
pa CO2 (arterial carbon dioxide tension). It is produced by
increase in frequency or depth of respiration, or both.
 Common emergency occur in dental office , almost always
occur is a result of extreme anxiety.
Prevention:
 Through prompt recognition and management of anxiety
 Physical evaluation of the patient
 The vital signs of apprehensive patients may deviate from
normal. Recording the vital signs at the patient‟s initial visit
 Stress reduction protocol is the primary means of preventing
hyperventilation

system Signs and symptoms
cardiovascular Palpitations
Tachycardia
Precordial”pain”
Neurologic Dizziness
Lightheadedness
Disturbance of consciousness
Disturbance of vision
Numbness and tingling of
extremities
Tetany (rare)
Respiratory Shortness of breath
Chest “pain”
Dryness of mouth
Gastro intestinal Globus hystericus (subjective
feeling of a lump in the throat)
Epigastric pain
Musculoskeletal Muscle pain and cramps
Tremor
Stiffness
Carpopedal tetany
Psychological Tension
Anxiety and nightmares

Pathophysiology:
Anxiety
Increased rate and depth of respiration
↑ exchange of O2 & CO2 by lungs
↑ blowing off of CO2 and paCO2 decreases
Hypocapnia
↑ in blood pH
Respiratory alkalosis

 Hypocapnia → vasoconstriction of cerebral vessels →
cerebral ischemia
 Respiratory alkalosis → ↓ ionized calcium

Management:
Recognize problem (rapid , deep, uncontrolled breathing)
P – Position patient comfortably usually upright
A → B → C – Basic life support as needed
Remove dental materials from patient‟s mouth
Calm patient
Correct respiratory alkalosis – instructed to breathe 7% CO2 &93% O2
or to rebreathe the exhaled air
Initial drug management – Benzodiazepines
Dental care may continue if both doctor and patient agree
Discharge patient

 In 1830 Eberle, a Philadelphia physician, defined it as
“paroxysmal affection of the respiratory organs,
characterized by great difficulty of breathing, tightness
across breast, and a sense of impending suffocation, without
fever or local inflammation.”
 Today it is defined as “a chronic inflammatory disorder that is
characterized by reversible obstruction of the airways.”

Extrinsic or allergic asthma,
 The allergens may be airborne – house dust, feathers, animal
dander, furniture stuffing, fungal spores, or plant pollens.
 Food and drugs – cow‟s milk, egg, fish, chocolate, shellfish,
tomatoes, penicillins, vaccines , asprin, and sulfites.
 Type I hypersensitivity reaction – Ig E antibodies produced in
response to allergen
 Approximately, 50% asthmatic children become
asymptomatic before reaching adulthood

Intrinsic or nonallergic, idiosyncratic, nonatopic asthma:
 Usually develops in adult age > 35 years
 Non – allergic factors – respiratory infection (viral infection is
more common causative factor), physical exertion,
environmental and air pollution, and occupational stimuli
 Psychological and physiologic stress can also contribute to
asthmatic episodes in susceptible individuals
 Acute episodes are usually more fulminant and severe than
those of extrinsic asthma. Long-term prognosis also less
optimistic.
Mixed asthma:
 Combination of extrinsic and intrinsic asthma. Major
precipitating factor is respiratory tract infection.

Status asthmaticus:
 More severe clinical form
 Experience wheezing, dyspnea, hypoxia
 Refractory to 2 – 3 doses of β-adrenergic agents
 If not managed adequately, patient may die due to
respiratory distress
Prevention:
Medical history regarding
 Lung diseases
 Allergies to drugs, food, medication, latex
 Usage of drugs, medications, natural remidies

Dialogue history:
 Asthma?
 Type extrinsic or intrinsic?
 Age of onset
 History of acute episodes
 Precipitating factor
 Management

Commonly prescribed drugs for the management:
Bronchodilators:
Sympathomimetic:
 Albuterol
 Salmeterol
 Metaproterenol
 Levalbuterol
 Epinephrine
 Theophylline
 Aminophylline
anticholinergic:
 Ipratropium
Corticosteroids:
 Beclomethasone , Triamcinolone, Flunisolide
 Mometasone , Fluticasone, Budesonide
Antimediator: Cromolyn sodium, Nedocromil sodium

