Dental Management of Patient with Diabetes Mellitus PresentationIraqi Dental Academy
This lecture discuss the topic of dental management of medically compromised patient who suffers from diabetes mellitus. it's simple lecture that directed to the level of mind of undergraduate students. thanks for viewing and reading, and please share the knowledge!
Dental Management of Patient with Diabetes Mellitus PresentationIraqi Dental Academy
This lecture discuss the topic of dental management of medically compromised patient who suffers from diabetes mellitus. it's simple lecture that directed to the level of mind of undergraduate students. thanks for viewing and reading, and please share the knowledge!
secondary impression / final impression in complete denture.
#prosthodontics
#prostho
BDS 4th year
Nischala Chaulagain
Nobel Medical College , Biratnagar
diabetes mellitus / dental implant courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
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secondary impression / final impression in complete denture.
#prosthodontics
#prostho
BDS 4th year
Nischala Chaulagain
Nobel Medical College , Biratnagar
diabetes mellitus / dental implant courses by Indian dental academy Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Sudden temporary change in PHYSICAL movement, SENSATION, BEHAVIOUR because of abnormal discharged of electrical impulses from nerve cells.
CLASSIFICATION
PARTIAL SEIZURE / FOCAL SEIZURE
>> Aimed to determine:
Type of seizure
Frequency
Severity
Aura
LOC
Dyspnea
Fixed and dilated pupil
Incontinence
Factors that precipitate them.
Developmental history taking (events of pregnancy and childbirth)
Questioned about illnesses or head injury
principles of preoperative evaluation and preparation.pptxMahmood Hasan Taha
The importance of preoperative assessment and evaluation to prepare the patient to surgical procedure is directly proportional with the degree of successful of any surgical procedure.
So, good preoperative assessment and evolution is necessary to avoid the morbidity and mortality that expected to the surgical procedures.
For those battling kidney disease and exploring treatment options, understanding when to consider a kidney transplant is crucial. This guide aims to provide valuable insights into the circumstances under which a kidney transplant at the renowned Hiranandani Hospital may be the most appropriate course of action. By addressing the key indicators and factors involved, we hope to empower patients and their families to make informed decisions about their kidney care journey.
India Clinical Trials Market: Industry Size and Growth Trends [2030] Analyzed...Kumar Satyam
According to TechSci Research report, "India Clinical Trials Market- By Region, Competition, Forecast & Opportunities, 2030F," the India Clinical Trials Market was valued at USD 2.05 billion in 2024 and is projected to grow at a compound annual growth rate (CAGR) of 8.64% through 2030. The market is driven by a variety of factors, making India an attractive destination for pharmaceutical companies and researchers. India's vast and diverse patient population, cost-effective operational environment, and a large pool of skilled medical professionals contribute significantly to the market's growth. Additionally, increasing government support in streamlining regulations and the growing prevalence of lifestyle diseases further propel the clinical trials market.
Growing Prevalence of Lifestyle Diseases
The rising incidence of lifestyle diseases such as diabetes, cardiovascular diseases, and cancer is a major trend driving the clinical trials market in India. These conditions necessitate the development and testing of new treatment methods, creating a robust demand for clinical trials. The increasing burden of these diseases highlights the need for innovative therapies and underscores the importance of India as a key player in global clinical research.
Navigating Challenges: Mental Health, Legislation, and the Prison System in B...Guillermo Rivera
This conference will delve into the intricate intersections between mental health, legal frameworks, and the prison system in Bolivia. It aims to provide a comprehensive overview of the current challenges faced by mental health professionals working within the legislative and correctional landscapes. Topics of discussion will include the prevalence and impact of mental health issues among the incarcerated population, the effectiveness of existing mental health policies and legislation, and potential reforms to enhance the mental health support system within prisons.
LGBTQ+ Adults: Unique Opportunities and Inclusive Approaches to CareVITASAuthor
This webinar helps clinicians understand the unique healthcare needs of the LGBTQ+ community, primarily in relation to end-of-life care. Topics include social and cultural background and challenges, healthcare disparities, advanced care planning, and strategies for reaching the community and improving quality of care.
Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
Join us as we delve into the crucial realm of quality reporting for MSSP (Medicare Shared Savings Program) Accountable Care Organizations (ACOs).
In this session, we will explore how a robust quality management solution can empower your organization to meet regulatory requirements and improve processes for MIPS reporting and internal quality programs. Learn how our MeasureAble application enables compliance and fosters continuous improvement.
PET CT beginners Guide covers some of the underrepresented topics in PET CTMiadAlsulami
This lecture briefly covers some of the underrepresented topics in Molecular imaging with cases , such as:
- Primary pleural tumors and pleural metastases.
- Distinguishing between MPM and Talc Pleurodesis.
- Urological tumors.
- The role of FDG PET in NET.
How many patients does case series should have In comparison to case reports.pdfpubrica101
Pubrica’s team of researchers and writers create scientific and medical research articles, which may be important resources for authors and practitioners. Pubrica medical writers assist you in creating and revising the introduction by alerting the reader to gaps in the chosen study subject. Our professionals understand the order in which the hypothesis topic is followed by the broad subject, the issue, and the backdrop.
https://pubrica.com/academy/case-study-or-series/how-many-patients-does-case-series-should-have-in-comparison-to-case-reports/
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
4. Prevention
Goals of physical evaluation
Physical evaluation –
Medical history questionnaire,
Physical examination
Dialogue history.
5. ASA Physical Status Classification
Class1: Healthy patient with no systemic disease.
Class 2: Mild Systemic disease with no limits on
activity.
Class 3: Severe systemic disease that limits
activity.
Class 4: Incapacitating systemic disease that is life
threatening.
Class 5: Moribund and E refers to emergency
of any kind.
6. Anxiety recognition & stress reduction
protocol
Recognize patient’s anxiety level.
Consider using pre-medication or sedation
Schedule morning appointments.
Minimize waiting time and watch appointment
length.
Make sure to use adequate pain control. This will
vary from patient to patient.
Monitor vital signs.
Medical consult if required.
7. Premedication
Drug Recommended dosage for adults
Alprazolam 4 mg / day
Diazepam 2-10 mg
Flurazepam 15-30 mg
Midazolam Rarely used
Oxazepam 10-30 mg
Triazolam 125-250µg
Eszopiclone 2-3 mg
Zaleplon 5-10 mg
Zolpidem 10 mg
8. Situation Agent Regimen
Standard general
prophylaxis
Amoxicillin Adults: 2g
Children: 50mg/kg
orally
1 hour before the procedure
Inability to take oral
medications
Ampicillin Adults: 2g
Children: 50 mg/kg
IM/IV
30 min before procedure
Allergy to penicillin Clindamycin or
Cephalexin/Cefadroxil or
Azithromycin/
Clarithromycin
Adults 600 mg
Children 20 mg /kg
Adults 2g
Children 50mg/kg
Adults 500 mg
Children 50 mg/kg
Orally
1 hour before the procedure
Allergy to penicillin and
inability to take oral
medications
Clindamycin or
Cefazolin
Adults 600mg
Children 20mg/kg
IV 30 min before
Adults 1g
Children 25 mg/kg
IM/IV 30 min before
9. 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
10. 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
15. Module one – critical or essential emergency drugs
Category Generic drug alternative quantity Availability
Allergy –
anaphylaxis
Epinephrine None 1 preloaded
