Survey
* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project
Download past medical history
Document related concepts
Psychopharmacology wikipedia , lookup
Electronic prescribing wikipedia , lookup
Pharmacognosy wikipedia , lookup
Drug design wikipedia , lookup
Drug discovery wikipedia , lookup
Drug interaction wikipedia , lookup
Pharmaceutical industry wikipedia , lookup
Prescription costs wikipedia , lookup
Prescription drug prices in the United States wikipedia , lookup
Neuropharmacology wikipedia , lookup
Pharmacokinetics wikipedia , lookup
Theralizumab wikipedia , lookup
Transcript
LECTURE 1: ALTERED CONSCIOUSNESS, PART II CVA, DIFF DX, SEIZURES Cerebrovascular Accident (CVA) CVA is a focal neurological disorder caused by destruction of brain substance as a result of intra cerebral hemorrhage, thrombosis, embolism or vascular insufficiency. CVA Apoplexy Stroke Brain Attack CVA - Types Lacunar TIA Occlusive (Ischemic) Hemorrhagic CVA - Lacunar Infarcts <5mm diameter poorly controlled HTN, DM deep arterial branches – cerebrum - brain stem good prognosis 4-6 weeks resolution CVA - TIA brief episodes of ischemia incidence:1/1000 elderly lasts < 24hours 10% major CVA in 2 weeks Ischemic Stroke - Cerebral Infarction 75% of all stroke patients male:female ratio 2:1 luminal reduction 85% 20% in sleep Ischemic stroke - Etiology embolic clot carotid stenosis atrial fibrillation mitral stenosis (RHD) Dental Management Post CVA 6 months: emergency Rx only stress reduction short appointments pain control psychosedation Anticoagulant Management Rx 2 1/2 X PT INR, 4-TXA-Amicar Management Acute CVA Dental Office call EMS position patient BLS - oxygen monitor V.S. supportive care Seizures A paroxysmal disorder of central CNS function characterized by an attack involving changes in the state of consciousness, motor activity, or sensory phenomena; a seizure is sudden in onset and usually of brief duration. not a disease - a symptom attacks - brief convulsions abnormal behavior 3-5% population, 1 seizure 0.5% have seizures Etiology - Primary Seizures 65% idiopathic/genetic family 3-5% incidence 6/10 X expected rate Etiology - Secondary Seizures 35% acquired - recurrent head trauma perinatal injuries congenital abnormalities tumors, space occupying lesions vascular disease degenerative disorders infectious diseases metabolic/toxic disorders Ischemic Stroke infarction core dies in five minutes ischemic penumbra surrounds core "idling cells" survive 3 hours Seizures - Dental Office -Etiology epileptic seizure Hypoglycemia (insulin) vasovagal syncope (hypoxia) L.A. overdose Hemorrhagic Stroke etiology:HTN - aneurysm 25% of total strokes intracerebral, vertibrobasilar, subarachnoid high mortality rate >50 years Seizure Types - Partial Seizures one hemisphere – simple - (limb jerks) both hemispheres – complex (facial gestures) no LOC reoriented rapidly (1 minute CVA treatment three hour window head CT without contrast TPA thrombolytic for ischemic stroke 50% post CVA die AMI or heart failure Symptoms Acute CVA HTN altered consciousness hemiparesis severe headache / blurred vision facial asymmetry pupillary asymmetry incontinence aphasia Cincinnati Stroke Scale Absence Attacks - Petit Mal primary epilepsy onset 3-15 years cease by 20 years 40%+EEG primary relatives Absence Attacks - Simple 1-2 seconds blank stare immediate recovery unaware of events Absence Attacks -Complex 15-30 seconds head droops arm jerks Generalized Tonic Clonic Seizures (GTCS) Grand Mal- Prodromal Phase aura-part of seizure recurrent aura lasts seconds olfactory, visual, gustatory, auditory no recall of aura Grand Mal - Preictal LOC falls to floor monoclonic flexion jerks vocalization autonomic changes Grand Mal - Ictal Phase Tonic Component flexion muscle contractions extremity-trunk rigidity brief dyspnea, cyanosis Clonic Component alternating relaxation-contraction tongue/cheek biting 2-5 minutes Grand Mal - Postictal Stage clonic-tonic movements cease normal respiration amnesia deep sleep urinary, bowel incontinence consciousness