 Stress reduction protocol in case of emotional stress
 Contraindication of barbiturates and opioids as increase the
risk of bronchospasm
 Some inhalational anesthetics like ether irritates respiratory
mucosa
 Special care should be taken while prescribing analgesics
 Some patients are sensitive to bisulphites, local anesthesia is
contraindicated

 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 - >40 in severe cases)
 Rise in B.P
 Increase in heart rate (>120 bpm in severe cases)
Only in respiratory distress
 Diaphoresis
 Agitation
 Somnolence
 Confusion
 Cyanosis
 Supraclavicular and intercostal retraction
 Nasal flaring

Pathophysiology:
 Neural control of airways
 Airway inflammation
 Immunological responses
 Bronchospasm
 Bronchial wall edema and hypersecretion of mucous glands
 Breathing

Management:
Recognize problem (respiratory distress, wheezing)
Discontinue dental treatment
Activate office emergency team
P – Position, usually upright with arms thrown forward
A → B → C –Assess and perform basic life support as needed
Administer O2
Administer bronchodilator via inhalation
(Episode terminates) (episode continues)
Dental care may continue Activate EMS
Discharge patient Administer parenteral drugs
Hospitalize or discharge patient, per EMS recommendation
Additional considerations: Sedatives which depress respiratory system and central
nervous system are absolutely contraindicated. 5mg IV or IM diazepam may be
indicated to decrease anxiety.

It is generally described as the inability of heart to supply sufficient
oxygenated blood for body‟s metabolic needs.
 Increase in the workload of the heart. E.g. high blood pressure
 Damaging muscular walls of the heart through coronary artery
disease and myocardial infarction
e.g. Stenosis of heart valves (aortic, mitral tricuspid, pulmonary)
Increase in body‟s requirement of O2 and nutrients (e.g. pregnancy,
hyperthyroidism, anemia, Paget‟s disease)
 Other factors are physical, psychological and climatic stress

Prevention:
 Medical history questionnaire
 Dialogue history
 Physical evaluation
 Physical examination
 ASA I – no dyspnea and fatigue with normal exertion. No
special dental modifications.
 ASA II – mild dyspnea and fatigue during exertion. Stress
reduction protocol should be considered
 ASA III – dyspnea and fatigue with normal activities - Medical
consultation, stress reduction protocol, other treatment
modifications.
 ASA IV – 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- Symptoms –
 Pallor, cool skin Weakness and undue fatigue
 Sweating (Diaphoresis) Dyspnea on exertion
 LVH Hyperventilation
 Dependent edema Nocturia
 Hepatomegaly and splenomegaly Paroxysmal
nocturnal dyspnea
 Narrow pulse pressure Wheezing (cardiac asthma)
 Pulsus alterans
 Ascities

Acute pulmonary edema –
 All of the signs & symptoms of heart failure
 Moist rales at lungs
 Tachypnea
 Cyanosis
 Frothy pink sputum
 increased anxiety, dyspnea at rest

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 is a drastic symptom of heart failure
Excess fluid in alveolar spaces and interstitial tissues
Suffocation and oppression of chest
Elevates heart rate and blood pressure
Increases additional load to the heart
Further decrease in cardiac function due to hypoxia
If this vicious circle is not interrupted, it may lead rapidly to death
v

Management:
Recognize problem (conscious patient exhibiting extreme difficulty in breathing)
P – Position, conscious patient in any comfortable position, usually upright
Calm the patient
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

It is a group of diseases marked by high levels of blood glucose resulting
from defects in insulin production, insulin action, or both
Type I diabetes:
 Genetic factors
 Environmental factors like drugs, toxins and viruses (mumps, rubella,
coxsackie)
 Autoimmune factors
Type II diabetes:
 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 tumors
Incorrectly used insulin pump
Malnutrition
Old age
Oral hypoglycemic agents
Over aggressive treatment of ketoacidosis
Pentamidine, Phenylbutazone, Propranolol
Recent change in dose
Salicylates
Sepsis