syringe +3x1
ml ampules
1:1000
(1mg/ml)
allergy –
histamine
blocker
Chlorphenira
mine
Diphenhydra
mine
(Benadryl)
3x1 ml
ampules
10 mg/ml
Oxygen Oxygen 1 “E” cylinder
Vasodilator Nitroglycerin Nitrostat
sublingual
tablets
1 metered spray
bottle
0.4 mg /metered
dose
Bronchodilator Albuterol Metaproterenol 1 metered dose
inhaler
Metered aerosol
inhaler
Antihypoglyce
mic
Sugar Insta – glucose
gel
1 bottle
Inhibitor of
platelet
aggregation
Asprin None 2 packets 325mg/tablet
16. Equipment Recommended Alternative Quantity
Oxygen delivery
system
Positive pressure and
demand valve
Pocket mask
Oxygen delivery
system with bag valve
mask device
Minimum: 1 large
adult, 1 child
1 per employee
Automated electronic
defibrillator(AED)
Many 1 AED
Syringes for drug
administration
Plastic disposable
syringes with needles
3x2 ml syringes with
needles for parenteral
drug administration
Suction and suction
tips
High volume suction
Large diameter, round
ended suction tips
Non electrical suction
system
Office suction system
Minimum 2
Tourniquets Robber and Velcro
tourniquet; rubber
tubing
spygmomanometer 3 torniquets and 1
spygmomanometer
Magill intubation
forceps
Magill intubation
forceps
1 pediatric Magill
intubation forceps
17. Module two – secondary/ noncritical drugs and equipment
Category Generic Drug Alternative Quantity Availability
Anticonvulsant Midazolam diazepam 1x5 ml vial 5 mg/ml
Analgesic Morphine
sulphate
Meperidine 3x1 ml ampules 10 mg/ml
Vasopressor Phenylephrine 3x1 ml ampules 10 mg/ml
Antihypoglycem
ic
50% dextrose Glucagon 1 vial 50 ml ampule
Corticosteroid Hydrocortisone
sodium succinate
Dexamethasone 2x2 ml mix- o –
vial
50 mg/ml
Antihypertensive Esmolol Propranolol 2x100 mg/ml
vial
100 mg/ml
Anticholinergic Atropine Scopolamine 3x1 ml ampules 0.5 mg/ml
Respiratory
stimulant
Aromatic
ammonia
2 boxes 0.3 ml/vaporole
Antihypertensive Nifedipine 1 bottle 10mg/capsule
18. Module three – Advanced Cardiac Life Support (ACLS) : essential
drugs
Category Generic Drug Alternative Quantity Availability
Cardiac Arrest epinephrine 3x10 ml
preloaded
syringes
1:10,000
(1mg/10ml
syringe)
Analgesic Morphine
sulphate
N2O – O2 3x1 ml ampules 10 mg/ml
Antidysrhythmic Lidocaine Procainamide 1 preloaded
syringe and 2x5
ml ampules
100 mg/ syringe
Symptomatic
Bradycardia
Atropine Isoproterenol 2x10 ml
syringes
1.0 mg/10 ml
Paroxysmal
Supraventricular
Tachycardia
verapamil 2x4 ml ampules 2.5 mg/ml
19. Module four – antidotal drugs
Category Generic Drug Alternative Quantity Availability
Opioid
antagonist
Naloxone nalbuphine 2x1 ml ampules 0.4 mg/ml
Benzodiazepine
antagonist
Flumazenil 1x 10 ml vial 0.1 mg/ml
Anticholinergic
toxicity
Antiemergence
delirium
Physostigmine 3x2 ml ampules 1 mg/ml
21. Vasodepressor Syncope
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)
22. 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
23. 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.
24. 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.
25. 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
26. Assess consciousness (loss of response to sensory stimulation)
Activate office emergency system
P- Position patient supine with feet elevated slightly
A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency&
breathing; assess circulation (palpation of carotid pulse)
D – Definitive care:
Administer O2
Monitor vital signs
Perform additional procedures:
Administer aromatic ammonia vaporole
Administer atropine if bradycardia persists
Do not panic!
