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Medical emergencies in dentisry
- 1. MEDICAL EMERGENCIES IN DENTISTRY PRESENTED BY:- ChETAN BARAI v.S.P.M DENTAL CoLLEGE NAGPuR
- 2. INTRODUCTION INCIDENCE TYPES OF EMERGENCIES • PREVENTION • PREPARATION • MANAGEMENT SUMMARY CONCLUSION REFERENCES CONTENTS
- 3. INTRODUCTION In spiteof the most meticulous protocols designed to prevent the development of life threatening situations, emergencies still occur. Such emergencies can occur in any environment, we as “Dental Surgeons” should be always alert and should have a thorough understanding about different emergency situation which may come across during ones practice.
- 4. Incidence A surveydone in the 90’s showed that, over a 10 year period, 90% of dentists have encountered at least one medical emergencies. TYPE OF EMERGENCYTYPE OF EMERGENCY NUMBERNUMBER PERCENTPERCENT AlteredAltered ConsciousnessConsciousness 17,78217,782 5959 CardiovascularCardiovascular 4,2804,280 1414 AllergyAllergy 2,8872,887 9.59.5 RespiratoryRespiratory 2,7182,718 99 SeizuresSeizures 1,5951,595 55 Diabetes-RelatedDiabetes-Related 999999 33
- 6. PREVENTION: Physical Evaluation •Medical history questionnaire • Physical examination (vital signs, visual inspection, auscultation of heart and lungs) • Dialogue history (recognition of anxiety)
- 7. Medical historyquestionnaire: • Thorough questionnaire • Past medical history • Familial disease history • Diet Anxiety Observation • Increased BP & Heart rate • Excessive sweating • Dilated pupils Psychological examination
- 8. Classification based clinicalsigns and symptoms: Unconsciousness Vasodepressor syncope Orthostatic hypotension Respiratory difficulty Airway obstruction Hyperventilation Asthma Heart failure and acute pulmonary edema
- 9. Altered consciousness Hyperglycemia and hypoglycemia Hyperthyroidism and hypothyroidism Cerebrovascular emergencies Seizure disorders Drug related emergency situations Drug overdose reactions Allergy Chest pain Angina pectoris Acute myocardial infarction.
- 10. DETERMINATION OF MEDICAL RISK Physical status classification system (1962, American Society of Anesthesiologists) ASA I : A patient without systemic disease, a normal healthy patient ASA II : A patient with mild systemic disease ASA III : A patient with severe systemic disease that limits activity but is not incapacitating
- 11. ASA IV :A patient with incapacitating systemic disease that is a constant threat to life. ASA V : A moribund patient not expected to survive 24 hrs with or with out surgery. ASA VI : Clinically dead patient being maintained for harvesting organs. ASA E : Emergency operation of any variety; E precedes the number, indicating the patients physical status ( ASA E-III)
- 12. Unconsciousness : Possible causesof unconsciousness Vasodepressor syncope Drug administration Orthostatic hypotension Epilepsy Hypoglycemic reaction Acute adrenaline insufficiency Acute allergic reaction Acute MI Hyperglycemic reaction Hyperventilation
- 13. Prevention Via preventionof predsposing factors Use of psychosedative drugs • Ingestion - Alprazolam (4mg), Diazepam (5mg) • I.M / I.V administration – Butorphenol (1mg), Midazolam (5mg) • Inhalation - N2O(15%) + O2(85%)
- 14. VASODEPRESSOR SYNCOPE Mostcommon form of emergency medical situation in Dental office. The terms syncope and faint commonly are used interchangeably to describe transient loss of consciousness caused by reversible disturbances in cerebral function.