gradually returns - 2 hours Status Epilepticus life threatening recurrent GTCS >5minutes 3-23% mortality Unterminated Grand Mal Seizures cardiac arrest cerebral hypoxia-encephalopathy increased ICP decreased intracerebral flow hypoglycemia Management GTCS - Ictal Stage Call EMS Patient position head/foot protect from injury BLS oxygen monitor V.S. Management GTCS Postictal Stage monitor airway, respiratory depression head/foot position oxygen monitor V.S. explain to patient/family Status Epilepticus EMS position ABC-BLS oxygen protect patient I.V. access anticonvulsant drugs Anticonvulsant Drugs diazepam 0.5mg/kg midazolam .1 mg/kg monitor respiratory depression Differential Diagnosis Vasovagal Syncope apprehensive brief hypoxia prodromal nausea, diaphoresis brief unconsciousness (+/_) convulsive movements hypotensive, bradycardic adolescents/young adults CVA patient history prodromal headache signs of neurological dysfunction Hypoglycemia patient history (DM) clinical signs symptoms Hyperventilation acute anxiety hyperventilation hypertension-tachycardia paresthesias extremities - circumoral 15-40 years rare LOC Hypoglycemia Hx-DM diaphoretic "drunk" demeanor tachycardic-tremors rapid LOC-seizures insulin shock CVA prodromal intense headache neurological deficits level of consciousness Hyperglycemia poorly controlled DM acetone breath hot/dry skin rapid deep respirations-Kusmaul's breathing gradual onset symptoms DKA Hypothyroidism sensitive to cold speech / mental capacity slow peripheral / face edema carotenemic skin oversensitive to CNS depressants weight gain / myxedema Hyperthyroidism nervous / hyperactive elevated BP, heart rate, temperature skin wet warm unexplained weight loss increased appetite exopthalmic LECTURE 2: ALTERED CONSCIOUSNESS, PART I GENERAL CONSIDERATIONS CONFUSION-A mental state marked by the mingling of ideas with consequent disturbances in comprehension and understanding , which eventually leads to bewilderment PREDISPOSING FACTORS GENETIC DISORDER PRIMARY DISTRUCTION: ISLETS OF LANGERHANS AN ENDOCRINE CONDITION STEROID ADMINISTRATION RELATIVE W/ DIABETES DELIRIUM-A mental disturbance marked by illusions, delusions, cerebral excitement, physical restlessness and incoherence PARENT PLUS DIZZINESS-A disturbed sense of relationship to space, a sense of unsteadiness accompanied by a feeling of movement within the head. PARENT PLUS CAUSES OF ALTERED CONSCIOUSNESS CAUSES DRUG OVERDOSE HYPERVENTILATION HYPOGLYCEMIA HYPERGLYCEMIA CVA, TIA HYPERTHYROIDISM HYPOTHYROIDISM FREQUENCY MOST COMMON COMMON COMMON LESS COMMON LESS COMMON RARE RARE MANAGEMENT OF ALTERED CONSCIOUSNESS RECOGNIZE, TERMINATE DENTAL PROCEDURE P- POSITION PATIENT, A-AIRWAY, B-BREATHING, C-CIRCULATION PERFORM BASIC LIFE SUPPORT AS NEEDED, D-DEFINITIVE CARE MONITOR VITAL SIGNS, MANAGE SIGNS AND SYMPTOMS DEFINITIVE MANAGEMENT DIABETES MELLITUS HYPERGLYCEMIA HYPOGLYCEMIA INCIDENCE OF DIABETES BY AGE IN THE UNITED STATES AGE GROUP (YEARS) BIRTH-17 25-40 45-65 65 OR OLDER INCIDENCE (PER 1000) 1.3 17 45 79 CHRONIC COMPLICATIONS OF DIABETES MELLITUS VASCULAR SYSTEM ATHEROSCLEROSIS LARGE VESSELS MICROANGIOPATHY KIDNEYS DIABETIC GLOMERULOSCLEROSIS ARTERIOLAR NEPHROSCLEROSIS PYELONEPHRITIS NERVOUS SYSTEM MOTOR, SENSORY AND AUTONOMIC NEUROPATHY EYES RETINOPATHY CATARACT FORMATION GLAUCOMA EXTRAOCULAR MUSCLE PALSIES SKIN XANTHOMA DIABETCORUM NECROBIOSIS LIPOIDICA DIABETICORUM PRURITIS FURUNCULOSIS MYCOSIS MOUTH GINGIVITIS INCREASED INCIDENCE OF CARIES & PERIODONTAL DISEASE ALVEOLAR BONE LOSS PREGNANCY INCREASED INCIDENCE INCREASED BIRTH WEIGHT STILL BIRTHS MISCARRIAGES NEONATAL DEATH CONGENITAL DEFECTS PARENT PLUS PARENT GRANDPARENT FIRST COUSIN RELATIVE ON OTHER SIDE OF FAMILY MAXIMUM RISK (%) GRANDPARENT AND AUNT OR UNCLE GRANDPARENT, AUNT OR UNCLE FIRST COUSIN . 