Post syncopal recovery- delayed recovery-
Postpone dental treatment Activate EMS
Determine precipitating factors
27. POSTURAL HYPOTENSION
Predisposing factors:
Administration and ingestion of drugs e.g. antihypertensives like
sodium depleting diuretics, calcium channel blockers &ganglion
blocking agents, sedatives and narcotics, histamine blockers, levo
dopa
Prolonged period of recumbency or convalescence
Inadequate postural reflex
Late stage pregnancy
Advanced age
Venous defects in legs (e.g. varicose veins)
Recovery from sympathectomy
Addisson’s disease
Physical exhaustion and starvation
Chronic postural hypotension (Shy – Drager syndrome)
28. 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
29. 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
30. P- Position patient supine with feet elevated slightly
A→B→C – Assess & open airway (head tilt &chin lift); assess airway
patency& breathing; assess circulation (palpation of carotid pulse)
D – Definitive care:
Administer O2
Monitor vital signs
Patient recovers consciousness-
slowly reposition chair delayed recovery -
activate EMS
Continue BLS as needed and discharge patient
31. ACUTE ADRENALINSUFFICIENCY: (ADRENAL
CRISIS)
A third potentially life - threatening situation that may result in the
loss of consciousness. The condition is uncommon, is potentially
life – threatening, but is readily treatable.
Predisposing factors:
Lack of gluco-corticosteroid hormones
Mechanism 1: sudden withdrawal of steroid hormones in the
patient who suffers primary adrenal insufficiency (Addison’s
disease)
Mechanism 2: After the sudden withdrawal of steroid hormones
from a patient with normal adrenal cortices but with a temporary
insufficiency resulting from cortical suppression through prolonged
exogenous gluco-corticosteroid administration (secondary
insufficiency)
Mechanism 3: Stress either physiologic or psychological.
32. 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
36. Management :
Conscious
Terminate dental treatment
P – Position patient comfortably if asymptomatic;
Supine with legs elevated slightly, if symptomatic
A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency&
breathing; assess circulation (palpation of carotid pulse)
D – Definitive care:
Monitor vital signs
Summon medical assistance
Obtain emergency kit and O2
Administer glucocorticosteroid
39. 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
40. 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
41. 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
42. 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
44. If foreign body is not retrieved
Consult radiologist
Obtain appropriate radiographs and initiate medical
consultation
Perform bronchoscopy to visualize and retrieve foreign body
45. Hyper ventilation
It is defined as ventilation in excess of that required to maintain
normal blood pa O2 (arterial oxygen tension) and pa CO2 (arterial
carbon dioxide tension). It is produced by increase in frequency
or depth of respiration, or both.
Common emergency occur in dental office , almost always occur is
a result of extreme anxiety.
Prevention:
Through prompt recognition and management of anxiety
Physical evaluation of the patient
The vital signs of apprehensive patients may deviate from normal.
Recording the vital signs at the patient’s initial visit
Stress reduction protocol is the primary means of preventing
hyperventilation
46. Clinical manifestations:
system Signs and symptoms
cardiovascular Palpitations
Tachycardia
Precordial”pain”
Neurologic Dizziness
Lightheadedness
Disturbance of consciousness
Disturbance of vision
Numbness and tingling of
extremities
Tetany (rare)
Respiratory Shortness of breath
Chest “pain”
Dryness of mouth
Gastro intestinal Globus hystericus (subjective
feeling of a lump in the throat)
Epigastric pain
Musculoskeletal Muscle pain and cramps
Tremor
Stiffness
Carpopedal tetany
Psychological Tension
Anxiety and nightmares
47. 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
49. Management:
Recognize problem (rapid , deep, uncontrolled breathing)
P – Position patient comfortably usually upright
A → B → C – Basic life support as needed
D – Definitive care:
Remove dental materials from patient’s mouth
Calm patient
Correct respiratory alkalosis – instructed to breathe 7% CO2 &93% O2 or to
rebreathe the exhaled air
Initial drug management – Benzodiazepines
Dental care may continue if both doctor and patient agree
Discharge patient
50. ASTHMA
In 1830 Eberle, a Philadelphia physician, defined it as “paroxysmal
affection of the respiratory organs, characterized by great
difficulty of breathing, tightness across breast, and a sense of
impending suffocation, without fever or local inflammation.”
Today it is defined as “a chronic inflammatory disorder that is
characterized by reversible obstruction of the airways.”
51. Predisposing factors:
Extrinsic or allergic asthma,
The allergens may be airborne – house dust, feathers, animal
dander, furniture stuffing, fungal spores, or plant pollens.