Prevention:
Medical history questionnaire
Dialogue history
Physical examination
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
phycisian or ↓ insulin dose by half
III  Monitor blood glucose levels more
frequently for several days following
surgery and modify insulin accordingly
 Consider medical consultation
IV  Consult physician before treatment

 Antibiotic coverage in the postsurgical period is appropriate
 Stress reduction protocol to be followed
Clinical manifestations of hyperglycemia:
Symptom Type I diabetes Type II diabetes
Polyuria ++ +
Polydipsia ++ +
Polyphagia with weight
loss
++ _
Recurrent blurred vision + ++
Vulvovaginitis or pruritis + ++
Loss of strength ++ +
Nocturnal enuresis ++ _
Absence of symptoms _ ++

Other symptoms of type I diabetes Other symptoms of type II diabetes
Repeated skin infections
Marked irritability Decreased vision
Headache Paresthesias
Drowsiness Loss of sensation
Malaise Impotence
Dry mouth Postural hypotension

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
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
 ↓ 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
 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
 Loss of consciousness
 Hypoglycemic coma and insulin shock
Patients may experience tonic – clonic convulsions

Management: Hyperglycemia
Recognize problem (lack of response to sensory stimulation)
P – Position, supine position with legs elevated
Summon EMS
Establish IV infusion, 5% dextrose and water or of normal saline
Administer O2
Transport to hospital

Hypoglycemia – conscious patient
Recognize problem (altered consciousness)
P – Position, patient comfotably
D – Definitive management:
Administer oral carbohydrates
If successful If unsuccessful
Permit patient to recover Activate EMS
Discharge the patient Administer parenteral
carbohydrates
Monitor patient
Discharge patient

Hypoglycemia: unconscious patient
P – Position patient in supine position with feet elevated
D – Definitive management
Summon EMS
Administer oral carbohydrates
IV 50% dextrose solution
1 mg glucagon via IM or IV
Transmucosal sugar, or rectal honey or syrup
Monitor vital signs every 5 minutes
Administer O2
Allow patient to recover and discharge per medical recommendations


The thyroid gland secretes three hormones (T3 T4 and
calcitonin)that are vital in the regulation of the level of
biochemical activity of most of the body‟s tissues.

Hypothyroidism: Hyperthyroidism:
Primary: Diffuse toxic goiter
 Auto immune Toxic multinodular goiter
 Idiopathic causes Factitious thyrotoxicosis
 Postsurgical thyroidectomy T3 thyrotoxocosis
 External radiation therapy Thyrotoxicosis with thyroiditis
 Radioiodine therapy Hashimoto‟s thyroiditis
 Inherited enzymatic defect Subacute thyroiditis
 Antithyroid drugs Jod – Basedow phenomenon
 Lithium, phenylbutazone Malignancies
TSH – producing tumors
Secondary:
 Pituitary tumor Hypothalamic hyperthyroidism
 Infiltrative disease of pituitary Struma ovarii with
hyperthyroidism

Prevention:
Dialogue history
Dental therapy considerations
 Euthyroid patient with normal hormone levels can be
managed normally
 Hypothyroid – avoidance of CNS depressants (opiods,
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

Clinical manifestations
Hypothyroidism:
Symptoms Signs
Paresthesias
Loss of energy
Intolerance to cold
Muscular weakness
Pain in muscles and joints
Inability to concentrate
Drowsiness
Constipation
Forgetfulness
Depressed auditory acuity
Emotional instability
Headaches
Dysarthria
Pseudomyotonic reflexes
Change in menstrual pattern
Hypothermia
Dry, scaly skin
Puffy eyelids
Hoarse voice
Weight gain
Dependent edema
Sparse axillary and pubic hair
Pallor
Thinning eyebrows
Yellow skin
Loss of scalp hair
Abdominal distension
Goiter
Decreased sweating

