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Medical emergencies dental office

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  • 1.  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  
  • 2. Goldberger 1990, “When you prepare for an emergency, the emergency ceases to exist.”
  • 3. Goals of physical evaluation Physical evaluation –  Medical history questionnaire,  Physical examination  Dialogue history.
  • 4.  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.
  • 5.  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.
  • 6. 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
  • 7. Situation Agent Regimen Standard general prophylaxis Amoxicillin Adults: 2g Children: 50mg/kg orally 1 hour before the procedure Inability to take oral medications Ampicillin Adults: 2g Children: 50 mg/kg IM/IV 30 min before procedure Allergy to penicillin Clindamycin or Cephalexin/Cefadroxil or Azithromycin/ Clarithromycin Adults 600 mg Children 20 mg /kg Adults 2g Children 50mg/kg Adults 500 mg Children 50 mg/kg Orally 1 hour before the procedure Allergy to penicillin and inability to take oral medications Clindamycin or Cefazolin Adults 600mg Children 20mg/kg IV 30 min before Adults 1g Children 25 mg/kg IM/IV 30 min before
  • 8.  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
  • 9. 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
  • 10. Module one – critical or essential emergency drugs Category Generic drug alternative quantity Availability Allergy – anaphylaxis Epinephrine None 1 preloaded syringe +3x1 ml ampules 1:1000 (1mg/ml) allergy – histamine blocker Chlorphenira mine Diphenhydra mine (Benadryl) 3x1 ml ampules 10 mg/ml Oxygen Oxygen 1 “E” cylinder Vasodilator Nitroglycerin Nitrostat sublingual tablets 1 metered spray bottle 0.4 mg /metered dose Bronchodilator Albuterol Metaproterenol 1 metered dose inhaler Metered aerosol inhaler Antihypoglyce mic Sugar Insta – glucose gel 1 bottle Inhibitor of platelet aggregation Asprin None 2 packets 325mg/tablet
  • 11. Equipment Recommended Alternative Quantity Oxygen delivery system Positive pressure and demand valve Pocket mask Oxygen delivery system with bag valve mask device Minimum: 1 large adult, 1 child 1 per employee Automated electronic defibrillator(AED) Many 1 AED Syringes for drug administration Plastic disposable syringes with needles 3x2 ml syringes with needles for parenteral drug administration Suction and suction tips High volume suction Large diameter, round ended suction tips Non electrical suction system Office suction system Minimum 2 Tourniquets Robber and Velcro tourniquet; rubber tubing spygmomanometer 3 torniquets and 1 spygmomanometer Magill intubation forceps Magill intubation forceps 1 pediatric Magill intubation forceps
  • 12. Module two – secondary/ noncritical drugs and equipment Category Generic Drug Alternative Quantity Availability Anticonvulsant Midazolam diazepam 1x5 ml vial 5 mg/ml Analgesic Morphine sulphate Meperidine 3x1 ml ampules 10 mg/ml Vasopressor Phenylephrine 3x1 ml ampules 10 mg/ml Antihypoglycem ic 50% dextrose Glucagon 1 vial 50 ml ampule Corticosteroid Hydrocortisone sodium succinate Dexamethasone 2x2 ml mix- o – vial 50 mg/ml Antihypertensive Esmolol Propranolol 2x100 mg/ml vial 100 mg/ml Anticholinergic Atropine Scopolamine 3x1 ml ampules 0.5 mg/ml Respiratory stimulant Aromatic ammonia 2 boxes 0.3 ml/vaporole Antihypertensive Nifedipine 1 bottle 10mg/capsule
  • 13. 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
  • 14. 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 toxicity Antiemergence delirium Physostigmine 3x2 ml ampules 1 mg/ml
  • 15. Syncope is a general term referring to a sudden, transient loss of consciousness that usually occurs secondary to a period of cerebral ischemia. Predisposing factors: Psychogenic factors  Fright  Anxiety  Emotional stress  Receipt of unwelcome news  Pain especially sudden &unexpected  Sight of blood/ surgical/ dental instruments  (e.g. local anesthetic syringe)
  • 16. 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
  • 17. 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.
  • 18. 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.
  • 19. 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
  • 20. Assess consciousness (loss of response to sensory stimulation) Activate office emergency system P- Position patient supine with feet elevated slightly A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency& breathing; assess circulation (palpation of carotid pulse) D – Definitive care: Administer O2 Monitor vital signs Perform additional procedures: Administer aromatic ammonia vaporole Administer atropine if bradycardia persists Do not panic! Post syncopal recovery- delayed recovery- Postpone dental treatment Activate EMS Determine precipitating factors
  • 21. Predisposing 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)
  • 22. 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
  • 23. 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
  • 24. 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
  • 25. 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.
