MEDICAL EMERGENCIES IN DENTAL OFFICE

PRESENTED BYMANASA.A

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

                       

Introduction

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

Prevention

Goals of physical evaluationPhysical evaluation –

Medical history questionnaire,

Physical examination

Dialogue history.

ASA Physical Status Classification 

  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. 

Anxiety recognition & stress reduction protocol

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.

Premedication 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: 2gChildren: 50mg/kgorally1 hour before the procedure

Inability to take oral medications

Ampicillin Adults: 2gChildren: 50 mg/kgIM/IV 30 min before procedure

Allergy to penicillin Clindamycin or

Cephalexin/Cefadroxil or

Azithromycin/ Clarithromycin

Adults 600 mgChildren 20 mg /kgAdults 2gChildren 50mg/kgAdults 500 mgChildren 50 mg/kgOrally1 hour before the procedure

Allergy to penicillin and inability to take oral medications

Clindamycin or

Cefazolin

Adults 600mgChildren 20mg/kgIV 30 min beforeAdults 1gChildren 25 mg/kgIM/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

Preparation

Basic life support (BLS)

Advanced Cardiovascular Life Support (ACLS)

Emergency drug kits

Module one – critical or essential emergency drugsCategory Generic drug alternative quantity Availability

Allergy – anaphylaxis

Epinephrine None 1 preloaded syringe +3x1 ml ampules

1:1000 (1mg/ml)

allergy – histamine blocker

Chlorpheniramine

Diphenhydramine (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

Antihypoglycemic

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 valvePocket mask

Oxygen delivery system with bag valve mask device

Minimum: 1 large adult, 1 child1 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 suctionLarge diameter, round ended suction tips

Non electrical suction system

Office suction systemMinimum 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 equipmentCategory 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

Antihypoglycemic

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

Category Generic Drug Alternative Quantity Availability

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

Category Generic Drug Alternative Quantity Availability

Opioid antagonist

Naloxone nalbuphine 2x1 ml ampules 0.4 mg/ml

Benzodiazepine antagonist

Flumazenil 1x 10 ml vial 0.1 mg/ml

Anticholinergic toxicityAntiemergence delirium

Physostigmine 3x2 ml ampules 1 mg/ml

UNCONSCIOUSNESS

Vasodepressor SyncopePostural HypertensionAcute Adrenal Insufficiency

Vasodepressor SyncopeSyncope 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 persistsDo not panic!

 Post syncopal recovery- delayed recovery-

Postpone dental treatment Activate EMSDetermine precipitating factors

POSTURAL HYPOTENSIONPredisposing 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)

D – Definitive care:Administer O2

Monitor vital signs

Patient recovers consciousness- slowly reposition chair delayed

recovery - activate EMS

Continue BLS as needed and discharge patient

ACUTE ADRENAL INSUFFICIENCY: (ADRENAL CRISIS)

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.

Predisposing factors: 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, latexDialogue historyRule 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 protocolClinical manifestations:

Symptom Sign Laboratory finding

1. Weakness, tiredness, fatigue

2. Anorexia3. GI symptoms like

nausea vomiting constipation, abdominal pain, diarrhea

4. Salt craving5. Postural dizziness6. Muscle or joint pain

1. Weight loss2. Hyperpigmentation3. Hypotension (<110

mm Hg systolic4. Vitiligo 5. Auricular

calcification

1. Electrolyte disturbance:

Hyponatremia Hyperkalemia Hypercalcemia1. Azotemia2. Anemia3. Eosinophilia

Pathophysiology

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)

D – Definitive care:Monitor vital signs

Summon medical assistanceObtain emergency kit and O2

Administer glucocorticosteroid

RESPIRATORY DISTRESS

Foreign Body Airway ObstructionHyperventilationAsthmaHeart Failure and Acute Pulmonary Edema

Foreign Body Airway ObstructionPrevention:

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 presentPlace 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 coughAspirated 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

Hyper ventilation 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

Clinical manifestations:system Signs and symptoms

cardiovascular PalpitationsTachycardia

Precordial”pain”Neurologic Dizziness

LightheadednessDisturbance of consciousness

Disturbance of visionNumbness and tingling of

extremitiesTetany (rare)

Respiratory Shortness of breathChest “pain”

Dryness of mouthGastro intestinal Globus hystericus (subjective

feeling of a lump in the throat)Epigastric pain

Musculoskeletal Muscle pain and crampsTremor

StiffnessCarpopedal tetany

Psychological TensionAnxiety 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

D – Definitive care: Remove dental materials from patient’s mouth

Calm patientCorrect 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 

ASTHMA

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.”

