CLASSIFICATION OF LIFE THREATENING EMERGENCIES UNCONSCIOUSNESS(vasodepressor syncope) RESPIRATORY DISTRESS (surgical management) tracheostomy, cricothyrotomy CARDIAC FAILURE (acute pulmonary oedema) ALTERED CONSCIOUSNESS ( DM, Thyroid, cerebrovascular accident) HYPERSENSITIVITY SEIZURE CHEST PAIN CARDIAC ARREST

1. MEDICAL EMERGENCIES
In the DENTAL OFFICE
PRESENTD BY- SAVITA SAHU, 1ST YR
PG,OMFS

2. CONTENT
 INTRODUCTION
 PREVENTION
 PREPARATION
 CLASSIFICATION OF LIFE THREATENING EMERGENCIES
 UNCONSCIOUSNESS(vasodepressor syncope)
 RESPIRATORY DISTRESS (surgical management)
tracheostomy, cricothyrotomy
 CARDIAC FAILURE (acute pulmonary oedema)
 ALTERED CONSCIOUSNESS ( DM, Thyroid, cerebrovascular accident)
 HYPERSENSITIVITY
 SEIZURE
 CHEST PAIN
 CARDIAC ARREST 5/15/2021
2
2

3. INTRODUCTION
Goldburger -WROTE - when you are prepared for an emergency, emergency ceases to
exist.
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4. EVALUATION - GOALS
1. Determine Patient’s ability to tolerate PHYSICAL STRESS
2. Determine patient’s ability to tolerate PSYCHOLOGICAL STRESS
3. To determine if any TREATMENT MODIFICATION is required to enable patient
tolerate the stress better
4. Determine whether the use of SEDATION is warranted
a) which sedation technique would be most appropriate.
b) to identify if any contraindications exist to any drug in planned treatment.
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5. ASA CLASSIFICATION
 ASA1:- A normal ,healthy patient without systemic disease
 ASA2:- A patient with mild systemic disease
 ASA3:-A patient with severe systemic disease
 ASA4:- A patient with severe incapacitating disease that is a constant threat to life
 ASA5:-A moribund patient not expected to survive without operation
 ASA6:-A declared brain dead patient whose organs are being removed for donor
purposes
 ASAE:-emergency operation of any variety , with E preceding the number to
indicate the patients physical status.
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6. PREVENTION- anxiety recoginition and
stress reduction
 NORMAL, HEALTHY, ANXIOUS PATIENT(ASA1)
 MEDICAL RISK PATIENT (ASA 2,3,4)-
o Recognise patient’s degree of medical risk
o Medical consultation
o Morning appointment
o Monitor preoperative and postoperative vital sign
o Consider sedation therapy, adequate pain control
o Length of patient appointment should not increase more than his tolerance
o Follow up with postoperative pain and anxiety control
o Arrange the appointment in the initial working week
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7. PREPARATION-emergency drug kit
These emergency drug and kits are available in following four modules
MODULE ONE-basic emergency kit(critical drugs and equipment) .
MODULE TWO-noncritical drugs and equipment.
MODULE THREE-advanced cardiovascular life supports(ACLS).
MODULE FOUR-antidotal drugs
The design of each module is based on doctors degree of training and experience in
medical emergency.
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8. MODULE ONE
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CATEGORY GENERIC DRUG PROPRITARY
DRUG
ALTERNATIVE QUANTITY AVAILABILITY
INJECTABLE
Allergy-
anaphylaxis
epinephrine adrenalin none 1 preloaded
syringe+3x 1ml
ampules
1:1000 (1mg/ml)
Allergy-histamine diphenhydramine benadryl chlorheniramine 3x 1ml ampules 50 mg/ml
NONINJECTABLE
Oxygen oxygen oxygen 1E cylinder
Vasodilator nitroglycerine Nitroglycerine
spray
Nitrostat,
sublingual tablets
1 metered spray
bottle
0.4mg/metered
dose
Bronchodilators albuterol proventil metaproterenol 1 metered dose
inhaler
Meterd dose
aerosol inhaler
Anti-holyglycemic sugar Orange juice,
nondiet soft drink
Insta glucose gel 1 bottle
Inhibitor of
platelet
aggregratyion
aspirin many Clopidrogel
(plavix)
2 packets of
powered aspirin
325mg/dose