  • 26. If the adrenal gland cannot meet the increased demand, clinical signs and symptoms of adrenal insufficiency develop.  Mechanism 4: After bilateral adrenalectomy  Mechanism 5: After sudden destruction of pituitary gland.  Mechanism 6: Injury to the both adrenal glands (trauma, infection, thrombosis, or tumor) Prevention:  History of rheumatic fever, asthma, TB, emphysema, other lung diseases, arthritis and rheumatism  Allergic history to drugs, food, medications, latex Dialogue history Rule of TWOs  In a dose of 20 mg or more of cortisone or its equivalent  Via oral or parenteral route for a continuous period of two weeks or longer  Within 2 years of dental therapy
  • 27. Dental therapy considerations:  Glucocorticosteroid coverage  Stress reduction protocol Clinical manifestations: Symptom Sign Laboratory finding 1. Weakness, tiredness, fatigue 2. Anorexia 3. GI symptoms like nausea vomiting constipation, abdominal pain, diarrhea 4. Salt craving 5. Postural dizziness 6. Muscle or joint pain 1. Weight loss 2. Hyperpigmentation 3. Hypotension (<110 mm Hg systolic 4. Vitiligo 5. Auricular calcification 1. Electrolyte disturbance:  Hyponatremia  Hyperkalemia  Hypercalcemia 1. Azotemia 2. Anemia 3. Eosinophilia
  • 28. Pathophysiology
  • 29. 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 assistance Obtain emergency kit and O2 Administer glucocorticosteroid
  • 30. Prevention:
  • 31. 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
  • 32. Visible objects – if assistant is present Place patient into supine or Trendelenburg position Use Magill intubation forceps or suction if assistant is not present Instruct patient to bend over arm of chair with their head down Encourage patient to cough Aspirated foreign bodies Place patient in left lateral decubitus position Encourage patient to cough
  • 33. 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
  • 34. 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
  • 35. Establishing an emergency airway – Non invasive procedures Invasive procedures
  • 36. If foreign body is not retrieved Consult radiologist Obtain appropriate radiographs and initiate medical consultation Perform bronchoscopy to visualize and retrieve foreign body
  • 37.  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
  • 38. Clinical manifestations: system Signs and symptoms cardiovascular Palpitations Tachycardia Precordial”pain” Neurologic Dizziness Lightheadedness Disturbance of consciousness Disturbance of vision Numbness and tingling of extremities Tetany (rare) Respiratory Shortness of breath Chest “pain” Dryness of mouth Gastro intestinal Globus hystericus (subjective feeling of a lump in the throat) Epigastric pain Musculoskeletal Muscle pain and cramps Tremor Stiffness Carpopedal tetany Psychological Tension Anxiety and nightmares
  • 39. 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
  • 40.  Hypocapnia → vasoconstriction of cerebral vessels → cerebral ischemia  Respiratory alkalosis → ↓ ionized calcium
  • 41. 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 patient Correct respiratory alkalosis – instructed to breathe 7% CO2 &93% O2 or to rebreathe the exhaled air Initial drug management – Benzodiazepines Dental care may continue if both doctor and patient agree Discharge patient
  • 42.  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.”
  • 43. 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
  • 44. 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.
  • 45. 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
  • 46. Dialogue history:  Asthma?  Type extrinsic or intrinsic?  Age of onset  History of acute episodes  Precipitating factor  Management
  • 47. 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
  • 48. 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
  • 49. 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
  • 50. Pathophysiology:  Neural control of airways  Airway inflammation  Immunological responses  Bronchospasm  Bronchial wall edema and hypersecretion of mucous glands  Breathing
  • 51. 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.
  • 52. 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
  • 53. Prevention:  Medical history questionnaire  Dialogue history  Physical evaluation  Physical examination Dental 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.