85 60 40 22 14 9 TYPES OF DIABETES TYPE I--IDDM TYPE II--NIDDM (NON-OBESE, OBESE) CLASSIFICATION OF DIABETES AND OTHER GLUCOSE INTOLERANCE DIABETES MELLITUS (DM) INSULIN-DEPENDENT (IDDM), TYPE I NON-INSULIN-DEPENDENT (NIDDM) ,TYPE II NONOBESE OBESE OTHER TYPES PANCREATIC DISEASE DISEASE OF HORMONAL ETIOLOGY DRUG OR CHEMICAL INDUCED CONDITION INSULIN RECEPTOR ABNORMALITIES CERTAIN GENETIC SYNDROMES MISCELLANEOUS IMPAIRED GLUCOSE INTOLERANCE (IGT) NONOBESE OBESE IGT W/ CERTAIN CONDITIONS & SYNDROMES PANCREATIC DISEASE DISEASE OF HORMONAL ETIOLOGY DRUG OR CHEMICAL INDUCED CONDITION INSULIN RECEPTOR ABNORMALITIES CERTAIN GENETIC SYNDROMES MISCELLANEOUS GESTATIONAL DIABETES (GDM) STATISTICAL RISK CLASSES PREVIOUS ABNORMALITY OF GLUCOSE TOLERANCE POTENTIAL ABNORMALITY OF GLUCOSE TOLERANCE COMPARISON OF TYPE I AND TYPE II DIABETES MELLITUS FACTORS COMPAIRED DKA COMPLICATIONS RATE OF CLINICAL ONSET STABILITY FAMILY HX OF DM HLA AND ABN. IMMUNE REACTION INSULIN RECEPTOR DEFECTS TYPE I (IDDM) COMMON 90% IN 20 YRS. RAPID UNSTABLE COMMON PRESENT TYPE II (NIDDM) UNCOMMON LESS COMMON SLOW STABLE LESS COMMON NOT PRESENT USUALLY NOT FOUND ----------- CLINICAL CLASSIFICATION OF IDIOPATHIC DM SYNDROME TYPE IDDM KETOSIS ISLET CELL ABs HLA ASSOC’N TREATMENT + + + INSULIN NIDDM NON-OBESE DIET OR DIET + INSULIN OR SULFONYLUREAS NIDDM OBESE WT. REDUCTION HYPOCALORIC DIET PLUS SULFONYLUREAS OR INSULIN COMPARISON OF TYPE I AND TYPE II DIABETES MELLITUS DIABETES MELLITUS--DENTAL THERAPY CONSIDERATIONS FACTORS COMPAIRED FREQUENCY AGE AT ONSET BODY BUILD SEVERITY USE OF INSULIN ORAL HYPO. AGENTS DKA COMPLICATIONS RATE OF CLINICAL ONSET STABILITY FAMILY HX OF DM HLA AND ABN. IMMUNE RXN INSULIN RECEPTOR DEFECTS PHYSICAL STATUS TREATMENT CONSIDERATIONS II USUAL ASA II CONSIDERATIONS PLUS: 1. EAT NORMAL BREAKFAST, TAKE USUAL INSULIN DOSE IN AM. 2. AVOID MISSING MEALS, PRE AND POSTOPERATIVELY 3. IF MISSING MEAL IS UNAVOIDABLE EITHER MEDICAL CONSULTATION OR DECREASE INSULIN DOSE BY HALF III USUAL ASA III CONSIDERATIONS, PLUS 1. FOLLOWING SURGERY OR EXTENSIVE PROCEDURES, MONITOR BLOOD GLUCOSE LEVELS MORE FREQUENTLY FOR SEVERAL DAYS & MODIFY INSULIN DOSES ACCORDINGLY 2. CONSIDER MEDICAL CONSULTATION IV USUAL ASA IV CONSIDERATIONS, PLUS 1. MEDICAL CONSULTATION PRIOR TO DENTAL TREATMENT TYPE I (IDDM) 5% 15 NORMAL OR THIN SEVERE ALMOST ALL FEW RESPOND COMMON 90% IN 20 YRS. RAPID UNSTABLE COMMON PRESENT USU. NOT FOUND TYPE II (NIDDM) 85% >40 OBESE MILD 25%-30% 50% RESPOND UNCOMMON LESS COMMON SLOW STABLE LESS COMMON NOT PRESENT ----------- 240 CONSECUTIVE CASES OF HYPOGLYCEMIA IN DM PTS. CAUSE INADEQUATE FOOD(CARBOHYDRATE) INTAKE EXCESSIVE INSULIN DOSE SULFONYLUREA THERAPY STRENUOUS EXERCISE ETHANOL INTAKE OTHER(KIDNEY FAILURE, LIVER FAILURE, DECREASE IN CORTICOSTEROID DOSE) PERCENT 66 12 12 4 4 2 CURENTLY AVAILABLE ORAL HYPOGLYCEMIC AGENTS GENERIC NAME TOLBUTAMIDE TOLAZAMIDE ACETOHEXAMIDE CHLORPROPAMIDE GLYBURIDE GLIPIZIDE METFORMIN PROPRIETARY NAME ORINASE TOLINASE DYMELOR DIABINASE GLYNASE, DIABETA, MICRONASE GLUCATROL GLUCOPHAGE LONG INSULIN TYPE REGULAR LENTE NPH ULTRALENTE ONSET 15 MIN 2 HR 2 HR DURATION (HRS) 5-7 18-24 18-24 24-36 PREVENTION WEIGHT GAIN OR LOSS MEDICATIONS SPECIAL DIET SIGNS OF INCREASED HUNGER, THIRST OR URINARY FREQUENCY HOW LONG HAVE YOU BEEN A DIABETIC? WHAT TREATMENT DO YOU TAKE TO CONTROL IT? DO YOU MONITOR YOUR BLOOD SUGAR? DO YOU EVER HAVE HYPOGLYCEMIC EPISODES? PHYSICAL EXAMINATION VITAL SIGNS SKIN SIGNS SWEET ACETONE BREATH OPTIMAL PHYSICAL STATUS OF DIABETIC PATIENTS TYPE TREATMENT SEVERITY I (IDDM) INSULIN + DIET SEVERE III MOD-SEVERE MILD-MOD II-III II MILD-MOD II II (NIDDM) -NONOBESE INSULIN + DIET ORAL MED. + DIET -OBESE ORAL MED. + DIET SYMPTOMS POLYURIA POLYDIPSIA POLY PHAGIA W/WEIGHT LOSS RECURRENT BLURRED VISION VULVOVAGINITIS OR PRURITIS LOSS OF STRENGTH NOCTURNAL ENURESIS OFTEN SYMPTOMATIC TYPE I (IDDM) ++ ++ ++ + + ++ ++ - TYPE II (NIDDM) + + ++ ++ + ++ OTHER SYMPTOMS: CURRENTLY AVAILABLE INJECTABLE INSULINS ACTION SHORT INTERMEDIATE CLINICAL MANIFESTATIONS OF HYPERGLYCEMIA OPTIMAL PHYSICAL STATUS TYPE I REPEATED SKIN INFECT. MARKED IRRITABILITY HEADAKE DROWSINESS MALAISE DRY MOUTH TYPE II 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 HYPOGLYCEMIA SWEATING TACHYCARDIA PILOERECTION INCREASED ANXIETY BIZARRE BEHAVIORAL PATTERNS BELLIGERENCE