Predisposing factors:

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

Dental therapy considerations:

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

Clinical manifestations: 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

D – Definitive care: 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.

HEART FAILURE AND ACUTE PULMONARY EDEMA

It is generally described as the inability of heart to supply sufficient oxygenated blood for body’s metabolic needs.

Predisposing factors: 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 examinationDental therapy considerations: 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.

Clinical manifestations:

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)

Discontinue dental treatment

P – Position, conscious patient in any comfortable position, usually upright

Activate office emergency team

Calm the patient

A → B → C –Assess and perform basic life support as needed

D – Definitive care: Administer O2

Monitor vital signsAlleviate symptoms of respiratory distress:

Perform bloodless phlebotomyAdminister vasodilator e. g. Nitroglycerine

Alleviate apprehension e.g. morphine

Discharge patient

Modify subsequent dental treatment

ALTERED CONSCIOUSNESS

Diabetes Mellitus: Hyperglycemia and HypoglycemiaThyroid Gland DysfunctionCerebro vascular Accident

DIABETES MELLITUS HYPO AND HYPERGLYCEMIA

It is a group of diseases marked by high levels of blood glucose resulting from defects in insulin production, insulin action, or both

Predisposing factors: Type I diabetes: Genetic factors Environmental factors like drugs, toxins and viruses (mumps,

rubella, coxsackie) Autoimmune factorsType 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 diseaseAnorexia nervosaDecrease in usual food intakeEthanolFactitious hypoglycemiaHepatic impairmentHyper and hypothyroidismIncrease in usual exerciseInsulin Islet cell tumorsIncorrectly used insulin pump MalnutritionOld ageOral hypoglycemic agentsOver aggressive treatment of ketoacidosisPentamidine, Phenylbutazone, PropranololRecent change in doseSalicylatesSepsis

Prevention:Medical history questionnaireDialogue historyPhysical examinationDental therapy considerations:

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 followedClinical 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 NauseaMore 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 shockPatients may experience tonic – clonic convulsions

Management: Hyperglycemia Recognize problem (lack of response to sensory stimulation)

Discontinue dental treatment

Activate office emergency team

P – Position, supine position with legs elevated

A → B → C –Assess and perform basic life support as needed

D – Definitive care: Summon EMS

Establish IV infusion, 5% dextrose and water or of normal salineAdminister O2

Transport to hospital

Hypoglycemia – conscious patientRecognize problem (altered consciousness)

Discontinue dental treatment

Activate office emergency team

P – Position, patient comfotably

A → B → C –Assess and perform basic life support as needed

D – Definitive management: Administer oral carbohydrates

If successful If unsuccessfulPermit 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 managementSummon EMS

Administer oral carbohydratesIV 50% dextrose solution

1 mg glucagon via IM or IVTransmucosal sugar, or rectal honey or syrup

Monitor vital signs every 5 minutesAdminister O2

 Allow patient to recover and discharge per medical

recommendations  

Thyroid gland dysfunction

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.