Food and drugs – cow’s milk, egg, fish, chocolate, shellfish,
tomatoes, penicillins, vaccines , asprin, and sulfites.
Type I hypersensitivity reaction – Ig E antibodies produced in
response to allergen
Approximately, 50% asthmatic children become asymptomatic
before reaching adulthood
52. 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.
53. Status asthmaticus:
More severe clinical form
Experience wheezing, dyspnea, hypoxia
Refractory to 2 – 3 doses of β-adrenergic agents
If not managed adequately, patient may die due to respiratory distress
Prevention:
Medical history regarding
Lung diseases
Allergies to drugs, food, medication, latex
Usage of drugs, medications, natural remidies
54. Dialogue history:
Asthma?
Type extrinsic or intrinsic?
Age of onset
History of acute episodes
Precipitating factor
Management
56. 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
57. 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
58. Pathophysiology:
Neural control of airways
Airway inflammation
Immunological responses
Bronchospasm
Bronchial wall edema and hypersecretion of mucous glands
Breathing
59. Management:
Recognize problem (respiratory distress, wheezing)
Discontinue dental treatment
Activate office emergency team
P – Position, usually upright with arms thrown forward
A → B → C –Assess and perform basic life support as needed
D – Definitive care:
Administer O2
Administer bronchodilator via inhalation
(Episode terminates) (episode continues)
Dental care may continue Activate EMS
Discharge patient Administer parenteral drugs
Hospitalize or discharge patient, per EMS recommendation
Additional considerations: Sedatives which depress respiratory system and central nervous system are absolutely contraindicated. 5mg IV
or IM diazepam may be indicated to decrease anxiety.
60.
61. HEART FAILURE AND ACUTE PULMONARY EDEMA
It is generally described as the inability of heart to supply sufficient
oxygenated blood for body’s metabolic needs.
Predisposing factors:
Increase in the workload of the heart. E.g. high blood pressure
Damaging muscular walls of the heart through coronary artery disease and
myocardial infarction
e.g. Stenosis of heart valves (aortic, mitral tricuspid, pulmonary)
Increase in body’s requirement of O2 and nutrients (e.g. pregnancy,
hyperthyroidism, anemia, Paget’s disease)
Other factors are physical, psychological and climatic stress
62. 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.
64. 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
65. Pathophysiology:
Structural and functional cardiac disorder
Impairs left ventricular ability to fill with or eject blood
Limit exercise tolerance and fluid retention
Pulmonary congestion and peripheral edema
Right ventricular failure signs and symptoms related to systemic venous and capillary congestion.
Acute pulmonary edema is a drastic symptom of heart failure
Excess fluid in alveolar spaces and interstitial tissues
Suffocation and oppression of chest
Elevates heart rate and blood pressure
Increases additional load to the heart
Further decrease in cardiac function due to hypoxia
If this vicious circle is not interrupted, it may lead rapidly to death
v
66. 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
68. DIABETESMELLITUS
HYPOAND HYPERGLYCEMIA
It is a group of diseases marked by high levels of blood glucose resulting from
defects in insulin production, insulin action, or both
Predisposing factors:
Type I diabetes:
Genetic factors
Environmental factors like drugs, toxins and viruses (mumps, rubella,
coxsackie)
Autoimmune factors
Type II diabetes:
Genetic factors
Insulin secretion
Insulin resistance
Obesity
Adipocyte derived hormones and cytokines
