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.
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