Predisposing factors: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 tumorsSecondary:

Pituitary tumor Hypothalamic hyperthyroidism Infiltrative disease of pituitary Struma ovarii with

hyperthyroidism

Prevention:Medical history questionnaireDialogue 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 manifestationsHypothyroidism:

Symptoms Signs

ParesthesiasLoss of energyIntolerance to coldMuscular weaknessPain in muscles and jointsInability to concentrateDrowsinessConstipationForgetfulnessDepressed auditory acuityEmotional instabilityHeadachesDysarthria

Pseudomyotonic reflexesChange in menstrual patternHypothermiaDry, scaly skinPuffy eyelidsHoarse voiceWeight gain Dependent edemaSparse axillary and pubic hairPallorThinning eyebrowsYellow skinLoss of scalp hairAbdominal distensionGoiterDecreased sweating

Thyrotoxicosis:

Symptoms signs

CommonWeight lossPalpitationsNervousnessTremorLess commonChest painDyspneaEdemaPsychosisDisorientationDiarrheaAbdominal pain

FeverTachycardiaSinus tachycardiaDysrhythmiasWide pulse pressureTremorThyrotoxic stare and eyelid retractionHyperkinesisHeart failureWeaknessComaTender liverInfiltrative ophthalmopathySomnolence or obtundenceJaundice

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 O2Discharge or hospitalize the patient

CEREBROVASCULAR ACCIDENT

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

Predisposing factors: Consistently elevated blood pressure is a major risk factor Diabetes mellitus Cardiac enlargement Hypercholesterolemia Use of oral contraceptives Cigarette smoking

Prevention:

Medical history questionnaire

Dialogue history

Physical examination

Dental therapy considerations: 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 therapyClinical manifestations: 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

Discontinue dental treatmentP – Position patient comfortably

A → B → C –Assess and perform basic life support as neededD – Definitive management:

Monitor vital signsManage 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

A → B → C –Assess and perform basic life support as neededMonitor vital signs

If B.P elevated, reposition patient (slight head &chest elevation)D definitive care: establish IV access & transport to EMT

SEIZURES

Types:

Causes: Congenital abnormalities Perinatal injuries Metabolic and toxic disorders Head trauma Tumors Vascular diseases Degenerative disorders Infectious diseases

Partial seizures Generalized seizures

Simple partialComplex partialPartial seizures evolving to generalized tonic – clonic

Absence seizures (true petitmal)Myoclonic seizuresTonic – clonic seizuresUnclassified epileptic seizures

Predisposing factors: 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

Dental therapy considerations: Conscious sedation – N2O – O2 & benzodiazepines

Clinical manifestations:

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

Discontinue dental treatment

Ictal phaseP – Position patient in supine position with feet elevated

Activation of EMSA → B → C –Assess and perform basic life support as needed

D – Definitive careProtect patient from injury

Post ictal phaseP – Position patient in supine position with feet elevated

A → B → C –Assess and perform basic life support as neededD – Definitive care

Administer O2

Monitor vital signsReassure patient and permit recovery

Discharge patient

To hospital To home To physician

DRUG RELATED EMERGENCIES

Drug Overdose Reactions

Allergy

Drug Overdose ReactionsLocal Anesthetic and Epinephrine Toxicity 

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. Monitor vital signs. 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.)

Monitor and record vital signs.

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

Allergic Reaction

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. Monitor vital signs. 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  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.

CHEST PAIN

Angina PectorisAcute Myocardial Infarction

Angina PectorisDefined 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

Dental therapy considerations: 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

Clinical manifestations: 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 substernallyRadiation 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)

Discontinue dental treatmentActivate office emergency team

P – Position, patient comfortably usually uprightA → B → C –Assess and perform BLS

D – definitive management

HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINAAdminister vasodilator and O2 Activate EMS

Transmucosal nitroglycerine spray O2 and consider nitroglycerine

Or sublingual nitroglycerine tablet Monitor and record0.3 – 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

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

Predisposing factors: Atherosclerosis and coronary artery disease Coronary thrombosis, occlusion and spasm Other risk factors are- Males 5th and 6th decades of life Undue stress

Location of infarction:

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

Dental therapy considerations: 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

Clinical manifestations:

Symptoms Signs

Pain – severe to intolerableProlonged, 30 minCrushing, chokingRetrosternalRadiates – left arm, hand, epigastrium, shoulders, neck, jawNausea and vomitingWeaknessDizzinessPalpitationsCold perspirationSense of impending doom

RestlessnessAcute distressSkin – cool, pale, moistHeart 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)

Discontinue dental treatmentActivate office emergency team

P – Position, patient comfortably usually uprightA → 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

   

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  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.