69. Other specific types of diabetes mellitus
Gestational diabetes mellitus
Impaired glucose tolerance
Impaired fasting glucose
70. Precipitants of hypoglycemia in diabetic patients:
Addison’s disease
Anorexia nervosa
Decrease in usual food intake
Ethanol
Factitious hypoglycemia
Hepatic impairment
Hyper and hypothyroidism
Increase in usual exercise
Insulin
Islet cell tumors
Incorrectly used insulin pump
Malnutrition
Old age
Oral hypoglycemic agents
Over aggressive treatment of ketoacidosis
Pentamidine, Phenylbutazone, Propranolol
Recent change in dose
Salicylates
Sepsis
71. Prevention:
Medical history questionnaire
Dialogue history
Physical examination
Dental therapy considerations:
ASA physical status Treatment considerations
II Eat normal breakfast and take usual
insulin dose in the morning
Avoid missing meals before and after
surgery
If missing meal is unavoidable, consult
phycisian or ↓ insulin dose by half
III Monitor blood glucose levels more
frequently for several days following
surgery and modify insulin accordingly
Consider medical consultation
IV Consult physician before treatment
72. Antibiotic coverage in the postsurgical period is appropriate
Stress reduction protocol to be followed
Clinical manifestations of hyperglycemia:
Symptom Type I diabetes Type II diabetes
Polyuria ++ +
Polydipsia ++ +
Polyphagia with weight
loss
++ _
Recurrent blurred vision + ++
Vulvovaginitis or pruritis + ++
Loss of strength ++ +
Nocturnal enuresis ++ _
Absence of symptoms _ ++
73. Other symptoms of type I diabetes Other symptoms of type II diabetes
Repeated skin infections
Marked irritability Decreased vision
Headache Paresthesias
Drowsiness Loss of sensation
Malaise Impotence
Dry mouth Postural hypotension
74. Clinical manifestations of hypoglycemia:
Early stage – mild reaction
Diminished cerebral function
Changes in mood
Decreased spontaneity
Hunger
Nausea
More severe stage
Sweating
Tachycardia
Piloerection
Increased anxiety
Bizarre behavioral patterns
Belligerence
Poor judgment
Uncooperativeness
Later severe stage
•Unconsciousness
•Seizure activity
•Hypotension
•Hypothermia
75. Pathophysiology:
Hyperglycemia:
Prolonged lack of insulin (type I) or prolonged lack of tissue response (type
II)
Blood glucose levels remains elevated for longer time coz of
glycogenolysis and ↓ uptake by peripheral tissues
Glucose exceeds 180mg/100 ml – glucosuria
Because of its large molecular size, glucose in urine carries away large
volumes of water and electrolytes (Na+ & K+) – polyuria
Dehydrated state – skin dry and flushing - polydipsia
Weight loss due to depletion of water, glycogen, triglyceride(TGA) stores
Loss of muscle mass due to aminoacids → glucose and ketone bodies
TGA → free fatty acids (FFA) in the liver
FFA – acetoacetate and β – hydroxybutyrate (BHA) – diabetic ketoacidosis
↓ cardiac contractility, catecholamine response, respiratory alkalosis
Diabetic coma
76. 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
77. 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
78. Hypoglycemia – conscious patient
Recognize problem (altered consciousness)
Discontinue dental treatment
Activate office emergency team
P – Position, patient comfotably
A → B → C –Assess and perform basic life support as needed
D – Definitive management:
Administer oral carbohydrates
If successful If unsuccessful
Permit patient to recover Activate EMS
Discharge the patient Administer parenteral
carbohydrates
Monitor patient
Discharge patient
79. 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
80. Thyroid gland dysfunction
The thyroid gland secretes three hormones (T3 T4 and
calcitonin)that are vital in the regulation of the
level of biochemical activity of most of the body’s
tissues.