9. MODULE ONE EQUIPTMENT
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EQUIPTMENT RECOMMENDED ALTERNATIVE QUANTITY
Oxygen delivery system Positive pressure and
demand valve
Pocket mask
O2 delivery system with
bag valve mask device
minimum: 1 large adult,1
adult
1 per employee
Automated electronic
defibrillator
many 1AED
Syringes for drug
administration
Plastic disposable
syringes with needles
3x2-ml syringes with
needles for parental
drug administration
Suction and suction tips High volume suction.
Large dia. With round
ended suction tips
Nonelectrical suction
system
Office suction system
Min. 2
tourniquets Robber or Velcro
tourniquet; rubber tubing
sphygmomanometer 3 tourniquet
1 sphygmomanometer
Magill intubation forceps Magill intubation forceps 1 paediatric Magill
intubation forceps
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10. MODULE TWO
CATEGORY GENERIC DRUG PROPRIETARY
DRUG
ALTERNATIVE QUANTITY AVAILABILITY
INJECTABLE
anticonvulsant midazolam midazolam diazepam 1x5-ml or 10 ml
vial
5mg/mml
analgesic Morphine sulfate generic N2O 3X1-ml ampules 10mg/ml
vasopressor ephedrine generic 3X1-ml ampules 50mg/ml
antihypoglycemic 50% dextrose glucagon 1 vial 50-ml ampule
corticosteroid Hydrocortisone
sodium succinate
Solu-cortef dexamethasone 2x2 ml mix-o-vial 50mg/ml
antihypertensive esmolol brevibloc labetalol 2x100ml-mg/ml
vial
100mg/ml
anticholinergic atropine generic scopolamine 3x1-ml ampules 0.5mg/ml
NONINJECTABLE
Respiratory stimulant Aromatic
ammonia
generic 2 boxes 0.3ml/vaporole
antihypertensive hydralazine nitroglycerine 1 bottle 25mg tablets
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11. MODULE THREE
CATEGORY GENRIC
DRUG
PROPRIETAR
Y DRUG
ALTERNATIV
E
QUANTITY AVAILABILIT
Y
INJECTABLE
Cardiac arrest epinephrine adrenaline 3x10ml
preloaded
syringes
1:10000 (1
mg/10ml
syringe)
Antidysrhythmi
c
amiodarone Cordarone.nex
terone,pacero
ne
lidocaine 1x3ml Vial 50mg/ml
Symptomatic
bradicardis
atropine isoproterenol 2x10-ml
syringe
1.0mg/10ml
Paroxysmal
supraventricul
ar tachy cardi
Verapamil Calan,isoptin,v
erelin
2x4-ml
ampules
2.5mg/ml
NONINJECTA
BLE
oxygen oxygen 1 E cylinder 1E cylinder
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12. MODULE FOUR
CATEGORY GENERIC
DRUG
PROPRIET
ARY DRUG
ALTERNATI
VE
QUANTITY AVAILABILI
TY
INJECTABL
E
Opioid
antagonist
naloxone narcan nalbuphine 2x1-ml
ampules
0.4mg/ml
Benzodiaze
pine
antagonist
flumazenil romazic 1x10-ml 0.1mg/ml
Anticholiner
gic toxicity
Physostigmi
ne
antilirium 3x2-ml
ampules
1mg/ml
vssodilator phentolamin
e
reginite procaine 2x1-ml
ampules
5mg/ml
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13. UNCONCIOUSNESS-CAUSES
• Vasodepressor syncope.
MOST COMMOM
CASUE
• drug administration.
COMMON
CAUSES
• Orthostatic hypotension, epilepsy,
hypoglycaemia.
LESS COMMON
CAUSE
• Acute Adrenal insufficiency, allergic reaction,
MI, cerebrovascular accident, hyperglycemia
RARE
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14. VASODEPRESSOR SYNCOPE
It is also known as vasovagal syncope commonly referred to as faint.
SNCOPE is an abrupt transient loss of consciousness associated with
inability to maintain postural tone. It is associated with hypo-perfusion
of cerebral cortex and cerebral reticular activating system.
It is the 1st leading cause of syncope.
It has male predilection.
Age commonly affected is 16-35yrs.
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15. PREDISPOSING FACTOR
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PSYCHOGENIC FACTORS
o Fright
o Anxiety
o Emotional stress
o Receipt of unwelcome news
o Pain
o Sight of blood
NONPSYCHOGENIC FACTORS
o Erect sitting
o Hunger from dieting Exhaustion
o Poor physical condition Hot,
humid
o Crowded environment
o Age between 16-35yrs
o Male gender

16. PRESYNCOPAL SIGN AND SYMPTOMS
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EARLY
1. Feeling of warmth
2. Ashey-gray skin
tone.
3. Diaphoresis
4. Feeling faint/bad
5. Nausea
6. B.P. is at base line
7. tachycardia
LATE
1. Pupillary dilation
2. Yawning
3. Hypercapnea
4. Cold hands and feet
5. Hypotension
6. Bradycardia
7. Visual disturbances
8. Dizziness
9. Loss of
consciousness

17. PATHOPHYSIOLGY-PRESYNCOPE
STRESS Activation of fight and
flight mechanism
Release of
catecolamine
↓ in vascular resistance
,increased in blood flow to
peripheral tissue
Pooling of blood in
peripheral muscle
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↓ in venous
return to heart
↓ in
circulating
blood
volume
↓ in arterial
blood pressure
↓in cerebral
blood flow
Presyncopal symptoms
appear

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Activation of
compensatory
mechanism
Baroreceptors
and carotid
,aortic arch reflex
Constricts
peripheral blood
vessels
Increases
venous return
to heart
Increase
in heart
rate
Increase
in cardiac
output
Maintains B.P.
close to normal
Syncope
is
prevented
If the
stress
continues
Compensatory
mechanism
becomes fatigue
Patient
lands in
syncope

19. SYNCOPE
If the
stress
continue
s
↓ in blood
supply to
brain
Hearts ability
to pump blood
to brain is
impaired
Convulsive
movement
occurs
Cerebral
ischemia
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20. RECOVERY
Elevation of legs
improves
venous return
Blood
supply to
brain is
increased
Consciousn
ess is gained
Fatigue,swe
ating, pallor
may persist
Removal of
syncopal factor
improves
recovery
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21. MANAGEMENT
STEP1 ASSESS CONCIOUSNESS
STEP2 TERMINATE DENTAL PROCEDURE
STEP3 ACTIVATE OFFICE EMERGENCY SYSTEM
STEP4 P position patient supine with feet elevation
STEP5 CAB assess circulation, airway, breathing
STEP6 D definitive care
administer O2
monitor vital signs
Loosen tight cloths, aromatic ammonia, atropine-iv/im
POST-SYNCOPAL RECOVERY DELAYED RECOVERY
Postpone dental treatment activate medical emergency
determine the precipitating factor 5/15/2021
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22.  STEP1 ASSESS CONCIOUSNESS
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23. STEP2 TERMINATE DENTAL PROCEDURE
STEP3 ACTIVATE OFFICE EMERGENCY SYSTEM
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24.  STEP 4 Position- head and heart at same level feet elevated at an
angle of 10-15 degree.
 Pregnancy in third trimester is right lateral to prevent suppression on
the inferior venacava .
 STEP 5 –assess and open airway
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25. 5/15/2021
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26.  STEP 5- assess airway patency and breathing, circulation-
 Look listen and feel- lean over patient nose
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27. POSTURAL HYPOTENSION
It is defined as drop in systolic blood pressure of at least 20mmof hg or of diastolic blood
pressure of at least 10 mm of hg within 3 minutes of standing when compared to BP from
the sitting or supine position.
PREDISPOSING FACTORS-
1)Administration and ingestion of drugs
2)Prolonged period of recumbences or convalescences
3)inadequate postural reflex
4)Late stage pregnancy
5)Advanced age
6)Venous defect in legs
7)Addisions disease
8)Physical exhaustion
9)Chronic postural hypotension(shy-dragger syndrome)
Prevalance-5%to11% in middle age to 30% in elderly.
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28. PATHOPHYSIOLOGY
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In trendelenburg the systolic
BP decrease decreases by
2mm Hg for each 25 mm
increase of height and vice
versa.

