INTRODUCTION PREVENTION PREPARATION CLASSIFICATION OF LIFE THREATENING EMERGENCIES UNCONSCIOUSNESS Vasodepressor Syncope Postural Hypertension Acute Adrenal Insufficiency

ncy RESPIRATORY DISTRESS Foreign Body Airway Obstruction Hyperventilation Asthma Heart Failure and Acute Pulmonary Edema ALTERED CONSCIOUSNESS Diabetes Mellitus: Hyperglycemia and Hypoglycemia Thyroid Gland Dysfunction Cerebro vascular Accident SEIZURES DRUG RELATED EMERGENCIES Drug Overdose Reactions Allergy CHEST PAIN Angina Pectoris Acute Myocardial Infarction

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

Goals of physical evaluation Physical evaluation

Medical history questionnaire, Physical examination Dialogue history.

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

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

Drug Alprazolam Diazepam Flurazepam Midazolam

Recommended dosage for adults 4 mg / day 2-10 mg 15-30 mg Rarely used

Oxazepam
Triazolam Eszopiclone

10-30 mg
125-250g 2-3 mg

Zaleplon
Zolpidem

5-10 mg
10 mg

Situation Standard general prophylaxis

Agent Amoxicillin

Regimen Adults: 2g Children: 50mg/kg orally 1 hour before the procedure Adults: 2g Children: 50 mg/kg IM/IV 30 min before procedure 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 Adults 600mg Children 20mg/kg IV 30 min before Adults 1g Children 25 mg/kg IM/IV 30 min before

Inability to take oral medications

Ampicillin

Allergy to penicillin

Clindamycin

or

Cephalexin/Cefadroxil or

Azithromycin/ Clarithromycin

Allergy to penicillin and inability to take oral medications

Clindamycin or

Cefazolin

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

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

Module one critical or essential emergency drugs

Category
Allergy anaphylaxis

Generic drug alternative

Epinephrine None

quantity
1 preloaded syringe +3x1 ml ampules 3x1 ml ampules
1 E cylinder

Availability
1:1000 (1mg/ml)

allergy histamine blocker

Oxygen Vasodilator

Chlorphenira mine

Diphenhydra mine (Benadryl)

10 mg/ml

Oxygen Nitroglycerin Nitrostat sublingual tablets Metaproterenol Insta glucose gel

1 metered spray 0.4 mg /metered bottle dose 1 metered dose inhaler 1 bottle Metered aerosol inhaler

Bronchodilator Antihypoglyce mic

Albuterol Sugar

Inhibitor of platelet aggregation

Asprin

None

2 packets

325mg/tablet

Equipment
Oxygen delivery system

Recommended
Positive pressure and demand valve Pocket mask Many Plastic disposable syringes with needles

Alternative
Oxygen delivery system with bag valve mask device

Quantity
Minimum: 1 large adult, 1 child 1 per employee 1 AED 3x2 ml syringes with needles for parenteral drug administration

Automated electronic defibrillator(AED) Syringes for drug administration

Suction and suction tips

High volume suction Large diameter, round ended suction tips Robber and Velcro tourniquet; rubber tubing Magill intubation forceps

Non electrical suction system

Office suction system Minimum 2

Tourniquets

spygmomanometer

3 torniquets and 1 spygmomanometer 1 pediatric Magill intubation forceps

Magill intubation forceps

Module two secondary/ noncritical drugs and equipment

Category Anticonvulsant Analgesic Vasopressor Generic Drug Midazolam Morphine sulphate Phenylephrine Alternative diazepam Meperidine Quantity 1x5 ml vial 3x1 ml ampules 3x1 ml ampules 1 vial 2x2 ml mix- o vial 2x100 mg/ml vial 3x1 ml ampules Availability 5 mg/ml 10 mg/ml 10 mg/ml 50 ml ampule 50 mg/ml 100 mg/ml

Glucagon Antihypoglycem 50% dextrose ic Corticosteroid Hydrocortisone Dexamethasone sodium succinate Antihypertensive Esmolol Propranolol

Anticholinergic

Atropine

Scopolamine

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 Cardiac Arrest

Generic Drug epinephrine

Alternative

Quantity 3x10 ml preloaded syringes 3x1 ml ampules 1 preloaded syringe and 2x5 ml ampules 2x10 ml syringes 2x4 ml ampules

Availability 1:10,000 (1mg/10ml syringe) 10 mg/ml 100 mg/ syringe

Analgesic Antidysrhythmic

Morphine sulphate Lidocaine

N2O O2 Procainamide

Symptomatic Bradycardia Paroxysmal Supraventricular Tachycardia

Atropine verapamil

Isoproterenol

1.0 mg/10 ml 2.5 mg/ml

Module four antidotal drugs

Category Opioid antagonist Generic Drug Naloxone Alternative nalbuphine Quantity Availability