Thyrotoxicosis:
Symptoms signs
Common
Weight loss
Palpitations
Nervousness
Tremor
Less common
Chest pain
Dyspnea
Edema
Psychosis
Disorientation
Diarrhea
Abdominal pain
Fever
Tachycardia
Sinus tachycardia
Dysrhythmias
Wide pulse pressure
Tremor
Thyrotoxic stare and eyelid
retraction
Hyperkinesis
Heart failure
Weakness
Coma
Tender liver
Infiltrative ophthalmopathy
Somnolence or obtundence
Jaundice

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 CO2 retention

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:
P – Position , supine position with feet elevated
D – Definitive management – activate EMS and if recovery is not
immediate, establish IV access
Hypothyroidism –IV doses of thyroid hormones (T3 & T4) for
several days
Thyrotoxicosis –administer large doses of antithyroid drugs,
additional therapy – propranolol, glucocorticoids
Administer O2
Discharge or hospitalize the patient

Defined as „any vascular injury that reduces cerebral blood flow
to a specific region of the brain, causing neurologic
impairment‟. „Stroke‟, „cerebral apoplexy‟ & „brain attack‟
Classification:
 cerebral ischemia and infarction – atherosclerosis &
thrombosis, cerebral embolism
 Intracranial hemorrhage – arterial aneurysms & hypertensive
vascular disease
 Others – TIA – transient ischemic attacks

 Consistently elevated blood pressure is a major risk factor
 Diabetes mellitus
 Cardiac enlargement
 Hypercholesterolemia
 Use of oral contraceptives
 Cigarette smoking
Prevention:
Dialogue history
Physical examination

 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
 Common signs and symptoms – headaches, dizziness, vertigo,
drowsiness, chills, nausea, vomiting. Loss of consciousness and
convulsive movements are less common. Weakness or paralysis
of extremities occurs in contralateral side. Speech defects may
be seen
 Neurological signs and symptoms – paralysis of one side of body,
difficulty in breathing and swallowing, inability to speak or slurring
of speech, loss of bladder and bowel control, unequal pupil size
 Infarction – gradual onset of signs and symptoms whereas
embolism and hemorrhage – abrupt onset of signs and
symptoms

Pathophysiology:
Cerebrovascular ischemia and
infarction
Hemorrhagic CVA
•At cellular level, ischemia
•Anaerobic glycolysis with
production of lactate
•Mitochondrial dysfunction →
disruption of membrane and
vascular endothelium
•BBB breaks down and edema
forms
•Edema ↑ tissue mass in cranium
causes mild headache
•Severe edema may forces the
portions of cerebral hemisphere
into tentorium cerebelli
•Ischemia and infarction of
upperbrain stem (medulla)
•Loss of consciousness and fatal
•Subarachnoid hemorrhage –
ruptured aneurysms
•Intracranial hemorrhage –
hypertensive vascular disease
•Once vessels rupture
•Arterial blood supply fills the
cranium
•↑ in intracerebral blood pressure
•Rapid displacement of brain stem
into tentorium cerebelli
•Ultimately death

Management of CVA & TIA:
Conscious patient
P – Position patient comfortably
D – Definitive management:
Monitor vital signs
Manage signs and symptoms
If B.P elevated, semi – fowler position (450 position)
Administer O2
Do not administer CNS depressants
Symptoms resolve (TIA) Symptoms persist CVA or TIA Loss of
consciousness
Follow up management Hospitalization P – position with
feet elevated slightly
Monitor vital signs
If B.P elevated, reposition patient (slight head &chest elevation)
D definitive care: establish IV access & transport to EMT

Types:
Causes:
 Congenital abnormalities
 Perinatal injuries
 Metabolic and toxic disorders
 Head trauma
 Tumors
 Vascular diseases
 Degenerative disorders
 Infectious diseases
Partial seizures Generalized seizures
Simple partial
Complex partial
Partial seizures evolving to generalized
tonic – clonic
Absence seizures (true petitmal)
Myoclonic seizures
Tonic – clonic seizures
Unclassified epileptic seizures

 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
 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 –
preictal phase: ↑in anxiety and depression , appearance of aura
and soon loses consciousness, a series of myoclonic jerks
occur (epileptic cry)
↑ HR, B.P, bladder pressure, piloerection, glandular
hypersecretion, mydriasis, apnea
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 sod. And pot. Ions
Ach. & GABA sustained membrane depolarization followed by
local hyper polarization
This abnormal discharge propagated through neuronal
pathways and partial seizure becomes generalized