POOR JUDGEMENT UNCOOPERATIVENESS LATER SEVERE STAGE UNCONSCIOUSNESS SEZURE ACTIVITY HYPOTENSION HYPOTHERMIA PATHOPHYSIOLOGY BRAIN REQUIRES CONTINUOUS SUPPLY OF GLUCOSE >50 Mg% INSULIN MOST IMPORTANT REGULATOR OF BLOOD GLUCOSE MUSCLE AND ADIPOSE CELLS ARE INSULIN DEPENDENT SEVERE INSULIN DEFICIENCY CAUSES: GLUCONEOGENESIS AND KETOGENESIS (DKA) BLOOD GLUCOSE REMAINS HIGH BECAUSE OF: LACK OF INSULIN (TYPE I) OR DECREASED INSULIN RECEPTOR SITES (TYPE II) GLYCOSEUREA--BLOOD GLUCOSE >180 Mg% HYPOGLYCEMIA: DIAGNOSTIC CLUES WEAKNESS, DIZZINESS PALE, MOIST SKIN SHALLOW RESPIRATIONS HEADACHE ALTERED LEVEL OF CONSCIOUSNESS MANAGEMENT OF HYPOGLYCEMIA RECOGNIZE HYPOGLYCEMIA TERMINATE DENTAL PROCEDURE P- POSITION PATIENT COMFORTABLY, A-B-C--BASIC LIFE SUPPORT D-DIFINITIVE CARE>> ADMINISTER ORAL CARBOHYDRATES: IF EPISODE TERMINATES: IF EPISODE CONTINUES: PERMIT PATIENT TO RECOVER SUMMON MEDICAL ASSISTANCE DISCHARGE PATIENT ADMINISTER PARENTERAL CARBOHYDRATE MONITOR PATIENT DISCHARGE PATIENT D-DIFINITIVE CARE>> SUMMON MEDICAL ASSISTANCE: 50% DEXTROSE IV, 1 MG GLUCAGON IM, TRANSMUCOSAL SUGAR, RECTAL HONEY OR SYRUP ALLOW PATIENT TO RECOVER AND DISCHARGE AS PER MEDICAL RECOMMENDATION HYPERGLYCEMIA: DIAGNOSTIC CLUES DRY, WARM SKIN KUSSMAUL’S RESPIRATIONS FRUITY OR SWEET BREATH ODOR RAPID, WEAK PULSE NORMAL TO LOW BLOOD PRESSURE ALTERED LEVEL OF CONSCIOUSNESS THYROID GLAND DYSFUNCTION HYPOTHYROID HYPERTHYROID CAUSES OF HYPOTHYROIDISM PRIMARY AUTOIMMUNE HYPOTHYROIDISM IDIOPATHIC POSTSURGICAL THYROIDECTOMY EXTERNAL RADIATION THERAPY RADIOIDINE THERAPY INHERITED ENZYMATIC DEFECT IODINE DEFICIENCY ANTITHYROID DRUGS LITHIUM, PHENYLBUTAZONE CAUSES OF HYPOTHYROIDISM SECONDARY PITUITARY TUMOR INFILTRATIVE DISEASE (SARCOID) OF PITUITARY CAUSES OF HYPERTHYROIDISM TOXIC DIFFUSE GOITER (GRAVES’ DISEASE) TOXIC MULTINODULAR GOITER TOXIC UNINODULAR GOITER FACTITIOUS THYROTOXICOSIS T3 THYROTOXICOSIS THYROTOXICISIS ASSOCIATED WITH THYROIDITIS HASHIMOTO’S THYROIDITIS SUBACUTE (deQUERVAIN’S) THYROIDITIS JOD-BASEDOW METASTATIC FOLLICULAR CARCINOMA MALIGNANCIES WITH CIRCULATING THYROID STIMULATORS TSH-PRODUCING PITUITARY TUMORS STRUMA OVARII WITH HYPERTHYROIDISM HYPOTHALAMIC HYPERTHYROIDISM PREVENTION MEDICATION WEIGHT GAIN OR LOSS CANCER OR TUMOR ALLERGY TO MEDICATION TYPE OF THYROID DISORDER TYPE OF TREATMENT BODY WEIGHT STABILITY SENSITIVITY TO COLD OR PAIN MEDICATION UNUSUALLY SENSITIVE TO HEAT IRRITABLE OR TENSE MEDICATIONS USED TO MANAGE HYPO- & HYPER-THYROIDISM HYPOTHYROIDISM 1. DESICCATED THYROID (PROLOID, S-P-T) 2. LEVOTHYROXINE (T4, LEVOTROID,LOVOXINE,SYNTHROID) 3. LIOTHYRONINE (T3, CYTOMEL, THYRAR) 4. LIOTRIX (EUTHROID, THYROLAR) HYPERTHYROIDISM 1. PROPYLTHIOURACIL 2. METHIMAXOLE (TAPOZOLE) 3. CARBIMAZOLE 4. PROPRANOLOL (INDERAL) PHYSICAL EXAMINATION HYPOTHYROID DRY,THICK, EDEMATOUS SKIN LARGE, THICK TONGUE PUFFY HANDS AND FACE LETHARGIC, SLOW SPEECH BRADYCARDIA, NORMAL BP HYPERTHYROID WARM, SWEATY, TREMOROUS HANDS TACHYCARDIA, ELEVATED BLOOD PRESSURE FEVER THYROMEGALY EXOPHTHALMOS DENTAL THERAPY CONSIDERATIONS EUTHYROID HYPOTHYROID MEDICAL CONSULT CAUTIOUS USE OF CNS DEPRESSANTS CARDIOVASCULAR DISEASE HYPERTHYROID MEDICAL CONSULTATION NO ATROPINE CAUTIOUS USE OF EPINEPHRINE LOCAL ANESTHETIC WITH VASOCONSTRICTOR LOWEST CONCENTRATION SMALLEST EFFECTIVE VOLUME ASPIRATION ESSENTIAL CLINICAL MANIFESTATIONS OF HYPOTHYROIDISM SYMPTOMS (>10% INCIDENCE) PARESTHESIAS LOSS OF ENERGY INTOLERANCE OF COLD MUSCULAR WEAKNESS MUSCLE AND JOINT PAIN INABILITY TO CONCENTRATE DROWSINESS CONSTIPATION FORGETFULNESS DEPRESSED AUDITORY ACUITY EMOTIONAL LABILITY HEADAKE DYSARTHRIA PERCENT 92% 79% 51% 34% 31% 31% 30% 27% 23% 15% 15% 14% 14% SIGNS “PSEUDOMYOTONIC” REFLEXS CHANGE IN MENSTRUAL PATTERN HYPOTHERMIA DRY, SCALY SKIN PUFFY EYELIDS HOARSE VOICE WEIGHT GAIN DEPENDENT EDEMA SPARSE AXILLARY AND PUBIC HAIR PALLOR THINNING OF EYEBROWS YELLOW SKIN LOSS OF SCALP HAIR ABDOMINAL DISTENSION GOITER DECREASED SWEATING PERCENT 95% 86% 80% 79% 70% 56% 41% 30% 30% 24% 24% 23% 18% 18% 16% 10% CLINICAL MANIFESTATIONS OF HYPERTHYROIDISM MANAGEMENT OF UNCONSCIOUS