- 15. PREDISPOSING FACTORS PSYCHOGENIC NONPSYCHOGENIC Fright Anxiety Emotional Pain (sudden) Sight of blood, syringe etc Erect sitting or standing posture Missed meal (hunger) Exhaustion Poor physical condition Hot humid environment
- 16. Critical levelof cerebral blood flow for maintenance of consciousness is estimated to be about 30ml/100gm/min. normal cerebral blood flow is 50 – 55 ml/100 gm/min. Systolic BP may descend to as low as 20 -40 mmHg Seizures may be precipitated depending upon the brain damage. SYNCOPE PATHOPHYSIOLOGY
- 17. CLINICAL FEATURES PRE SYNCOPE Feeling of warmth in neck and face Colour changes to pale to ashen grey Pupillary dilatation Yawning Cold extremities Hypotension Bradycardia
- 18. Loss ofconsciousness Pulse becomes weak, thready, irregular. Respiration becomes irregular, jerky, shallow, or may entirely cease Death like appearance of the patient SYNCOPE POST SYNCOPE Pallor Nausea Weakness Sweating
- 19. Management Terminate alldental treatment Supine position with legs raised Attempt to calm the patient Monitor vital signs Assessment of consciousness (“shake and shout”) Check for breathing
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- 23. SHOCK Type of shocks 1.Hypovolaemic shock 2. Cardiogenic shock 3. Septic shock 4. Anaphylactic shock 5. Neurogenic shock A critical condition that is brought on by a sudden drop in blood flow through the body. Shock is a major medical emergency which is common after serious injury.
- 24. Haemorrhage, severe vomitingand Diarrhoea. Acute Myocardial infarction Gram-positive and gram- negative bacterial infection, other organisms. Drugs, insect stings High cervical cord injury, severe Head injury. Causes
- 26. Management ABC includinghigh flow oxygen Position patient in Trendelenburg position Identify underlying cause Establish haemostatis Administration of intravascular fluids Monitor vitals signs Improving systemic perfusion and oxygenation
- 27. Anaphylaxis Clinical features Wheezing Abdominal pain Nausea Urticaria Flushing of face It is a serious allergic reaction that is rapid in onset and may cause death. Par aesthesia Pallor Rapid and weak pulse Cyanosis Edema of face
- 28. Management Terminate dentaltreatment Maintenance of IV line Supine position legs elevated 0.2-0.5ml of 1:1000 epinephrine IM Followed by chlorpheniramine 10mg IV Hydrocortisone 20mg IV Monitor vital signs
- 29. POSTURAL HYPOTENSION Decline >20-25 mm Hg in SBP or a decline >10 mm Hg in DBP. HR baseline or > 30 bpm When moves from a supine to a sitting or standing position
- 30. PREDISPOSING FACTORS Ingestionof drugs Prolonged period of recumbency Inadequate postural reflex Late stage pregnancy Venous defects in the legs Physical exhaustion and starvation
- 31. CLINICAL FEATURES Asymptomatic,BP changes without symptoms. Symptomatic, such as dizziness and faintness occur with BP changes. Acute or reversible , typically caused by volume loss or medication use. Chronic or irreversible , caused by endocrine and neurogenic factors.
- 32. MANAGEMENT –Positioning Theunresponsive patient should be placed into the supine position with the feet slightly elevated this position immediately enhances cerebral perfusion, and in most instances individual regains consciousness within a few seconds. Prevalence of OH with labetalol is 1.4%. Enalapril (5-20 mg/d) reduces OH episodes, whereas long-acting nifedipine (30-90 mg/d) increases episodes.
- 33. Affects ~50million people in the US Types: 1. Primary:- Chronic high blood pressure without a source or associated with any other disease - Most common form of hypertension 2. Secondary:- Elevation of blood pressure associated with another disease such as kidney disease HYPERTENSION Category Systolic mmHg Diastolic mmHg Optimal < 120 < 80 Normal < 130 < 85 High Normal 130 - 139 85 - 89 Hypertension Stage I 140 - 159 90 - 99 Hypertension Stage II 160 - 179 100 - 109 Hypertension stage III ≥ 180 ≥ 110
- 34. Causes Genetics-some peopleare prone to hypertension simply based off of their genetic makeup Family History- your risk for high blood pressure/hypertension increases if it is in your family history Environment – Inactivity – Stress – Obesity – Alcohol – High Sodium Diet – Tobacco Use – Age – Menopausal Medications
- 35. Treatments Step 1: –Lifestyle modifications • Diet and exercise • Limit alcohol and tobacco use • Reduce stress factors Step 2: – If lifestyle changes are not enough, drug therapy will be introduced Step 3: – If previous steps don’t work, drug dose or type will be changed or another drug is added Step 4: – More medications are added until blood pressure is controlled
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- 37. A clinicalstate of hyper reactivity of the tracheobronchial tree, characterized by recurrent paroxysms of dyspnea and wheezing. In diagnosed pts, not an emergency. Results from constriction of smooth muscles of the tracheobronchial tree resulting from infection, inflammation or a genetic disposition. ASTHMA
- 38. Predisposing factors- INTRINSIC &EXTRINSIC 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 – IgE antibodies produced in response to allergen Approximately, 50% asthmatic children become symptomatic before reaching adulthood
- 39. INTRINSIC OR IDIOSYNCRATIC ORNON-ATOPIC ASTHMA Usually develops in adult age > 35 years Non allergic factors – respiratory infection, physical exertion, environmental and air pollution, and occupational stimuli. Psychological and physiologic stress can also contribute to asthmatic episodes. Acute episodes are usually more fulminant and severe than those of extrinsic asthma. Long-term prognosis also less optimistic.