Management of petitmal seizures:
P – position patient with feet elevated
Seizure ceases: reassure patient seizure continues (> 5 min)
Allow patient to recover before discharge A → B → C
–Assess and perform BLS

Management of tonic clonic seizure:
Prodromal phase
Ictal phase
Activation of EMS
D – Definitive care
Protect patient from injury
Post ictal phase
D – Definitive care
Administer O2
Monitor vital signs
Reassure patient and permit recovery
Discharge patient
To hospital To home To physician

Signs and Symptoms of Epinephrine Toxicity
 Agitation, weakness, and headache.
 Pallor, tremor, palpitation.
 Sharp rise in blood pressure and heart rate.
Signs and Symptoms of Local Anesthetic Toxicity
 Agitation.
 Muscular twitching and tremors.
 Increased blood pressure and heart rate.
 Light-headedness.
 Visual and auditory disturbances (Tinnitis, Difficulty focussing.)
 If moderate to high overdose of Local anesthetic can also have
convulsions and depression of blood pressure, heart rate, and
respiration.

MANAGEMENT OF TOXIC REACTIONS TO EPINEPHRINE:
 Toxic effect of epinephrine is transitory rarely lasting more
than a few minutes
 Stop dental treatment.
 Place patient in most comfortable position.
 Consider administering oxygen.
 Allow time for the patient to recover.
Dental Treatment Considerations for use of Epinephrine
 Due to its cardiovascular effects limit use in patients with
history of heart disease or stroke.
 Can cause uterine contractions in the pregnant female.
 Possible drug interactions (Especially MAO inhibitors and
Cocaine.)
 Remember the patient has endogenous epinephrine
production of this is increased in stressful situations.

MANAGEMENT OF TOXIC REACTIONS TO LOCAL ANESTHETIC:
treatment varies with the onset and severity of the reaction.
MILD REACTION/RAPID ONSET (Example is an intravascular
injection)
 Reassure patient.
 Administer Oxygen.
 Monitor and record vital signs.
 Allow for recovery; determine if patient can be allowed to
leave unescorted.
MILD REACTION/SLOW ONSET
 Toxic reaction with a delayed onset is most likely a result of
impaired biotransformation.
 Evolves slowly, use caution.
 Monitor patient, record vital signs.

SEVERE OVERDOSE/RAPID ONSET, SEVERE OVERDOSE/SLOW ONSET
 ABC‟s.
 Activate EMS.
 Administer Oxygen by mask at 10-15L/minute.
 Start IV if available (18 gauge catheter with Normal Saline.)
 If needed and available administer anticonvulsant, Versed
(Midazolam)
2mg, then 1mg/min to effect (Monitor respiration.)
 Allow for recovery and discharge with appropriate escort or
transport to hospital if required.

Treatment Considerations to Avoid Adverse Drug Reaction
 Prevention is the key. Take a complete medical history.
Determine if there are any diseases present that affect the use
of a drug.
 Know what medications the patient is taking and possible drug
interactions.
 Careful injections make sure to aspirate to avoid an
intravascular injection.
Maximum Recommended Doses of Local Anesthetic
 Lidocaine “Plain” 4.4mg/kg
 Lidocaine 2% with 1:100k Epinephrine 7.0mg/kg
 Mepivicaine “Plain” 4.4mg/kg
 Mepivicaine with 1:20k Neocobefrine 6.6mg/kg
 Bupivicaine with 1:200k Epinephrine 3.2mg/kg
Maximum Recommended Doses of Epinephrine
 Healthy Adult 0.2mg
 Cardiac Patient 0.04mg

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 shock including; pallor, syncope, palpitations,
tachycardia, hypotension, arrythmias, and convulsions.
 Respiratory symptoms include; sneezing, cough, wheezing,
tightness in chest, bronchospasm, laryngospasm.
 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.