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A number of intricate mechanism have developed to protect the brain , ensuring that it
receives an adequate supply of oxygen and glucose
The mechanisms are as follows
1)Reflex arteriolar constriction
2)reflex increase in heart rate
3)Reflex venous constriction
4)An increase in muscle tone and contraction in legs and abdomen
5)A reflex increase in respiration
6)The release into the blood of various neurohumoral substance like norepinephrine,
antidiuretic hormones, renin, and angiotensin

30. CLINICAL SIGN
 Prodromal signs and symptoms of vasodepressor syncope –
 Light-headedness
 Pallor
 Dizziness
 Blurred vision
 Nausea
 Diaphoresis
 Heart rate < 30 beats/min
 Unconsciousness >10 sec.
 Systolic pressure drop to 30 mm of hg
 Diastolic pressure drop to 10 mm of hg
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31. MANAGEMENT
STEP1 ASSESS CONCIOUSNESS(lack of response to sensory
stimulation)
STEP2 ACTIVATE OFFICE EMERGENCY SYSTEM
STEP3 P position patient supine with feet elevation
STEP4 CAB assess circulation , airway, breathing
STEP5 D definitive care
administer O2
monitor vital signs
POST-SYNCOPAL RECOVERY DELAYED
RECOVERY
Postpone dental treatment activate medical emergency
service
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32. ACUTE ADRENAL INSUFFICIENCY
 Third potentially life threatening situation resulting in loss of
consciousness.
 It is uncommon but, if identified at right time its readily treatable
 Incidence - 0.3-1/1,00,000 individuals.
 Clinical manifestations :- unless & until 70%-80% of the adrenal
cortex is destroyed.
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33. PREDISPOSING FACTORS
 Lack of glucocorticosteroid hormone is major predisposing factor in
all cases of acute adrenal insufficiency.
 The deficiency develops through following 6 mechanism
1)sudden withdrawal of steroid hormone in a patient who suffers from
Addisons disease
2)Sudden withdraw of steroid hormone in a patient suffering from
secondary insufficiency
3)Stress
4)Bilateral adrenalectomy
5)Sudden destruction of pituitary gland
6)Injury to adrenal gland
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34. CLINCAL FEATURES
 GENERAL SYMPTOMS
Weakness ,fatigue
Anorexia
Gastrointestinal symptoms
Weightloss
Hyponatremia
Blood pressure decreases
Fever mild
Depression
Myalgia
Auricular calcification
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35. PRIMARY SIGNS SECONDARY SIGN
Hyperpigmentation hyperkalaemia
Salt craving hyperpigmentation
Orthostatic, syncope hypoglycaemia
Vitiligo orthostatic ,hypotension
Hyperkalaemia amenorrhea
Hypercholemia and acidosis axillary and pubis hair loss
Hypoglycaemia decreased libido
CRISIS SIGN
Refractory hypotension
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36. PREVENTION
 1)DIALOGUE HISTORY
 2)DENTAL THERAPY CONSIDERATION-
-2-4 folds increase in glucocorticosteroid on the day of treatment should be
given
-stress reduction protocol should be followed
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37. MANAGEMENT IN CONSCIOUS PATIENT
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• Asses the patient (conscious )
• Terminate the dental treatment
• P position the patient with feet elevated
• CAB provide with BLS
• D definitive care
• Monitor vital signs

38. 5/15/2021
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• 1L of normal saline should be infused if hypovolemia
present(3L in 8Hrs)
• If hypoglycaemic administer 5% dextrose, if i.v. line
is available
• 1-2 mg of glucagon can be administered via i.m.
route
• obtain Emergency kit
• Administer dexamethasone phosphate 4mg i.v
• Administer glucocorticosteroid (hydrocortisone sodium
succinate)50-100mg. it should be given every 6-8 hrs

39. MANAGEMENT IN UNCONSCIOUS PATIENT
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• Asses the patient (unconscious)
• Terminate the dental treatment
• P position the patient with feet elevated
• CAB provide with BLS
• D definitive care
• Monitor vital signs

40. • Administer glucocorticosteroid (hydrocortisone sodium
succinate50-100mg over 30 sec)
• 1L of normal saline should be infused if hypovolemia
present(3L in 8Hrs)
• If hypoglycemic administer 5% dextrose, via i.v. line. 1-2
mg of glucagon can be administered via i.m. route.
TRANSFER PATIENT TO HOSPITAL.
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• obtain Emergency kit
• Administer oxygen.
• Administer dexamethasone phosphate4mg i.v