PATIENT W/ THYROID DISEASE SYMPTOMS PERCENT WEIGHT LOSS 72%-100% <20 LB. UP TO 14% 20-40 LB. 27%-36% >40 LB. 23%-45% PALPITATIONS DYSPNEA EDEMA CHEST PAIN NERVOUSNESS WEAKNESS TREMOR PHYCHOSIS DIARRHEA HYPERDEFICATION ABDOMINAL PAIN MYALGIAS DISORIENTATION HYPOTHYROID PATIENT (MYXEDEMA COMA) HYPERTHYROID PATIENT (THYROID STORM) TERMINATE DENTAL PROCEDURE P-POSITION THE PATIENT (SUPINE WITH LEGS ELEVATED SLIGHTLY) A-B-C—ASSESS AND PERFORM BLS, AS NEEDED D-DEFINITIVE CARE: SUMMON EMERGENCY ASSISTANCE ESTABLISH INTRAVENOUS LINE, IF POSSIBLE ADMINISTER OXYGEN PERFORM NECESSARY DEFINITIVE MANAGEMENT SIGNS FEVER <103 F >103 F TACHYCARDIA 100-139 140-169 170-200 SINUS TACHYCARDIA DYSRHYTHMIAS THYROMEGALY WIDE PULSE PRESSURE 40-59 TORR (MM HG) 60-100 TORR TREMOR THYROTOXIC STARE/LID RETRACTION HYPERKINESIS CONGESTIVE HEART FAILURE WEAKNESS COMA TENDER LIVER INFILTRATIVE OPHTHALMOPATHY SOMNOLENT/OBTUNDENT PSYCHOSIS JAUNDICE PERCENT 100% 57%-70% 30%-43% 100% 24% 62% 14% 67% 37% 100% 86%-100% 38% 62% 73% 60% 55% 50% 23% 18%-23% 17% 17% 14%-46% 9%-29% 9%-24% PATHOPHYSIOLOGY HYPOTHYROID DECREASED BMR MYXEDEMA-- INFILTRATION OF SKIN BY MUCOPOLYSACCHARIDES AND MUCOPROTEINS PERICARDIAL AND PLEURAL EFFUSIONS ACCELERATED CORONARY ARTERY DISEASE CNS DEPRESSION-- HYPOTHERMIA, HYPOGLYCEMIA AND CARBON DIOXIDE RETENTION HYPERTHYROID INCREASED BMR-- INCREASED TEMPERATURE INCREASED THYROID HORMONE ACTIVITY ON MYOCARDIUM DECREASED LIVER FUNCTION HYPOTHYROID DIAGNOSTIC CLUES COLD INTOLERANCE WEAKNESS FATIGUE DRY, COLD, YELLOW , PUFFY SKIN THICK TONGUE HYPERTHYROID DIAGNOSTIC CLUES HEAT INTOLERANCE SWEATING TACHYCARDIA WARM, THIN, SOFT, MOIST SKIN EXOPHTHALMOS TREMOR LECTURE 3: DRUG-RELATED EMERGENCIES, PART I GENERAL CONSIDERATIONS & DRUG OD RXNS Practice Caveat -“Never treat a stranger!” PAST MEDICAL HISTORY Medical History Questionnaire Are you currently taking any medicine or drugs? Have you taken any medicine or drugs during the past 2 years? Are you allergic to any medication or drug? Do you currently have or have you had any of the following: Asthma Allergy or hives Hay fever Environmental Allergies Food Allergies Chemotherapy Steroid medication Dialogue History Follow-up questions Pertinent Positives Pertinent Negatives MAJOR DRUG CATEGORIES USED IN DENTISTRY Local Anesthetics Amides Esters Prescription Drugs Analgesics Non-opioids Acetaminophen ASA NSAIDS Ibuprofen Naprosyn Ketoprofen Opioids Agonists Morphine Codeine Tylenol w/ Codeine (#1,#2,#3,#4) Dihydrocodone Oxycodone Meperidine Fentanyl Propoxyphene Tramadol Agonist/Antagonists Butarphanol Nalbuphine Pentazocine Dezocine Antagonists Naloxone Naltrexene Antibiotics Penicillin E-mycin Tetracycline Cephalosporin Minor Tranquilizers Barbiturates Anxiolytics / Sedative Hypnotics Benzodiazepines Chloral Hydrate Hydroxyzine Promethazine Nitrous Oxide ADVERSE DRUG REACTIONS (ADR’s) Definition: Any response to a drug that is noxious (harmful), unintended and that occurs at doses used in man for purposes of prophylaxis, diagnosis, or therapy but specifically excludes failure to accomplish the intended purpose of the drug. GENERAL PRINCIPLES OF TOXICOLOGY No drug ever exerts a single action. No clinically useful drug is entirely devoid of toxicity. Potential toxicity of a drug rests in the hands of the user. Classification of Adverse Drug Reactions Toxicity resulting from direct extension of pharmacologic effects Side effects Abnormal dosage (overdose) Local toxic effects Toxicity resulting from altered recipient (patient) Presence of pathology Emotional disturbances Genetic aberrations (idiosyncrasy) Teratogenicity Drug-drug interactions Toxicity resulting from drug allergy ADR CATEGORIES: Probability Severity Severe Moderate Mild Outcome Recovered Recovered with sequelae Died Cause of Death Related Unrelated DRUG OVERDOSE REACTIONS Absolute overdose Relative overdose LOCAL ANESTHETIC OVERDOSE / TOXICITY REACTIONS CAUSES OF HIGH BLOOD LEVELS OF LOCAL ANESTHETICS Biotransformation of the drug is unusually slow Drug is slowly eliminated from the body through the kidneys