2x1 ml ampules 0.4 mg/ml 1x 10 ml vial 0.1 mg/ml

Benzodiazepine Flumazenil antagonist Anticholinergic Physostigmine toxicity Antiemergence delirium

3x2 ml ampules 1 mg/ml

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

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

Prevention: Proper positioning and Anxiety relief

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

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

Pathophysiology:
Stress Catecholamines release Decreased peripheral vascular resistance & blood flow to peripheral muscles venous return circulatory blood vol. & drop in arterial B.P. Activation of Compensatory mechanisms Reflux bradycardia develops (< 50)

Significant drop in cardiac output associated with fall in B.P below the critical level
Cerebral ischemia & loss of consciousness

Assess consciousness (loss of response to sensory stimulation) Activate office emergency system P- Position patient supine with feet elevated slightly ABC 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 recoverydelayed recoveryPostpone dental treatment Activate EMS Determine precipitating factors

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 Addissons 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 ABC 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 consciousnessslowly reposition chair

delayed recovery activate EMS

Continue BLS as needed and discharge patient

A third potentially life - threatening situation that may result in the loss of consciousness. The condition is uncommon, is potentially life threatening, but is readily treatable. Predisposing factors: Lack of gluco-corticosteroid hormones Mechanism 1: sudden withdrawal of steroid hormones in the patient who suffers primary adrenal insufficiency (Addisons 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 glucocorticosteroid administration (secondary insufficiency) Mechanism 3: Stress either physiologic or psychological.

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

Dental therapy considerations: Glucocorticosteroid coverage Stress reduction protocol Clinical manifestations:
Symptom 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 Sign 1. Weight loss 2. Hyperpigmentation 3. Hypotension (<110 mm Hg systolic 4. Vitiligo 5. Auricular calcification Laboratory finding 1. Electrolyte disturbance: Hyponatremia Hyperkalemia Hypercalcemia 1. Azotemia 2. Anemia 3. Eosinophilia

Pathophysiology

Management :
Conscious Terminate dental treatment P Position patient comfortably if asymptomatic; Supine with legs elevated slightly, if symptomatic ABC 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

Prevention:

General Signs and Symptoms Gasping for breath Patient grabs at throat Panic Suprasternal or supraclavicular retraction Inability to speak, breathe, cough
If Partial Obstruction

Snoring Gurgling Wheezing Crowing sound on inspiration Forceful cough Wheezing between cough Absent or altered voice sounds Possible cyanosis, lethargy, disorientation

If Total Obstruction - No noise

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

CONSCIOUS victim with obstructed airway

Identify complete airway obstruction Ask Are you choking

Apply abdominal thrusts until foreign body is expelled

Have medical or paramedical personnel to evaluate the patient

CONSCIOUS victim with known obstructed airway who loses consciousness

Place victim in supine position with head in neutral position

Maintain airway (head tilt chin lift) Look in mouth for foreign object prior to ventilation. If INEFFECTIVE: Perform abdominal thrust, repeating until the object is expelled Check for foreign body. If visible, perform finger swipe to remove

Establishing an emergency airway Non invasive procedures

Invasive procedures

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

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

Clinical manifestations:
system cardiovascular Signs and symptoms Palpitations Tachycardia Precordialpain Dizziness Lightheadedness Disturbance of consciousness Disturbance of vision Numbness and tingling of extremities Tetany (rare) Shortness of breath Chest pain Dryness of mouth Globus hystericus (subjective feeling of a lump in the throat) Epigastric pain Muscle pain and cramps Tremor Stiffness Carpopedal tetany Tension Anxiety and nightmares

Neurologic

Respiratory

Gastro intestinal

Musculoskeletal

Psychological

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 patients mouth Calm patient Correct respiratory alkalosis instructed to breathe 7% CO2 &93% O2 or to rebreathe the exhaled air Initial drug management Benzodiazepines

Dental care may continue if both doctor and patient agree Discharge patient

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

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 cows 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 -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) Dental care may continue Discharge patient Hospitalize or discharge patient, per (episode continues) Activate EMS Administer parenteral drugs EMS recommendation

Additional considerations: Sedatives which depress respiratory system and central nervous system are absolutely contraindicated. 5mg IV or IM diazepam may be indicated to decrease anxiety.

It is generally described as the inability of heart to supply sufficient oxygenated blood for bodys 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 bodys requirement of O2 and nutrients (e.g. pregnancy, hyperthyroidism, anemia, Pagets disease)

Other factors are physical, psychological and climatic stress

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.