- 40. CAUSATIVE FACTORS Allergy Respiratory infection Physical exertion Pollution Occupational stimuli Pharmacologic stimuli Psychologic factors
- 41. MANIFESTATIONS MILD SEVERE Wheezing Dyspnoea Tachycardia Coughing Anxiety Intense dyspnoeawith flaring of nostrils Use of accessory muscles Cyanosis of mucous membrane & nailbed Flushing of face & anxiety
- 42. MANAGEMENT Episode terminates Episodecontinues Continue treatment Administer O2 Injection of aqueous epinephrine Hydrocortisone sodium succinate 100-200mg iv
- 43. HYPERVENTILATION CLINICAL MANIFESTATIONS Palpitations Tachycardia Dizziness Light headedness Numbness of extremities Chest pain Dryness of mouth Short breath Muscle pain and cramps Tremors Stiffness Tension Anxiety Excessive rate and depth of respiration leading to abnormal loss of carbon dioxide from the blood primarily predisposed to anxiety.
- 44. Anxiety Increased rate anddepth of respiration Increased O2/CO2 exchange by lungs Excessive CO2 blow off>>paCO2 decreases Hypocapnia= decreased HCO3 ion conc. Increased blood pH>>RESPIRATORY ALKALOSIS P A T H O L O G Y
- 45. MANAGEMENT Terminate dentaltreatment Position-sitting Verbally calm the patient Carbon dioxide rich air (paper bag) if it continues Diazepam 10mg IM/ IV Monitor vital signs Continue dental treatment
- 46. AIRWAY OBSTRUCTION Duringdental treatment the potential is great that objects may fall into the posterior portion of the oral cavity and subsequently into the pharynx. PREVENTION Rubber dam Oral packing Chair position Suction Magill intubation forceps
- 47. MANAGEMENT RECOGNITION OF THEAIRWAY OBSTRUCTION Signs of complete airway obstruction Inability to speak, breathe, cough Universal sign for choking (choking sign) Panic Signs of partial airway obstruction Forceful cough Wheezing between coughs Ability to breathe Altered voice sounds Possible disorientation ‘Crowing’ sound on inspiration
- 48. BASIC AIRWAY MANEUVERS Position Headtilt- chin lift A+B Jaw thrust maneuver Artificial ventilation
- 49. ESTABLISHMENT OF EMERGENCY AIRWAY Noninvasive Invasive Back blows Finger sweep Chest thrustHeimlich maneuver Manual thrusts Non invasive Tracheostomy Cricothyrotomy
- 50. DIABETES MELLITUS Serum glucoselevel can fall because of: Increased administration of insulin Decreased dietary caloric intake Increased metabolic utilization of glucose (exercise, emotional stress WHIPPLE’S TRIAD: 1. Symtoms consistent with hypoglycaemia 2. Low plasma glucose concentration measured by precise method (Not with glucose monitor) 3. Relief of symptoms after plasma glucose level is raised.
- 51. Types of diabetesmellitus Type 1-(beta cell destruction ,usually leading to absolute insulin deficiency) Type 2-(due to progressive insulin secretory defect on the background of insulin resistance) Gestational diabetes mellitus (GDM)-diabetes diagnosed in the second or third trimester of pregnancy .