Total dose of local anesthetic administered is too large Absorption of local anesthetic from the injection site is unusually rapid Local anesthetic is inadvertently administered intravascularly Predisposing Factors Patient Factors Age (<6 & >65) Body wt. – ( body wt. risk) Presence of pathology Liver dz. CHF Pulmonary dz. ( CV toxicity) Hypoxia Acidosis Genetic (atypical plasma cholinesterase def.) Mental attitude (anxiety seizure threshold) Sex (slight risk during pregnancy) Drug Factors Vasoactivity of drug (vasodilation increases risk) Dose of drug Route of administration Rate of injection Vascularity of injection site Presence of vasoconstrictor Related to high blood levels of local anesthetic Lidocaine / Mepivacaine CNS effects at 5 g /ml Cardiotoxic effects at 20g/ml Bupivacaine CNS effects at 1-2g/ml Cardiotoxic effects 1-2 g/ml Rate of clearance in decreasing order is: Prilocaine>etidocaine>lidocaine>mepivacaine & ropivacaine>bupivacaine Clinical manifestations of local anesthetic overdose: Low to moderate overdose levels Signs Confusion Talkativeness Apprehension Excitedness Slurred speech Generalized stutter Muscle twitching & tremor Nystagmus Elevated blood pressure Elevated heart rate Elevated respiratory rate Symptoms Headache Lightheadedness Dizziness Blurred vision, unable to focus Ringing in ears Perioral numbness Flushed or chilled feeling Drowsiness Disorientation Loss of consciousness LECTURE 4: DRUG-RELATED EMERGENCIES, PART II DRUG ALLERGY AND DIFFERENTIAL DX Classification of Allergic Disease Moderate to high levels Generalized tonic-clonic seizure Generalized CNS depression Depressed Bp, HR, RR Death TREATMENT Prevention Oxygen Seizure control Diazepam (0.1-0.3 mg/kg) EPINEPHRINE OVERDOSE Predisposing Factors Preexisting cardiovascular dz. Unstable angina Hx. Of MI Cardiac dysrhythmias Heart failure CVA Uncontrolled HTN Renal dz. Hepatic dz. TCA’s MAO-I Manifestations of epinephrine overdose Symptoms Signs anxiety after injection Elevated Bp Restlessness Elevated HR Tremor of limbs PVC’s VT VF Diaphoresis Throbbing headache Weakness Dizziness Florid pallor Respiratory difficulty Palpitations (tachycardia) Drug Allergy: Factors & Prevention Previous history of allergy Age (more common in children) Sex? (no effect) Prior exposure to drug Amount of drug? (no effect) Dental Drugs With High Allergic Potential Penicillins (up to 10-15% of population, >500 deaths per year/US) Aspirin, NSAIDs Opioids (morphine, codeine) Barbiturates Ester local anesthetics (topical, local sloughing of tissues at site of application) Bisulfite preservatives (steroid-dependent asthmatics) Contents of the Local Anesthetic Cartridge Local anesthetic (hydrochloride salt) Vasoconstrictor Sodium Metabisulfite (anti-oxidant) Sodium chloride (for isotonicity) Sterile water Selected Sources of Sulfites Restaurant salads Sausage Fruits Cheese Wine, beer Shrimp Sparkling grape juices No evidence of latex reactions to local anesthetic cartridges Shojaei AR & Haas DA. Journal of the Canadian Dental Association, 68:622-626, 2002 TREATMENT Reassurance Oxygen CONCLUSION Be prepared for emergencies Individualize the drug dosage Recognize and expect adverse drug effects Medical History Questions Pertinent to Drug Allergy What drug was used? (NOVOCAIN) What amount of drug was used? (dose-related or dose-independent) Did the drug contain vasoconstrictor or preservative (paraben)? What other medications were being taken at the time of the reaction? What position was the patient in? How did the reaction manifest itself? What treatment was given? (especially what kind of drugs were used?) Was a physician required? Was the patient hospitalized? Name, address & phone/fax number of treating physician? How about testing the patient with a small dose first? DON’T EVEN THINK ABOUT IT! Alternatives to Dental Drugs With High Allergic Potential Acetaminophen Synthetic opioid analgesics (e.g., meperidine, pentazocine) Clarithromycin Clindamycin Diphenhydramine (for local anesthesia) Options for emergency care of “allergic” patient