41. RESPIRATORY SYSTEM
FOREIGN BODY OBSTRUCTION
HYPER VENTILATION
ASTHMA
ACUTE PULMONARY EDEMA AND HEAT FAILURE
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42. FOREIGN BODY AIRWAY
OBSTRUCTION
More than 90% of the death from foreign body aspiration in pediatric
age group occur in children in younger than 5 yrs.
Elderly patients-neurological disorders and decreased gag reflexes
due to alcohol, seizures, strokes, parkinsonism, trauma, and senile
dementia are also at a greater risk of aspiration.
Third category of risk are those undergoing procedures with sedation,
particularly dental procedure and emergency intubation.
If the object has entered the trachea bronchial tree it is most likely to
be located in the right bronchos as it takes the more direct pathway as
compared with the left bronchos. The right main bronchos branches off
the trachea at 25-degree angle, the left branches off at 45-degree
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43. PREVENTION
Rubber dam
Oral packing
Chair position
Dental assistant and suction
Magil intubation forceps tongue grasping forceps
Ligature
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44. SIGNS OF PARTIAL AIRWAY
OBSTRUCTION
INDIVIDUAL WITH GOOD AIR FLOW-
Forceful cough
Wheezing between cough
Ability to breath
INDIVIDUAL WITH POOR AIR EXCHANGE-
Weak ineffective cough
Crowing sound on inspiration
Paradoxical respiration
Absence or altered voice sounds
Possible cyanosis
Possible lethargy
Possible disorientation
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45. SIGNS IF COMPLETE AIRWAY
OBSTRUCTION
 Inability to breath
 Inability to speak
 Inability to cough
 Universal sign of chocking
 panic
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46. ASSESSMENT OF UPPER AIRWAY
OBSTRUCTION
 Researches have documented in dogs the physiologic events that occur with
asphyxia.
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PHASES SIGNS AND SYMPTOMS
First phase
(1-3 mins)
Conscious; universal chocking signs; struggling,
paradoxical respiration without air movement or
voice; increased blood pressure and heart rate.
Second
phase
(2-5 mins)
Loss of consciousness; decreased respiration, blood
pressure, heart rate
Third phase
(4-5 mins)
Coma, absent vitals signs; dialted pupils

47. BASIC AIRWAY MANEUVERS
STEP1- P (POSITION)-supine, with feet elevated slightly
STEP2- C (CIRCULATION)-check for pulse if not present start chest compression. If present
start with step3
STEP3- (HEAD TILT CHIN LIFT)-If tongue is the cause of obstruction it will be relieved by this
method
STEP4- A+B (airway, breathing)-go for look, listen and feel technique.
STEP4a – jaw thrust maneuverer, if indicated.
STEP 5-A+B. repeat step 4 if necessary
STEP6-rescue breathing, if indicated. If step 6 is performed and patient is not able to establish
airway it implies that the obstruction is in lower airway
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48. ESTABLISHING PATENT
AIRWAY
INVASIVE METHOD NONINVASIVE METHOD
1)TRACHEOSTOMY 1)BACK BLOWS
2)CRICOTHYROTOMY 2)ABDOMINAL THRST
3) CHEST THRUST
4)FINGER SWEEP
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49. NONINVASIVE METHOD- BACK BLOWS
 It remains an integral part of the protocol for obstructed airway management in infants.
 TECHNIQUE
the infant is straddled over rescuers arms with head lower than trunk and with the head
supported with the rescuers firm hold on the infants jaw.
Using heel of hand, deliver up to 5 back slaps forcefully between the infants shoulder blades
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50. ABDOMINAL THRUST AND CHEST
THRUST
 It acts by increasing the intrathoracic pressure, thereby acting as an artificial cough
that can help dislodge a foreign body.
 Condition to use chest thrust
Obese patient
Pregnant patient
For infant >1yr of age
Hand should be superior to xiphoid process
 Condition to use abdominal thrust
oldage people
young people
Hand should be placed below the xiphoid process
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51. HEIMLICH MANEUVER(abdominal thrust )
 It was described by dr. henry J. helmich .
 Used when there is severe obstruction
 Signs of severe obstruction
o a weak ineffective cough or no cough at all
o high pitched noise during inhalation or no noise at all
o increased respiratory difficulty
o presence of cyanosis of mucus membrane e
o aphonia
o universal chocking sign( clutching at neck thumb and finger)
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52. Management in conscious patient
 Ask victim if he /she is chocking
 If victim nods yes
 Ask for permission to attempt to relive obstruction patient
 Incase of unconscious patient the consent is applied
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Stand behind the victim
Wrap your hand around victims waist
Stabalize yourself

53. Make a fist with one hand
Place the thumb of your fist against the abdomen
Grab your fist with one hand
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Press your fist in the abdomen
(quickly,forcefully,with upward thrust)
Repeat the thrust until the object is out
Victim should be evaluated for
complications before dismissing

54. Management in unconscious patient
Place victim in supine position, call for EMS
Begin basic life support-30 chest compression
(prior pulse checking)
Open airway, deliver breath, look for object,
remove if visible
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If object not visible , repeat above steps
Repeat until object is removed or until EMS
arrives

55. Management in conscious patient with chest thrust
Stand behind the patient, place your arms under armpit
encircling the chest
Grasp one fist with other
Place your thumb side for fist on the middle of sternum
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Stabilize yourself
Perform backward thrust until foreign object is
retrieved

56. Management in unconscious patient with
chest thrust
Place the victim supine, contact EMS
Begin BLS with 30 chest compression ( prior checking
pulse)
Open airway, deliver breath, look for object, remove if
visible
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If object not visible , repeat above steps
Repeat until object is removed or until EMS
arrives