- 52. Pathophysiology of Hyperglycemia Prolonged lack of insulin ( type1) or prolonged lack of tissue response(type2). Blood glucose levels remains elevated for longer time because of glycogenolysis and decreased uptake by peripheral tissues. Glucose exceeds 180mg/100ml-glucosuria
- 53. Clinical manifestations of hyperglycemia symptoms: Polyuria Polydipsia Polyphagia with weight loss Recurrent blurred vision pruritis Loss of stength Noctural enuresis
- 54. Hypoglycaemia Blood glucose levelbelow 50 mg% usually indicates hypoglycemia in adults, less than 40mg% in children.
- 55. Clinical manifestations Rapidonset Sweating Tachycardia Anxiety Irritability Disorientation Nausea
- 56. MANAGEMENT Terminate all dentaltreatment Administer glucose source monitor vital signs If symptoms do not rapidly improve administer 30ml of 50% Dextrose solution IV 1mg glucagon IV or IM 0.5mg of 1:1000 epinephrine IM/ SC (every 15 Minutes)
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- 58. Eye signs VONGRAEFE’S SIGN – Lid lag. JOFFROY’S SIGN – Absence of wrinkling of forehead on looking up. STELLWAG’S SIGN – Decreased frequency of blinking. DALRIMPLE’S SIGN – Lid retraction exposing the upper sclera. MOBIUS SIGN – Absence of convergence.
- 59. MANAGEMENT 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
- 60. P – Position, supine position with feet elevated D – Definitive management – activate Emergency Medical Services 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
- 61. SEIZURES A seizureis defined as an episodic disturbance of movement, feeling, or consciousness that can be caused by sudden synchronous, inappropriate, and excessive electrical discharges that interfere with the normal function of the brain. The term epilepsy is defined as a disease of frequent seizures that do not have a reversible metabolic cause Epilepsy can be caused by either abnormal neuronal membrane function or an alteration between the excitatory and inhibitory neurons
- 62. Pathophysiology In epilepsyabnormal neurons undergo spontaneous firing Cause of abnormal firing is unclear Firing spreads to adjacent or distant areas of the brain Often area of brain from which epileptic activity arises.
- 64. MANAGEMENT OF SEIZURES Treatment Anti- epileptic drugs: ABC’ (+ monitor / O2 / large iv’s) Start pharmacotherapy immediately Metabolic acidosis common - if severe, give sodium bicarbonate Benzodiazepines Phenytoin / fosphenytoin Barbiturates Others / new possibilities
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- 67. ANGINA PECTORISANGINA PECTORIS Definition- “A condition marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, owing to an inadequate blood supply to the heart.” Types: Stable (classic or exertional) Variant (prinzmetal , vasospastic) Unstable (crescendo, acute coronary insufficiency Prevention includes stress reduction protocol, reassurance & psychosedation.
- 68. ANGINA PECTORIS PREDISPOSING FACTORS Physical activity Hot humid environment Cold weather Large meals Emotional stress Fever, anaemia or thyrotoxicosis. Cigarette smoking High altitudes CLINICAL MANIFESTATIONS Chest pain Radiation of pain
- 69. PREVENTION Long actingnitrates- isosorbide dinitrate Beta blockers- atenolol Calcium channel blockers- verapamil, nefedepine Nitroglycerine Drugs
- 70. Recognize problem (chestpain – 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 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 continue with dental procedure summon medical care Administer aspirin Continue to monitor and record vital signs MANAGEMENT
- 71. MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION DEFINITION- “A clinical syndrome caused by deficient coronary arterial blood supply resulting in ischaemia to a region of the myocardium and causing cellular death and necrosis.” Predisposing Factors: Atherosclerosis and coronary artery disease Coronary thrombosis, occlusion and spasm Males 5th and 6th decades of life Undue stress
- 72. MANAGEMENTMANAGEMENT Protocol commonfor both ACS outcomes PORTABLE AUTOMATICPORTABLE AUTOMATIC EXTERNALEXTERNAL DEFIBRILLATOR (AED)DEFIBRILLATOR (AED) Immediate recognition of cardiac arrest and activation of the emergency response system. Early CPR with an emphasis on chest compressions Rapid defibrillation Effective advanced life support Integrated post-cardiac arrest care.