Consultation (most practical and best way, manage pain w/o local anesthetic) General anesthesia (high risk high $) Antihistamine Allergic Skin Reactions Usual Sequence of Anaphylactic Allergic Reactions Skin > Eyes, Nose > Respiratory > Cardiovascular > GI Tract Pathophysiology of Immediate Allergic Reactions Antigen-induced stimulation of IgE antibodies (“sensitizing” dose) (B lymphocytes, mature plasma cells) Latent period for sensitization of mast cells & basophils Re-exposure to antigen (“challenge” dose) Properties of Immunoglobulins Respiratory Allergic Reactions Defense Mechanisms Anatomic barriers (skin, mucosa) Mobilization of phagocytic blood cells Production of enzymes IgA (external secretions) 3 Possible Outcomes of Antigen-Antibody Reactions 1. Production of additional antibodies with neutralization of antigen (beneficial outcome) 2. Antigen-antibody complex precipitates & occludes blood vessels (Arthus Reaction) (pathologic outcome) 3. Antigen-antibody complex activates mediators, results in anaphylaxis (pathologic outcome) Mediators of Anaphylaxis Allergic Cardiovascular Reactions Histamine Widely distributed (“shock organs”) Stored in mast cells & basophils Produces capillary dilation & leakage with edema Relaxes vascular smooth muscle Constricts bronchiolar smooth muscle Stimulates secretions (respiratory, GI) Slow-Reacting Substance of Anaphylaxis (SRS-A) Produced by antigen-IgE-mast cell interaction Actually a mixture of leukotrienes Produces a slow-onset powerful bronchial constriction Potentiates actions of histamine Not susceptible to antihistamine block Other Anaphylactic Factors Eosinophilic chemotactic factor (eosinophils release enzymes) High MW neutrophil chemotactic factor Basophil kallikreins, bradykinin (vasodilation, edema, pain) Prostaglandins (PGD2, PGF2, contract) Platelet activating factor Drugs Used in Management of Allergic Reactions 100% oxygen (required by Texas law) Epinephrine (1:1,000 i.m. or subcu, 1:10,000 i.v.) Antihistamines (diphenhydramine, chlorpheniramine, oral or i.m.) Corticosteroids (i.m. or i.v.) Other bronchodilators (aminophylline) Management of Delayed-Onset Skin Reaction Management of Respiratory Allergic Reaction Management of Rapid-Onset Allergic Skin Reaction Management of Laryngeal Edema Note: definitive care includes epinephrine Management of Generalized Anaphylaxis (signs & symptoms of allergy present) Note: definitive care includes epinephrine & oxygen Diagnostic Features of Allergy Signs/symptoms develop after drug administration Prior administration of drug necessary Usually presents as skin reaction Nervousness not commonly seen Loss of consciousness with anaphylaxis Seizures rarely occur (usually due to hypoxia) Respiratory symptoms common & represent severe reactions HR elevated, pulse weak & thready Blood pressure significantly depressed REMEMBER: The more rapid the onset of the allergic reaction, the more severe it is likely to be! Management of Generalized Anaphylaxis (no signs/symptoms of allergy) Note: definitive care DOES NOT include epinephrine LECTURE 5: DR. MCMAHON CHEST PAIN (HANDED OUT IN CLASS) LECTURE 6: VENTILATION AND INTUBATION Learning and Skills Objectives Describe ACLS Approach (Primary and Secondary ABCD Surveys) in CPR Describe and demonstrate the “airway hierarchy”: Supplemental oxygen: Nasal cannulae Face masks Noninvasive airway devices: Nasopharyngeal airway Oropharyngeal airway Recommended invasive airway devices: Laryngeal mask airway (LMA) Esophageal-tracheal (Combitube) tube Tracheal tube Primary/secondary confirmation of tracheal tube placement: Physical exam criteria End-tidal CO2 detection Devices to detect esophageal placement Devices to prevent TT dislodgment Primary ABCD Survey Focus: Basic CPR and Defibrillation Check responsiveness Activate emergency response system Call for defibrillator A = Airway: open the airway B = Breathing: check breathing, provide positive-pressure ventilations C = Circulation: check circulation, give chest compressions D = Defibrillation: assess for and shock