82. 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
83. Clinical manifestations
Hypothyroidism:
Symptoms Signs
Paresthesias
Loss of energy
Intolerance to cold
Muscular weakness
Pain in muscles and joints
Inability to concentrate
Drowsiness
Constipation
Forgetfulness
Depressed auditory acuity
Emotional instability
Headaches
Dysarthria
Pseudomyotonic reflexes
Change in menstrual pattern
Hypothermia
Dry, scaly skin
Puffy eyelids
Hoarse voice
Weight gain
Dependent edema
Sparse axillary and pubic hair
Pallor
Thinning eyebrows
Yellow skin
Loss of scalp hair
Abdominal distension
Goiter
Decreased sweating
84. Thyrotoxicosis:
Symptoms signs
Common
Weight loss
Palpitations
Nervousness
Tremor
Less common
Chest pain
Dyspnea
Edema
Psychosis
Disorientation
Diarrhea
Abdominal pain
Fever
Tachycardia
Sinus tachycardia
Dysrhythmias
Wide pulse pressure
Tremor
Thyrotoxic stare and eyelid
retraction
Hyperkinesis
Heart failure
Weakness
Coma
Tender liver
Infiltrative ophthalmopathy
Somnolence or obtundence
Jaundice
85. 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
86. Thyrotoxicosis:
Thyroid hormones ↑ body’s energy consumption and BMR
Fatigue &weight loss
Direct actions on myocardium - ↑ HR, ↑ myocardial irritability
↑ cardiac work load
Palpitations, dyspnea, chest pain
↑ incidence of angina pectoris and heart failure
↑ thyroid hormones also affects liver function
End point – thyroid storm and crisis
87. 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
88. CEREBROVASCULAR ACCIDENT
Defined as ‘any vascular injury that reduces cerebral
blood flow to a specific region of the brain,
causing neurologic impairment’. ‘Stroke’,
‘cerebral apoplexy’ & ‘brain attack’
Classification:
cerebral ischemia and infarction – atherosclerosis
& thrombosis, cerebral embolism
Intracranial hemorrhage – arterial aneurysms &
hypertensive vascular disease
Others – TIA – transient ischemic attacks
89. 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
90. 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
91. Pathophysiology:
Cerebrovascular ischemia and
infarction
Hemorrhagic CVA
•At cellular level, ischemia
•Anaerobic glycolysis with
production of lactate
•Mitochondrial dysfunction →
disruption of membrane and
vascular endothelium
•BBB breaks down and edema
forms
•Edema ↑ tissue mass in cranium
causes mild headache
•Severe edema may forces the
portions of cerebral hemisphere
into tentorium cerebelli
•Ischemia and infarction of
upperbrain stem (medulla)
•Loss of consciousness and fatal
•Subarachnoid hemorrhage –
ruptured aneurysms
•Intracranial hemorrhage –
hypertensive vascular disease
•Once vessels rupture
•Arterial blood supply fills the
cranium
•↑ in intracerebral blood pressure
•Rapid displacement of brain stem
into tentorium cerebelli
•Ultimately death
92. 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
94. 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
95. 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
96. 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
97. 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
98. Management of petitmal seizures:
P – position patient with feet elevated
Seizure ceases: reassure patient seizure continues (> 5 min)
Allow patient to recover before discharge A → B → C
–Assess and perform BLS
99. 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
101. Drug Overdose Reactions
Local Anesthetic and EpinephrineToxicity
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.
102. 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.
103. 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.
104. SEVERE OVERDOSE/RAPID ONSET, SEVERE OVERDOSE/SLOW ONSET
ABC’s.
Activate EMS.
Administer Oxygen by mask at 10-15L/minute.
Start IV if available (18 gauge catheter with Normal Saline.)
If needed and available administer anticonvulsant, Versed (Midazolam)
2mg, then 1mg/min to effect (Monitor respiration.)
Monitor and record vital signs.
Allow for recovery and discharge with appropriate escort or transport
to hospital if required.
105. Treatment Considerations to Avoid Adverse Drug Reaction
Prevention is the key. Take a complete medical history. Determine if there
are any diseases present that affect the use of a drug.
Know what medications the patient is taking and possible drug interactions.
Careful injections make sure to aspirate to avoid an intravascular injection.
Maximum Recommended Doses of Local Anesthetic
Lidocaine “Plain” 4.4mg/kg
Lidocaine 2% with 1:100k Epinephrine 7.0mg/kg
Mepivicaine “Plain” 4.4mg/kg
Mepivicaine with 1:20k Neocobefrine 6.6mg/kg
Bupivicaine with 1:200k Epinephrine 3.2mg/kg
Maximum Recommended Doses of Epinephrine
Healthy Adult 0.2mg
Cardiac Patient 0.04mg
106. Allergic Reaction
Signs and Symptoms of an Allergic Reaction
Cutaneous reactions are the most common occurrence and include
urticarial, exanthematous, and eczemoid reactions. Itching is
common and can also find exfoliative dermatitis and bullous
dermatosis.