  • 54. 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
  • 55. 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
  • 56. 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
  • 57. 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 signs Alleviate symptoms of respiratory distress: Perform bloodless phlebotomy Administer vasodilator e. g. Nitroglycerine Alleviate apprehension e.g. morphine Discharge patient Modify subsequent dental treatment
  • 58. 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 factors Type II diabetes:  Genetic factors  Insulin secretion  Insulin resistance  Obesity  Adipocyte derived hormones and cytokines
  • 59. Other specific types of diabetes mellitus  Gestational diabetes mellitus  Impaired glucose tolerance  Impaired fasting glucose
  • 60. Precipitants of hypoglycemia in diabetic patients: Addison‟s disease Anorexia nervosa Decrease in usual food intake Ethanol Factitious hypoglycemia Hepatic impairment Hyper and hypothyroidism Increase in usual exercise Insulin Islet cell tumors Incorrectly used insulin pump Malnutrition Old age Oral hypoglycemic agents Over aggressive treatment of ketoacidosis Pentamidine, Phenylbutazone, Propranolol Recent change in dose Salicylates Sepsis
  • 61. Prevention: Medical history questionnaire Dialogue history Physical examination Dental 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
  • 62.  Antibiotic coverage in the postsurgical period is appropriate  Stress reduction protocol to be followed Clinical manifestations of hyperglycemia: Symptom Type I diabetes Type II diabetes Polyuria ++ + Polydipsia ++ + Polyphagia with weight loss ++ _ Recurrent blurred vision + ++ Vulvovaginitis or pruritis + ++ Loss of strength ++ + Nocturnal enuresis ++ _ Absence of symptoms _ ++
  • 63. 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
  • 64. Clinical manifestations of hypoglycemia: Early stage – mild reaction  Diminished cerebral function  Changes in mood  Decreased spontaneity  Hunger  Nausea More severe stage  Sweating  Tachycardia  Piloerection  Increased anxiety  Bizarre behavioral patterns  Belligerence  Poor judgment  Uncooperativeness Later severe stage •Unconsciousness •Seizure activity •Hypotension •Hypothermia
  • 65. 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
  • 66. Hypoglycemia:  Hypoglycemia in adults – blood sugar < 50 mg/dl, in children - < 40 mg/dl  Alters normal functioning of the cerebral cortex  Mental confusion and lethargy  Lack of glucose → ↑ activities of sympathetic and parasympathetic nervous systems  With the mediation of epinephrine,↑ systolic and mean blood pressures  ↑ sweating and tachycardia  When the blood sugar level drops even further  Loss of consciousness  Hypoglycemic coma and insulin shock Patients may experience tonic – clonic convulsions
  • 67. 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 saline Administer O2 Transport to hospital
  • 68. Hypoglycemia – conscious patient Recognize 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 unsuccessful Permit patient to recover Activate EMS Discharge the patient Administer parenteral carbohydrates Monitor patient Discharge patient
  • 69. Hypoglycemia: unconscious patient P – Position patient in supine position with feet elevated D – Definitive management Summon EMS Administer oral carbohydrates IV 50% dextrose solution 1 mg glucagon via IM or IV Transmucosal sugar, or rectal honey or syrup Monitor vital signs every 5 minutes Administer O2 Allow patient to recover and discharge per medical recommendations 
  • 70. 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.
  • 71. 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 tumors Secondary:  Pituitary tumor Hypothalamic hyperthyroidism  Infiltrative disease of pituitary Struma ovarii with hyperthyroidism
  • 72. Prevention: Medical history questionnaire Dialogue history Dental therapy considerations  Euthyroid patient with normal hormone levels can be managed normally  Hypothyroid – avoidance of CNS depressants (opiods, sedative hypnotics)  Hyperthyroid – avoidance of atropine and vasoconstrictors, least concentrated solution is preferred 1:200,000, smallest effective volume of anesthetic and vasodepressor, aspiration prior to every injection  Evaluation of cardio vascular disease
  • 73. Clinical manifestations Hypothyroidism: Symptoms Signs Paresthesias Loss of energy Intolerance to cold Muscular weakness Pain in muscles and joints Inability to concentrate Drowsiness Constipation Forgetfulness Depressed auditory acuity Emotional instability Headaches Dysarthria Pseudomyotonic reflexes Change in menstrual pattern Hypothermia Dry, scaly skin Puffy eyelids Hoarse voice Weight gain Dependent edema Sparse axillary and pubic hair Pallor Thinning eyebrows Yellow skin Loss of scalp hair Abdominal distension Goiter Decreased sweating
  • 74. Thyrotoxicosis: Symptoms signs Common Weight loss Palpitations Nervousness Tremor Less common Chest pain Dyspnea Edema Psychosis Disorientation Diarrhea Abdominal pain Fever Tachycardia Sinus tachycardia Dysrhythmias Wide pulse pressure Tremor Thyrotoxic stare and eyelid retraction Hyperkinesis Heart failure Weakness Coma Tender liver Infiltrative ophthalmopathy Somnolence or obtundence Jaundice
  • 75. 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
  • 76. 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
  • 77. Management: P – Position , supine position with feet elevated D – Definitive management – activate EMS and if recovery is not immediate, establish IV access Hypothyroidism –IV doses of thyroid hormones (T3 & T4) for several days Thyrotoxicosis –administer large doses of antithyroid drugs, additional therapy – propranolol, glucocorticoids Administer O2 Discharge or hospitalize the patient
  • 78. 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
  • 79. 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
  • 80. 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 therapy Clinical 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
  • 81. 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