VF/pulseless VT Secondary ABCD Survey A = Airway: insert advanced airway device as soon as able (new: 3 types) B = Breathing: confirm placement by PE (primary tube confirmation) Bag-Mask Ventilation Advantages Provides immediate ventilation and oxygenation Operator gets sense of compliance and airway resistance May provide excellent short-term support of ventilation High oxygen concentrations are possible Can be used to assist spontaneous respirations Potential complications Hypoventilation Gastric inflation Airway Adjunct Devices Nasal cannula: 24-44% O2 concentration Face mask with O2 reservoir 60-100% O2 concentration Equipment for Intubation Laryngoscope with several blades Tracheal tubes Malleable stylet 10-mL syringe Magill forceps Water-soluble lubricant Suction unit, catheters, and tubing Curved Blade Attaches to Laryngoscope Handle Curved Blade Laryngoscope Inserted Against Epiglottis Straight-Blade Laryngoscope Inserted Past Epiglottis Cricothyroid Membrane With Horizontal Cricothyrotomy Incision PLUS B = Breathing: confirm placement with esophageal detector device or end-tidal CO2 detector or both (secondary tube confirmation) B = Breathing: use a commercial tube holder to prevent dislodgment B = Breathing: confirm effective oxygenation/ventilation by 02 sat, CO2 levels, pH Airway Obstruction Most common cause: tongue and/or epiglottis Opening the Airway Jaw thrust, Head tilt – chin lift Malposition of Oropharyngeal Airway (Too Short) Nasopharyngeal Airway Insertion technique Mouth-to-Mask Ventilation Advantages Eliminates direct contact Enables positive-pressure ventilation Oxygenates well if O2 attached 1-rescuer technique; performed from side Easier to perform than Rescuer slides over for chest compressions bag-mask ventilation Fingers: head tilt–chin lift Best for small-handed rescuers Mouth-to-Mask Ventilation Bag-Mask Ventilation Key—ventilation volume: “enough to produce obvious chest rise” Cricoid Pressure Thyroid cartilage Cricoid Visualization of Vocal Cords Anatomy: Vallecula, Epiglottis, Arytenoid Cartilage Tracheal Intubation Advantages Protects airway from aspiration of foreign material Facilitates ventilation and oxygenation Facilitates suctioning of trachea and bronchi Provides route for drug administration Prevents gastric inflation if used with cuff Allows faster chest compressions Indications Inability to ventilate the unconscious patient After insertion of pharyngeal airway Inability of patient to protect own airway (coma, areflexia, or cardiac arrest) Need for prolonged mechanical ventilation Recommendations Intubate as soon as possible after ventilation and oxygenation in cardiac arrest Intubation should be done by most experienced person Do not take longer than 30 seconds per attempt Auscultate the thorax and epigastrium after intubation Complications Trauma—teeth, lips, tongue, mucosa, vocal cords, trachea Esophageal intubation Vomiting and aspiration Hypertension and arrhythmias Esophageal-Tracheal Combitube A = esophageal obturator; ventilation into trachea through side openings = B C = tracheal tube; ventilation through open end if proximal end inserted in trachea D = pharyngeal cuff; inflated through catheter = E F = esophageal cuff; inflated through catheter = G H = teeth marker; blindly insert Combitube until marker is at level of teeth Esophageal-Tracheal Combitube Inserted in Esophagus A = esophageal obturator; ventilation into trachea through side openings = B D = pharyngeal cuff (inflated) F = inflated esophageal/tracheal cuff H = teeth markers; insert until marker lines at level of teeth Laryngeal Mask Airway (LMA) The LMA is an adjunctive airway that consists of a tube with a cuffed mask-like projection at distal end. LMA Introduced Through Mouth Into Pharynx Once the LMA is in position, a clear, secure airway is present. Esophageal Detector Device (Bulb-Type) Confirmation: Tracheal Tube Placement End-tidal colorimetric CO2 indicators Qualitative End-Tidal CO2 Detector What should the operator’s next action be? Tracheal Tube Holders: Adult and Infant