Clinical manifestations:
Heart failure SignsSymptoms 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

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

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

Other specific types of diabetes mellitus

Gestational diabetes mellitus Impaired glucose tolerance Impaired fasting glucose

Precipitants of hypoglycemia in diabetic patients:

Addisons disease Anorexia nervosa Decrease in usual food intake Ethanol Factitious hypoglycemia Hepatic impairment Hyper and hypothyroidism Increase in usual exercise Insulin Islet cell tumors Incorrectly used insulin pump Malnutrition Old age Oral hypoglycemic agents Over aggressive treatment of ketoacidosis Pentamidine, Phenylbutazone, Propranolol Recent change in dose Salicylates Sepsis

Prevention: Medical history questionnaire Dialogue history Physical examination Dental therapy considerations:
ASA physical status II Treatment considerations 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 Monitor blood glucose levels more frequently for several days following surgery and modify insulin accordingly Consider medical consultation Consult physician before treatment

III IV

Antibiotic coverage in the postsurgical period is appropriate Stress reduction protocol to be followed Clinical manifestations of hyperglycemia:

Symptom Polyuria

Type I diabetes ++

Type II diabetes +

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 Repeated skin infections Marked irritability Headache Drowsiness Malaise Dry mouth

Other symptoms of type II diabetes

Decreased vision Paresthesias Loss of sensation Impotence Postural hypotension

Clinical manifestations of hypoglycemia: Early stage mild reaction Diminished cerebral function Changes in mood Decreased spontaneity Hunger Nausea More severe stage Later severe stage Unconsciousness Sweating Seizure activity Tachycardia Hypotension Piloerection Hypothermia Increased anxiety Bizarre behavioral patterns Belligerence Poor judgment Uncooperativeness

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 hydroxybutyrate (BHA) diabetic ketoacidosis cardiac contractility, catecholamine response, respiratory alkalosis Diabetic coma

Hypoglycemia: Hypoglycemia in adults blood sugar < 50 mg/dl, in children < 40 mg/dl Alters normal functioning of the cerebral cortex Mental confusion and lethargy Lack of glucose activities of sympathetic and parasympathetic nervous systems With the mediation of epinephrine, systolic and mean blood pressures sweating and tachycardia When the blood sugar level drops even further Loss of consciousness Hypoglycemic coma and insulin shock Patients may experience tonic clonic convulsions

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

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 Permit patient to recover Discharge the patient If unsuccessful Activate EMS Administer parenteral carbohydrates Monitor patient Discharge patient

Hypoglycemia: unconscious patient

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

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

Predisposing factors: Hypothyroidism: Primary: Auto immune

Hyperthyroidism: Diffuse toxic goiter Toxic multinodular goiter

Idiopathic causes Factitious thyrotoxicosis Postsurgical thyroidectomy T3 thyrotoxocosis External radiation therapy Thyrotoxicosis with thyroiditis Radioiodine therapy Hashimotos thyroiditis Inherited enzymatic defect Subacute thyroiditis Antithyroid drugs Jod Basedow phenomenon Lithium, phenylbutazone Malignancies TSH producing tumors Secondary:

Pituitary tumor Hypothalamic hyperthyroidism Infiltrative disease of pituitary Struma ovarii with hyperthyroidism

Prevention: 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

Clinical manifestations Hypothyroidism:

Symptoms 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 Signs Pseudomyotonic reflexes Change in menstrual pattern Hypothermia Dry, scaly skin Puffy eyelids Hoarse voice Weight gain Dependent edema Sparse axillary and pubic hair Pallor Thinning eyebrows Yellow skin Loss of scalp hair Abdominal distension Goiter Decreased sweating

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

Pathophysiology: Hypothyroidism: Insufficient levels of thyroid hormones Body functions slow down Infiltration of mucopolysaccharides and mucoproteins in skin Hard nonpitting mucinous edema myxedema Cardiac enlargement, pericardial and pleural effusions Cardiovascular and respiratory difficulties End point is myxedema coma- loss of consciousness due to hypothermia, hypoglycemia and CO2 retention

Thyrotoxicosis: Thyroid hormones bodys energy consumption and BMR

Fatigue &weight loss Direct actions on myocardium - HR, myocardial irritability cardiac work load Palpitations, dyspnea, chest pain incidence of angina pectoris and heart failure thyroid hormones also affects liver function End point thyroid storm and crisis

Management: P Position , supine position with feet elevated

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

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

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 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

Pathophysiology:

Cerebrovascular ischemia and infarction

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

Hemorrhagic CVA
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 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

Types:
Partial seizures Simple partial Complex partial Partial seizures evolving to generalized tonic clonic Generalized seizures Absence seizures (true petitmal) Myoclonic seizures Tonic clonic seizures Unclassified epileptic seizures

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

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 ABC Assess and perform BLS

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

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 ABCs.