TREATMENT
General Treatment
 ABC‟s
 Maintain airway, administer oxygen, and determine possible need for
intubation or surgical airway.
 If in shock put patient in a horizontal or slight Trendelenburg position.
Mild Reactions
 Antihistamines usually effective. (Benadryl 50-100mg or
Cholpheniramine maleate 4-12 mg IV, or IM.)
 Identify and remove allergen.
 Follow up medications in 4-6 hours.
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 (Itching) are present can use
Corticosteroids. However these drugs are to slow acting to be
used for an emergency situation.
 Hydrocortisone sodium succinate (Solu-cortef) 100-500mg IV or
IM. Dexamethasone (Decadron) 4-12mg IV or IM.
 Repeat dose at 1, 3, 6, and 10 hours as indicated by severity of
symptoms.
Other Considerations
 Seizures are possible as a result of circulatory or respiratory
insufficiency.
 Most severe allergic reactions require hospitalization and
observation for 24 hours.

Defined as „ 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

Types:
 Stable (classic or exertional)
 Variant (prinzmetal , vasospastic)
 Unstable (crescendo, acute coronary insufficiency)
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 – type of pain, radiation, precipitating
factors and effect of nitro glycerine

 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
 Vasodepressor administration should be minimized in
increased risk patients
 Psychosedation – N2O – O2 is preferable
 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

Management:
Recognize problem (chest pain – angina attack)
P – Position, patient comfortably usually upright
A → B → C –Assess and perform BLS
D – definitive management
HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA
Administer vasodilator and O2 Activate EMS
Transmucosal nitroglycerine spray O2 and consider nitroglycerine
Or sublingual nitroglycerine tablet Monitor and record
0.3 – 0.6 mg for every 5 min (3 doses)
IF PAIN RESOLVES IF PAIN DOES NOT RESOLVE
Future dental treatment modifications Activate EMS
Administer aspirin
Monitor and record vital signs
Medical management of unstable angina – Nitrates, β – blockers, calcium
channel blockers and psychological stress management and
reassurance

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

 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 antiplatelet
therapy need not be altered
 Inferior alveolar NB and Posterior superior alveolar NB – risk of
hemorrhage – should be avoided

Symptoms Signs
Pain – severe to intolerable
Prolonged, 30 min
Crushing, choking
Retrosternal
Radiates – left arm, hand,
epigastrium, shoulders,
neck, jaw
Nausea and vomiting
Weakness
Dizziness
Palpitations
Cold perspiration
Sense of impending doom
Restlessness
Acute distress
Skin – cool, pale, moist
Heart rate – bradycardia
to tachycardia; PVC
(premature ventricular
contractions) 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

Management:
Recognize problem (chest pain – no history of angina)
P – Position, patient comfortably usually upright
A → B → C –Assess and perform BLS
D – definitive management
HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA
Follow protocol of angina (presumptive
diagnosis: Acute MI)
Activate EMS
Administer O2,consider
nitroglycerine
Administer aspirin
Manage pain (parenteral
opioids, N2O – O2)
Monitor and record vital signs
Prepare to manage complications (sudden
cardiac arrest)
Transfer to emergency department

 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
 Caroline, Nancy L., Emergency Medicine in the Streets,
2nd Ed., 1983, Little and Brown.
 Malamed, Stanley, Managing Medical Emergencies,
Journal of the American Dental Association, Vol. 124,
pp40-59, August 1993.
 Malamed, Stanley, Emergency Medicine: Beyond the
Basics, Journal of the American Dental Association, Vol.
128, pp843-854, July 1997.
 Malamed, Stanley, Medical Emergencies in the Dental
Office, 4th Ed. 1993, Mosby.
 Prusinski, L., Fundamentals of Corticosteroid Therapy, Oral
Medicine Department, Nation Naval Dental Center,
Bethesda, MD, 1997.
 Walker, H.K., Hall, W.D., Hurst, J.W., Clinical Methods, The
History, Physical, and Laboratory Examinations, 2nd Ed.,
1980, Butterworths.
 Whitehouse, Michael, Medical Emergencies for Dental
Officers, 2nd Dental Battalion/Naval Dental Center, Camp
Lejeune, NC, 1998.

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