Angioedema (Swelling) this varies from localized slight swelling of
the lips, eyelids, and face to more uncomfortable swelling of the
mouth, throat, and extremities.
107. 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.
108. 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.
109. Evaluation of Allergic Reactions: Things to remember.
Skin manifestations may precede more serious cardiorespiratory
problems.
Recognition of skin reactions and early treatment may abort more
serious problems.
Most important factor is assessing the seriousness of the
condition is the rate of onset.
Reactions that occur greater than one hour after the
administration of the allergen will usually be of a non-emergent
nature.
110. TREATMENT
General Treatment
ABC’s
Maintain airway, administer oxygen, and determine possible need for intubation or
surgical airway.
Monitor vital signs.
If in shock put patient in a horizontal or slight Trendelenburg position.
Mild Reactions
Antihistamines usually effective. (Benadryl 50-100mg or Cholpheniramine maleate 4-12
mg IV, or IM.)
Identify and remove allergen.
Follow up medications in 4-6 hours.
Severe Reactions
If available start IV Fluids
Epinephrine is drug of choice. Usually prepackaged 1:1,000 in 1mg vials or syringe
If IV in place titrate 1:1,000 solution to effect.
If drop in blood pressure is minimal, start with 0.5ml (0.5mg.)
111. 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.
113. Angina Pectoris
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
114. 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
115. 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
116. 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
117. 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
118. Management:
Recognize problem (chest pain – angina attack)
Discontinue dental treatment
Activate office emergency team
P – Position, patient comfortably usually upright
A → B → C –Assess and perform BLS
D – definitive management
HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA
Administer vasodilator and O2 Activate EMS
Transmucosal nitroglycerine spray O2 and consider nitroglycerine
Or sublingual nitroglycerine tablet Monitor and record
0.3 – 0.6 mg for every 5 min (3 doses)
IF PAIN RESOLVES IF PAIN DOES NOT RESOLVE
Future dental treatment modifications Activate EMS
Administer aspirin
Monitor and record vital signs
Medical management of unstable angina – Nitrates, β – blockers, calcium channel blockers and psychological stress
management and reassurance
119. Acute myocardial infarction
It is a clinical syndrome caused by a deficient coronary
arterial blood supply to a region of myocardium that
results in cellular death and necrosis
Predisposing factors:
Atherosclerosis and coronary artery disease
Coronary thrombosis, occlusion and spasm
Other risk factors are-
Males
5th and 6th decades of life
Undue stress
121. 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
122. 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
123. Clinical manifestations:
Symptoms Signs
Pain – severe to intolerable
Prolonged, 30 min
Crushing, choking
Retrosternal
Radiates – left arm, hand,
epigastrium, shoulders,
neck, jaw
Nausea and vomiting
Weakness
Dizziness
Palpitations
Cold perspiration
Sense of impending doom
Restlessness
Acute distress
Skin – cool, pale, moist
Heart rate – bradycardia
to tachycardia; PVC
(premature ventricular
contractions) common
124. 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
125. Management:
Recognize problem (chest pain – no history of angina)
Discontinue dental treatment
Activate office emergency team
P – Position, patient comfortably usually upright
A → B → C –Assess and perform BLS
D – definitive management
HISTORY OF ANGINA PRESENT NO HISTORY OF ANGINA
Follow protocol of angina (presumptive
diagnosis: Acute MI)
Activate EMS
Administer O2,consider
nitroglycerine
Administer aspirin
Manage pain (parenteral
opioids, N2O – O2)
Monitor and record vital signs
Prepare to manage complications (sudden cardiac
126. conclusion
Prompt recognition and efficient management of
medical emergencies by a well-prepared dental
team can increase the likelihood of a satisfactory
outcome. The basic algorithm for managing
medical emergencies is designed to ensure that
the patient’s brain receives a constant supply of
blood containing oxygen.
127. 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.