57. 5/15/2021
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58. SURGICAL AIRWAY
MANAGEMENT-
-TRACHEOSTOMY
-CRICOTHROTOMY
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59. TRACHEOSTOMY
INDICATIONS
1)Major laryngeal trauma
2)Inability to intubate or perform needle cricothyrotomy
3)Stable patient requiring controlled airway
4)Laryngeal foreign body
5)Prolonged ventilation
6)Cervical spine injury
7)Oncological resection of head and neck
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60. CONTRAINDICATIONS
 If there is expanding hematoma
 In patient whom other means can be used eg- rescue airway, needle or
open cricothyrotomy.
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61. PROCEDURE
Incision is made on patient with head in normal position.
Head is then hyperflexed
Types of incision
Vertical Horizontal
#Done in emergency #electively to have better
From cricoid cartilage to cosmetic results. 4-5 cm long
suprasternal notch through incision below cricoid cartilage,
Subcut tissue and platsyma muscle through Subcut tissue and
platsyma muscle.
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62.  The space of burns is bluntly entered, inferior thyroid vein are
clamped.
 Frequent palpation and spreading of tissue vertically in midline is done
towards trachea
 pretracheal fascial and thyroid isthmus -exposed .
 Thyroid isthmus-transected if not retractable
 Cut suspensory ligament at inferior border of cricoid
cartilage-allows mobilisation
 Isthmus is cut and oversewn
 Tracheal ring is now visible.
 Dissection should be sufficient enough to see 1st and 4 the tracheal ring
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63.  Tracheostomy hook is placed between 1st and 2nd ring
 Gentle superior traction given to lift trachea
 Tracheal entrance incision( U , INVERTED U, T, CRUCIFORM)
 Traction suture of 2-0 silk is placed through tip of flap and inferior margin
of skin and is tied.
 Trousseau dilator or Kelly haemostat is inserted and spread vertically,
tracheal lumen is visible at present
 Appropriate tube is selected and inserted.
 The cuff of EET should be just inferior to vocal cord.
 Once the tube is in place and proper fit auscultate the lungs and see the
chest movement.
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64.  Skin can be loosely sutured or left open
 A gauze dressing should be placed under the tube phalanges and around
cannula.
 Tube should be secured with cloth tape tied around the patients neck.
 Chest x-ray should be taken to confirm and rule pneumothorax , a special
complication in paediatric population.
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65. COMPLICATIONS
PERIOPERATIVE POSTOPERATIVE
Haemorrhage Plugging of tube with secretion
Pneumothorax Haemorrhage
Subcutaneous emphysema Infection
Oesophageal injury Tracheal stenosis
False passage Tracheoesophageal fistula
Aspiration Vocal cord injury
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66. POST OPERATIVE CARE
 The cuff pressure should be maintained at 20 mmofhg
 40% humidified air is required all the time
 TRACH CARE-tracheostomy tube should be aspirated frequently –
hyperventilate patients lung with 100%O2 for 2-3 min before suctioning.
5 ml of sterile saline is injected into tracheal tube, followed by deep
suctioning procedure. Suctioning should be intermittent for 2 or 3 sec.
repeat until no secretion is seen
 Tach care should be performed every hour for 1st 2 days, every 2hrs. For
next 2 days , every 4 hrs thereafter.
 The tracheostomy tube should be changed weekly
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67. PERCUTANEOUS TRACHEOSTOMY
 This technique is based on seldinger’s description of arterial
catheterization.
 STEPS ARE AS FOLLOWS
1)Insertion of needle with a saline filled syringe
2) Removal of syringe and introduction of guidewire
3)Insertion of dilators
4)Remove dilator and placement of tracheostomy tube
5)Confirmation of airway maintenance
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67

68. CRICOTHYROTOMY
It is considered more than tracheostomy because it prevents the
following complications like
Trauma to isthmus gland
Perforation of oesophagus
Haemorrhage
Pneumothorax
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68

69. ADVANTAGES OF CRICOTHYROTOMY
OVER TRACHEOSTOMY
 Faster than tracheostomy, generally requires less than 2 min
 Easier to perform with less instrumentation required
 Fewer surgical complication and less bleeding
 Dose not require extension of neck
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70. PROCEDURE
 preparation of the neck
 identification of land mark
 immobilization of larynx
 incision on the skin-2-3 cm
 Reidentification of the membrane
 Incision of the cricothyro membrane-1.5 cm
 Dilation of the incision
 Insertion of the tube
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70

71. INDICATIONS
 Maxillofacial trauma
 Oropharyngeal obstruction
 Condition in which tracheal intubation from above is contra
indicated-eg- congenital malformation, massive haemorrhage,
persistent vomiting
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72. CONTRAINDICATION
 Age-children under 11yrs
 Crush injury to larynx
 Pre-existing laryngeal or tracheal pathology
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72

73. COMPLICATION OF CRICOTHYROTOMY
PERIOPERATIVE POSTOPERATIVE
Improper tube placement dysphonia, hoarseness
Haemorrhage subglottic stenosis
Prolonged execution time infection
Pneumomediastinum haemorrhage
Subcutaneous emphysema aspiration
Thyroid gland injury occlusion of tube
Oesophageal injury persistent stoma
Cartilage fracture vocal cord paralysis
Recurrent laryngeal nerve injury
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73

74. HYPERVENTILATION
 is defined as ventilation in excess of that required to maintain normal
blood PaO2 and PaCO2.
 Predisposing factors
 Acute anxiety & Patient hiding their fear
 Prevalence
 Age 15-40 years
 Female predominance
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75. CLINICAL SIGN AND SYMPTOMS
1)Patient may complain of chest tightness and will do over
breathing
2)Patient feel lightheaded
3)Palpitation
4)Patient may feel of a lump in the throat
5)Dryness of month
6)Epigastric pain
7)Muscular tremor and stiffness
8)Numbness and tingling of the extremities
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76. 5/15/2021
76

77. MANAGEMENT
 STEP 1-Terminate the dental treatment
 STEP2 -P position the patient.
 STEP3-CAB provide with BLS
 STEP4-D definitive care
 STEP4a –removal of material from mouth
 4b-calming the patient . Ask the patine to breath at the rate of 4-6 breath
per min. OR to keep his hand over mouth and breath exhaled air
 4c-correction of respiratory alkalosis(7%C02&93%O2).
 4d-drug management, if necessary 10 mg diazepam or 3-5 mg midazolam
 STEP 5- either continue or postpone
 STEP6- discharege if patient is well or escorted eith some body.
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78. ASTHMA
 It is a respiratory disorder characterized by reversible obstruction of airway
 TYPES-
o Extrinsic- it is allergic asthma.
o Intrinsic – it is non allergic asthma.
o •Mixed – it is combination of extrinsic and intrinsic asthma.
o •Status asthmatics – it is the most severe form of asthma
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79. EXTRINSIC ASTHMA
 It occurs most commonly occurs in children and younger adults .
 Patient with this form of asthma demonstrate an inherited allergic
predisposition .
 Patient may be allergic to methyl-paraben , sodium metabisulfite or latex
 Now a days in local anaesthesia cartridges methylparaben are not added
by most of the manufacturers
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79

80. INSTRIC ASTHMA
 Non allergic
 Developed >35 yr of age
 Causes- physiological or psychological stress
MIXED ASTHMA
 combination of extrinsic or intrinsic factor. Major cause – upper
respiratory infection.
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81. STATUS ASTHAMATICUS
 Most severe clinical form
 It’s a true medical emergency
 If not managed patient may die due to respiratory distress
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81