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 Cardiac Patient

0.2mg 0.04mg

Signs and Symptoms of an Allergic Reaction

Cutaneous reactions are the most common occurrence and include urticarial, exanthematous, and eczemoid reactions. Itching is common and can also find exfoliative dermatitis and bullous dermatosis.
Angioedema (Swelling) this varies from localized slight swelling of the lips, eyelids, and face to more uncomfortable swelling of the mouth, throat, and extremities.

Respiratory (Tightness in chest, sneezing, bronchospasm) bronchospasm is a generalized contraction of bronchial smooth muscles resulting in the restriction of airflow. This may also be accompanied by edema of the bronchiolar mucosa. Bronchospasm is more common with pre-existing pulmonary disease such as asthma or infection but can also be caused by the inhalation of a foreign substance. Ocular reactions include conjunctivitis and watering of eyes. Hypotension can occur with any allergic reaction.

Anaphylaxis: Signs and symptoms include:

Cardiovascular shock including; pallor, syncope, palpitations, tachycardia, hypotension, arrythmias, and convulsions. Respiratory symptoms include; sneezing, cough, wheezing, tightness in chest, bronchospasm, laryngospasm. Skin is warm and flushed with itching, urticaria, and angioedema.

Nausea, vomiting, abdominal cramps, and diarrhea also possible.

Evaluation of Allergic Reactions: Things to remember.

Skin manifestations may precede more serious cardiorespiratory problems. Recognition of skin reactions and early treatment may abort more serious problems. Most important factor is assessing the seriousness of the condition is the rate of onset. Reactions that occur greater than one hour after the administration of the allergen will usually be of a nonemergent nature.

TREATMENT General Treatment ABCs 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.

Defined as a characteristic thoracic pain, usually substernal, precipitated chiefly by exercise, emotion, or a heavy meal; relieved by vasodilator drugs, and a few minutes rest; and a result of a moderate inadequacy of the coronary circulation Precipitating factors: Physical activity Hot, humid environment Cold whether Large meals Emotional stress Caffeine ingestion Fever, anemia, thyrotoxicosis Cigarette smoking Smog High altitudes Second hand smoke

Types:

Stable (classic or exertional) Variant (prinzmetal , vasospastic) Unstable (crescendo, acute coronary insufficiency)

Prevention:

Medical history questionnaire chest pain, shortness of breath, history of heart disease, stroke, high B.P, family history of diabetes & heart problems, thyroid and diabetes, previous surgeries and medications
Dialogue history type of pain, radiation, precipitating factors and effect of nitro glycerine

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 substernally Radiation of pain: most commonly to left shoulder and arm (ulnar nerve distribution) Less frequently to right shoulder, arm, left jaw, neck and epigastrium

Pathophysiology: Imbalance between myocardial oxygen demand and supply Compensatory mechanism by coronary arteries

If myocardial oxygen requirement reaches this critical level

Myocardial ischemia

Clinical manifestation of angina pain due to adenosine , bradykinin, histamine and serotonin from ischemic cells
If there is consistent high B.P and tachycardia work load of the heart Ventricular dysrhythmias and becomes fatal

Management: Recognize problem (chest pain angina attack) 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, blockers, calcium channel blockers and psychological stress management and reassurance

It is a clinical syndrome caused by a deficient coronary arterial blood supply to a region of myocardium that results in cellular death and necrosis 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 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

Signs Restlessness Acute distress Skin cool, pale, moist Heart rate bradycardia to tachycardia; PVC (premature ventricular contractions) common

Pathophysiology: Infarction of myocardium Left ventricle is commonly involved in acute MI

Blood supply leaving the heart may be diminished

Signs and symptoms of acute MI Larger the infarct, greater the circulatory insuficiency Signs and symptoms of heart failure Increased left ventricular pressure Left ventricular failure hypotension, cardiac output, cardiogenic shock Fatal

Management:

Recognize problem (chest pain no history of angina) 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 Follow protocol of angina

NO HISTORY OF ANGINA (presumptive diagnosis: Acute MI) Activate EMS Administer O2,consider nitroglycerine Administer aspirin Manage pain (parenteral opioids, N2O O2) Monitor and record vital signs Prepare to manage complications (sudden cardiac arrest) Transfer to emergency department

Prompt recognition and efficient management of medical emergencies by a well-prepared dental team can increase the likelihood of a satisfactory outcome. The basic algorithm for managing medical emergencies is designed to ensure that the patients 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.