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- 74. CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS Confusion, blurred speech Muscular twitching, facial tremor Headache, tinnitus Drowsiness, disorientation Elevated BP,HR,RR If uncontrolled, generalized tonic clonic seizures.
- 75. MANAGEMENTMANAGEMENT Termination ofthe dental procedure Positioning the patient comfortably Reassurance of the patient Basic life support ( BLS) as needed Definitive care Administration of O2 Monitoring of vital signs ( Blood pressure, heart rate and respiratory rate) Administration of an anticonvulsant drug, if needed : Diazepam or midazolam
- 76. Gingivitis :-91% Anaemia :- 82% Taste Alteration :-66% Halitosis :-52% Xerostomia :-48% Morning Sickness :-48% Burning Sensation :-42% Pigmentation :-34% Tongue Changes :-17% Angular Cheilitis :-8% Oral Findings Management in Pregnancy
- 77. Preventive Program General GuidelinesFor Management An accurate History Preventive Oral Hygiene Measures Short Appointment in Patients convenience
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- 82. NEEDLE STICKNEEDLE STICK INJURYINJURY Stop procedure immediately. Wash skin with disinfectant. Treat with running water and encourage bleeding Dry area and cover with antiseptic dressing Recording medical history vital in case of an exposed needle situation. Seek antidotal vaccination or treatment if necessary. Invariably associated with faulty techniques such as: bending the needle while administering LA inserting the needle up to the hub directing the needle against resistance May also occur if pt jerks head during administration. Most commonly with IANB. Elasticity of soft tissue produces rebound, burying the fragment within. NEEDLENEEDLE BREAKAGEBREAKAGE
- 83. MANAGEMENTMANAGEMENT Inform ptof the occurrence, tell him/her to remain calm, keep mouth open and refrain from any jaw movements. Retrieve the fragment, if visible, with a haemostat. A buried fragment needs to be located ASAP using radiographs or CT scans & retrieved surgically.
- 84. Basic Life Support Primary response to all emergencies P-A-B-C-D Position >Airway >Breathing >Circulation >Defebrilation P-A-B-C-D MODIFIED TO P-C-A-B-D 15 compressions – 2 rescue breaths 4 cycles – 1 minute Cardio Pulmonary Resuscitation CPR
- 85. Steps in CPR Recognizecardiac arrest Check for unresponsiveness SHAKE AND SHOUT CPR Cardio Pulmonary Resuscitation
- 86. ABC of CPR A– Airway B- Breathing C- Circulation Airway Head tilt / chin lift Sniffing morning air position Jaw thrust method Check for Carotid pulse
- 87. Breathing Look for riseand fall of chest Listen and feel for movement of air Breathing Mouth to mouth Mouth to nose Endotracheal intubation Oesophageal obturator airway Position of hands to administer chest compression
- 92. OFFICE EMERGENCY KIT Oxygen, Ambu bag with mask Suction Syringes and needles Tourniquets Cricothyrotomy equipment Airways, laryngoscope Epinephrine Diphenhydramine Diazepam Hydrocortisone Morphine Dextrose 50%
- 93. FUTURE OF CPR “DON’TWORRY ABOUT BEING SCRUTINIZED FOR DOING IT RIGHT-DOING SOMETHING IS BETTER THAN DOING NOTHING”
- 94. CONCLUSION Commonly seensigns and symptoms include alterations of consciousness, respiratory distress, seizures, drug related emergencies and chest pain. In each situation a successful outcome depends on our adherence to defined treatment protocol. Once such steps are employed successfully additional (secondary) steps can lead us towards a more definitive diagnosis which can help correct the problem.
- 95. REFERENCES 1. Medical emergenciesin dental office- Stanley F. Malamed 2. Medicine 3rd Edition- K.George Mathew 3. Contemporary oral and maxillofacial surgery- Peterson 5. Principles and practice of medicine-Davidson