82. SIGN AND SYMPTOMS
1. Cough & Feeling of chest congestion
2. Wheezing & Dyspnoea
3. Patient wants to sit or stand
4. rise in heart rate > 120 beats/min & rise in BP.
5. Diaphoresis & Agitation
6. tachypnoea (breaths > 20-40 beats/min)
7. Confusion , Cyanosis & Nasal flaring
8. Supraclavicular & intercostal retraction
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83. MANAGEMENT OF ACUTE EPISODE
 STEP 1-Terminate the dental treatment
 STEP2 -P position the patient
 STEP3- removal of material from mouth
 STEP4- calming the patient
 STEP5- –CAB provide with BLS
 STEP 6-D definitive care
 6a-administer oxygen
 6b-bronchodilator inhaler-beta agonist-(epinephrine ,ventolin ,isoproterenol, etc)
Or selective beta2 agonist-(metaprolol)
ALBUTEROL is more frequently used for patient with asthma and
concomitent medical problem.
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83

84. MANAGEMENT OF SEVERE BRONCHOSPAM
 Step 6c- call for assistance
 Step 6d- administration of parental bronchodilators
Epinephrine-(1:10000)-3 ml subcute or i.m
Epinephrine-(1:1000)-0.3 ml i.v
Step 6e-administration o iv medications(optional)-hydrocortisone sodium
succinate 100 to 200 mg via i.v route
STEP 6f-2mg midaz i.v to decrease anxiety
STEP7-hospitalization so that long term asthma therapy could be reevaluated
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85. CARDIAC FAILURE AND
ACUTE PULMONARY EDEMA
 HEART FAILURE- it is generally described as its inability of heart to
supply sufficient oxygenated blood for body's metabolic need.
 PREDISPOSING FACTOR-
1)INCREASE THE WORK LOAD O THE HEART- increased blood pressure
2)DAMAGED MUSCUALAR WALL OF THE HEART- coronary artery
disease,myocardial infraction.
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85

86. PHYSICAL EVALUATION
VITAL SIGNS
 BLOOD PRESSURE- increases. Pulse pressure narrows to 30.
 HEART RATE AND R.R- increases
 WEIGHT GAIN- recent 3 pounds in 7 days.
PHYSICAL EXAMINATION
 SKIN AND MUCOU S MEMBRANE- ashen- gray apperance, cyanosis
 NECK-JUGULAR vein distension develop in patient with right ventricular
failure.
 ANKLES- pitting edema
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86

87. SIGN AND SYMPTOMS
HEART FAILURE-
SIGN SYMPTOMS
Pallor , cool skin weakness and fatigue
Diaphoresis dyspnoea on exertion
Left ventricular hypertrophy hyperventilation
Piting eodema, nocturia
Hepatomegaly and splenomegaly paroxysmal noctural dyspnoea
Narrow pulse pressure wheezing
ascites
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87

88. SIGN AND SYMPTOMS OF PULMONARY
EDEMA
 Moist rales at lung base
 Tachypnoea
 Cyanosis
 Frothy pink sputum
 Increased anxiety
 Dyspnoea at rest
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89. MANAGEMENT
 STEP 1-Terminate the dental treatment
 STEP2 -P position the patient
 STEP 3- removal of material from mouth
 STEP4- ACTIVATE OFFICE EMERGENCY SYSTEM
 STEP 5- calming of patient
 STEP6-CAB provide with BLS
 STEP7-D definitive care
 7a-administer 02
 7b-monitoring of vital signs
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90.  STEP 7c)- alleviation of symptoms
 STEP7d)-bloodless phlebotomy- 400-500ml of blood is removed
from the body
Torniquet is applied to three extremities , using wide, soft, rubber
tubing.
One is placed 6 inches below the groin
4 inches below the shoulder
 STEP 7e)administration of vasodilator-0.8 to 1.2 mg of nitroglycerin
tablet ‘every 15-30 minutes.
 STEP7F)alleviate apprehension-morphine 2-4 mg i.v. or subcut, or
im every 15 min
 STEP8- discharge
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90

91. 1)Diabetes mellitus
2)Thyroid gland function
3)Cerebrovascular accident
ALTERED
CONSCIOUSNESS
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91

92. DIABETES MELLITUS
It is a clinical syndrome characterised by an increase in plasma blood glucose.
Environmental factor combine with genetic factor determine which people will
develop clinical syndrome and the timing of its onset .
TYPES
TYPEI
TTPE II
GESTATIONAL DIABETES MELLITUS
IMPAIRED GLUCOSE TOLERANCE/ IMPAIRED FASTING GLUCOSE
TOLERANCE.
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93.  TYPE I- it is T- cell a mediated auto autoimmune disease involving
destruction of the insulin secreting β cells in pancreatic isletts . The
symptoms appear only when there is functional capacity is lost by 80-
90% .
 TYPEII- it results from complex genetic interactions, the expression of
which is modified by the environmental factor. They are thought to be
resistant to insulin action.
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94.  OTHER SPECIFIC TYPE-
genetic defect of beta cell function
Genetic defect of insulin action(lipodystrophies)
Disease of exocrine pancreas(neoplastic,fibrosis,pancreatectomy)
Drug or chemical induced (corticosteroids)
Infection
Associated with genetic syndrome(turners syndrome)
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95.  GESTATIONAL DIABETES MELLITUS-Is characterised by abnormal
result on the oral glucose tolerance test taken during pregnancy that may
either revert back to normal after postpartum or may remain abnormal.
18% of pregnancies are affected by gestation diabetes
Undiagnosed diabetes may cause perinatal illness or death
 IMPAIRED GLUCOSE TOLERANCE/IMPAIRED FASTING
GLUCOSE- it is an intermittent condition between diabetes and
normality.
140 & 199mg/dl glucose -2 hrs after food (ogtt) cant be classifed as diabetes.
100-125 after an overnight fasting. The level is high but, not high enough to
classify as diabetes.
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95