  • 82. Management of CVA & TIA: Conscious patient Discontinue dental treatment P – Position patient comfortably A → B → C –Assess and perform basic life support as needed D – Definitive management: Monitor vital signs Manage signs and symptoms If B.P elevated, semi – fowler position (450 position) Administer O2 Do not administer CNS depressants Symptoms resolve (TIA) Symptoms persist CVA or TIA Loss of consciousness Follow up management Hospitalization P – position with feet elevated slightly A → B → C –Assess and perform basic life support as needed Monitor vital signs If B.P elevated, reposition patient (slight head &chest elevation) D definitive care: establish IV access & transport to EMT
  • 83. Types: Causes:  Congenital abnormalities  Perinatal injuries  Metabolic and toxic disorders  Head trauma  Tumors  Vascular diseases  Degenerative disorders  Infectious diseases Partial seizures Generalized seizures Simple partial Complex partial Partial seizures evolving to generalized tonic – clonic Absence seizures (true petitmal) Myoclonic seizures Tonic – clonic seizures Unclassified epileptic seizures
  • 84. 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
  • 85. 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
  • 86.  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
  • 87. 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
  • 88. 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
  • 89. Management of tonic clonic seizure: Prodromal phase Discontinue dental treatment Ictal phase P – Position patient in supine position with feet elevated Activation of EMS A → B → C –Assess and perform basic life support as needed D – Definitive care Protect patient from injury Post ictal phase P – Position patient in supine position with feet elevated A → B → C –Assess and perform basic life support as needed D – Definitive care Administer O2 Monitor vital signs Reassure patient and permit recovery Discharge patient To hospital To home To physician
  • 90. 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.
  • 91. 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.
  • 92. 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.
  • 93. 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.
  • 94. 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
  • 95. 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.
  • 96.  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.
  • 97. 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.
  • 98. 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.
  • 99. 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.)
  • 100.  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.
  • 101. Defined as „ a characteristic thoracic pain, usually substernal, precipitated chiefly by exercise, emotion, or a heavy meal; relieved by vasodilator drugs, and a few minutes rest; and a result of a moderate inadequacy of the coronary circulation‟ Precipitating factors:  Physical activity  Hot, humid environment  Cold whether  Large meals  Emotional stress  Caffeine ingestion  Fever, anemia, thyrotoxicosis  Cigarette smoking  Smog  High altitudes  Second – hand smoke
  • 102. 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
  • 103. 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
  • 104. 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 substernally Radiation of pain: most commonly to left shoulder and arm (ulnar nerve distribution)  Less frequently to right shoulder, arm, left jaw, neck and epigastrium
  • 105. 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
  • 106. Management: Recognize problem (chest pain – angina attack) Discontinue dental treatment Activate office emergency team P – Position, patient comfortably usually upright A → B → C –Assess and perform BLS D – definitive management HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA Administer vasodilator and O2 Activate EMS Transmucosal nitroglycerine spray O2 and consider nitroglycerine Or sublingual nitroglycerine tablet Monitor and record 0.3 – 0.6 mg for every 5 min (3 doses) IF PAIN RESOLVES IF PAIN DOES NOT RESOLVE Future dental treatment modifications Activate EMS Administer aspirin Monitor and record vital signs Medical management of unstable angina – Nitrates, β – blockers, calcium channel blockers and psychological stress management and reassurance
  • 107. 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
  • 108. Location of infarction:
  • 109. 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
  • 110. 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
  • 111. Clinical manifestations: Symptoms Signs Pain – severe to intolerable Prolonged, 30 min Crushing, choking Retrosternal Radiates – left arm, hand, epigastrium, shoulders, neck, jaw Nausea and vomiting Weakness Dizziness Palpitations Cold perspiration Sense of impending doom Restlessness Acute distress Skin – cool, pale, moist Heart rate – bradycardia to tachycardia; PVC (premature ventricular contractions) common
  • 112. Pathophysiology: Infarction of myocardium Left ventricle is commonly involved in acute MI Blood supply leaving the heart may be diminished Signs and symptoms of acute MI Larger the infarct, greater the circulatory insuficiency Signs and symptoms of heart failure Increased left ventricular pressure Left ventricular failure → hypotension, ↓ cardiac output, cardiogenic shock Fatal
  • 113. Management: Recognize problem (chest pain – no history of angina) Discontinue dental treatment Activate office emergency team P – Position, patient comfortably usually upright A → B → C –Assess and perform BLS D – definitive management HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA Follow protocol of angina (presumptive diagnosis: Acute MI) Activate EMS Administer O2,consider nitroglycerine Administer aspirin Manage pain (parenteral opioids, N2O – O2) Monitor and record vital signs Prepare to manage complications (sudden cardiac arrest) Transfer to emergency department
  • 114.  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.
  • 115. 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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