96. INVESTIGATIONS
URINE TESTING-
 1)glucose-testing should be performed 1-2 hrs after meal to maximise
sensitivity. Disadvantage –different glucose threshold
 2)ketones – it can be identified by nitropruside reaction , it measures
acetoacetate using either tablets or dipstick
 3)protein-microalbuminuria or proteinuria, in absence of urinary tract
infection is an indicator of diabetic nephropathy/increased risk of
microvascular disease.
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97.  BLOOD TESTING-
 GLUCOSE- laboratory glucose testing relies upon enzymatic
reaction(glucose oxidase). It is cheap, reliable. however the glucose level
depends wheater the patient has eaten readily in which blood sample was
taken.
-It can also be measured by colorimetric or other testing stick, which has a
electronic reader(fingerprick)
Values-The normal blood glucose level – 50 - 150mg/dl.
Individuals with overnight fasting – 78 – 115mg/.
KETONES-whole blood ketone monitoring detects β-OHB and is usefull in
assisting with insulin adjustment during intercurrent illness or sustained
hyperglycemia to prevent or detect DKA
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98.  INTERPRETATION OF CAPILLARY BLOOD KETONE
<0.6 mmol/L-normal to no action is required
0.6-1.5mmol/L-suggests metabolic control may be deteriorating; control to
monitor and seek medical advice if sustained/progressive
1.5-3.0mm0l/L- high risk of DK
>3.0- severe ketosis
GLYCELATED HAEMOGLOBIN- HbA1c indicates the integrated blood
glucose control over the life span of erythrocytes
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98

99. SIGN AND SYMPTOMS OF HYPERGLYCEMIA
 Thirst, dry mouth DK
 Polyuria, leg cramps
 Nocturia abdominal pain
 Tiredness, fatigue, lethargy dehydration
 Weight loss hypotension
 Blurring of vision tachycardia
 Hyperphagia hyeprthermia
 Nausea, vomiting drownsiness
 Mood change, irritabilty, difficulty in concentrating
 Kussmauls respiration
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100. PREVENTION
1) Proper medical history
2) Physical examination
3) Dental therapy consideration-patient with type1 (more prone to
DK).phentolamine mesylate(αadrenergic blocker) inj. Reduces soft
tissue anesthesia. Type2 diabetes are less prone to acute complications
-antibiotic coverage post treatment
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101. MANAGEMENT OF DK
 TIME (0-60 mins)
1.)commence 0.9% sodium chloride. 1L over 60 mins
2)commence insulin treatment-50 U human soluble insulin in 50 ml 0.9% sodium
chloride infused iv at 0.1 U/kg body weight/hr
3)perform further investigation-hourly blood glucose and ketone testing.
 TIME(60mins-12hrs)-IV infusion of 0.9%sodium chloride with potassium
chloride with potassium chloride as indicated below
1L over 2hr
1L over 2hrs
1Lover 4 hrs
1L over 4 hrs
1L over 6 hrs
Add 10 % glucose 125ml/hr iv when glucose <14 mmol/L
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102.  TIME 12-24 hrs
 Ketonameia and acidosis must have been resolved. If not eating and
drinking
 Continue IV insulin infusion at slower rate of 2-3 U/hr
 Continue iv fluid replacement
 Reinitiate SC insulin . Donot disconitue IV infusion until 30 mins after
SC-short acting insulin injection
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103. HYPOGLYCEMIA
 It is the 2nd and much more common acute complication of diabetes
mellitus.
 It develops very quickly as compared to hyperglycemia.
 Episodes of hypoglycemia usually develops when the patient has not
eaten for several hours.
 The normal blood glucose level – 50 - 150mg/dl.
 Individuals with overnight fasting – 78 – 115mg/dl.
 If its less than 63 . It will cause hypoglycemia
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103

104. CAUSES OF HYPOGLYCEMIA
 missed or inadequate meal
 Unexpected or unusual exercise
 Alcohol
 Lipohypertrophy
 Malabsorbtion
 Poorly designed insulin regimen.
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105. SIGN AND SYMPTOMS
EARLY STAGE
Diminished cerebral function •Changes in mood •Hunger & nausea
MORE SEVRE STAGE-
Sweating •Tachycardia •Increased anxiety •Bizzare behavioral patterns
•Belligerence •Poor judgement •Uncooperativeness
LATER SEVERE STAGE
Unconsciousness •Seizure activity •Hypotension •Hypothermia
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106. MANAGEMENT
 CONSCIOUS AND RESPONSIVE PATIENT
 Oral fast actng carbohydrate(10-15 g)is taken.
 Follow by snacking(complex carbohydrate)
 HYPOGLYCEMIC UNRESOPNSIVE PATIENT
 Iv 75ml 20% dextrose
 4)Im or iv injection of 1mg glucagon
 5)0.5mg of 1:1000 epinephrine im
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106

107. THYROID GLAND
DYSFUNCTION
HYPOTHYROIDISM
HYPER THYROIDISM
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107

108. HYPOTHYROIDISM
 CAUSES
 1)Disease to thyroid gland (primary hypothyroidism)
 2)Disease to pituitary gland (secondary hypothyroidism)
 3)Disease to hypothalamus (tertiary hypothyroidism)
 Prevalence :- 3-10 times more in FEMALE
 Clinically – these patients are sensitive to most CNS depressant
 drugs, sedatives, opioids and antianxiety drugs.
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109. CLINICAL SIGN AND SYMPTOMS
 Loss of energy
 2)Intolerance to cold
 3)Muscular weakness & Pain in muscles and joints
 4)Drowsiness & Forgetfulness
 5)Bradycardia & Hypotension
 6)Hypothermia (29.5 C- 30 C)
 7)Hypoglycaemia
 8)Loss of consciousness
 9)If not treated leads to myxedema coma with mortality rate up to 50%
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110. MANAGEMENT
IF THE PATIENT IS CONSCIOUS
Give desiccated thyroid hormone.
IF THE PATIENT GOES UNCONSCIOUS
Follow the basic protocol
give iv infusion of 5% dextrose and water, RL or normal saline
give O2
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111. HYPERTHYROIDISM
 Dental procedure for any patient is a stressful condition.
 This stressful situations lead to release of adrenaline from the body.
 This adrenaline along with the adrenaline used in the la , can act on the
thyroid gland.
 Leads to thyrotoxicosis due to excess release of T3& T4.
 SIGNS :-
 a)The skin becomes soft, warm and flushed, heat intolerance and
excessive sweating.
 b)It increases palpitations and trachycardia in middle aged people, in aged
people there may be congestive heart failure.
 c)Pt experience nervousness, tremor, irritability.
 d)Muscle weakness.
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112. THYROID STROM
 It is the late stage of thyrotoxicosis.
 It is rare but life threatening complication of thyrotoxicosis
 FEATURE
 fever
 •Agitation
 •Confusion
 •Tachycardia
 •Cardiac failure
 •Abdominal pain
 •sweating
FEATURES IF NOT TREATED COMA
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113. MANAGEMENT
IF THE PATIENT GOES UNCONSCIOUS AND HAS A
HISTORY OF THYROXICOSIS
Follow the basic protocol
Administer 5% solution of dextrose and water, RLM or normal saline
DEFINATIVE MANAGEMENT –
Antithyroidal drug
Beta blockers –propranolol
Glucocorticosteriod
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114. CEREBROVASCULAR ACCIDENT
 A cerebrovascular event (stroke) is a clinical syndrome caused by
disruption of blood supply to the brain, characterised by rapidly
developing signs of focal or global disturbance of cerebral functions,
lasting for more than 24 hours or leading to death.
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115. TYPES
 LACUNAR INFRACTION
 CEREBRAL INFRACTION
 TRANSIENT ISCHEMIC ATTACK
 HEMORRHAGIC STROKE
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116. PREDISPOSING FACTOR
1) DIABETES MELLITUS
2) DISORDER OF HEART RHYTHM
3) FAMILY HISTORY AND GENETICS
4) SMOKING
5) PHYSICAL INACTIVITY
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117. DENTAL THERAPY CONSIDERATION
 1)LENGTH OF TIME ELAPSED SINCE THE CVA
 2)MINIMIZATION OF STRESS
 3)ASSESSMENT OF WHEN THE POST-CVA PATIENT IS TOO
GREAT A RISK FOR TREATMENT .
 4)ASSESSMENT OF BLEEDING
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118. CLINICAL MANIFESTATION
 TRANSIENT ISCHEMIC ATTACK-onset is abrupt, recovery is rapid.
Most TIA cause transient numbness or weakness of contralateral
extremities, transient monocular blindness.
 CEREBRAL INFRACTION-onset may be sudden or slow-mild
headache, vomiting, symptoms occur on the contralateral side of patient.
seizure rarely precedes the stroke.
 CEREBRAL HEMORRHAGE-can occur in stressful dental treatment
Signs- severe headache, nausea, vomiting, chills, sweating ,dizziness and
vertigo
Omnious sign- conscious loss(occur in half of patient)
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119. MANAGEMENT
 THE STROKE CHAIN OF SURVIVAL
1)Rapid recognition and reaction to stroke warning signs
2)Rapid EMS dispatch
3)Rapid EMS transport and hospital prenotification
4)Rapid diagnosis and treatment in the hospital
IV. THROMBOLYTIC AGENT S
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120. HYPERSENSITIVITY
 Hypersensitivity is defined as an exaggerated or inappropriate state
of normal immune response with onset of adverse effects on the body.
 TYPES-
 Immediate type in which on administration of antigen, the reaction occurs
immediately (within seconds to minutes). Includes
type1,2,3hypersensitivity reaction.
 Delayed type in which the reaction is slower in onset and develops within
24-48 hours and the effect is prolonged. It includes type 4 hypersensitivity
reaction
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121. TYPES OF TYPE1 ALLERGIC REACTION
1)generalized(systemic) anaphylaxis
2)Localised anaphylaxis
3)Urticaria
4)Bronchospasm
5)Food allergy
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122. 5/15/2021
122

123. ACTION OF HISTAMINE
 Histamine receptors are present all over the body, especially in CVS
system, smooth muscle and glands.
 The clinical manifestation of histamine depends upon the ratio of H1 and
H2 activation
 CVS action of histamine- dilation of capillaries ,↑ capillary permeability
(prominent on the face and chest). ↑permeability lead to outward passage
of plasma protein and fluid into extracellular space, resulting in
formation of oedema.
 It decreases the venous return thereby ↓BP and cardiac output
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124.  Smooth muscle action of histamine-
-It relaxes the vascular smooth muscle, however nonvascular smooth
muscle is contracted-eg- bronchi and uterus.
-Smooth muscle of GIT are moderately contracted,
-Urinary bladder & gallbladder are slightly contracted
 action of histamine on glands-it stimulates the gastric gland, salivary,
lacrimal, pancreatic, and intestinal glands.
 ↑ secretion from mucous glands leads to rhinitis
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125. Slow-reacting substance of anaphylaxis or SRS-It is a
mixture of the leukotrienes LTC4, LTD4 and LTE 4.leukotrienes produce
a marked and prolonged bronchial smooth muscle contraction’
-It is 6000 times more potent as that of histamine
-Its onset is slower and longer than histamine.
eosinophilic chemotactic factor of anaphylaxis
basophil kallikreins-vasodilation ,production of pain, increased
permeability of blood vessel
Prostaglandin-smooth muscle contraction, increased vascular
permeability
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125

126. CLINICAL SIGN AND SYMPTOMS
 RESPIRATORY-↑mucous secretion
Laryngeal oedema
Angioedema
Asphyxia
Bronchospasm
Coughing
Wheezing
Chest tightness
Dyspnoea
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127. 5/15/2021
127

128. MANAGEMENT
 FOR SKIN REACTION- if mild diphenhydramine orally -50 mg(wt.>30 kg) 25
mg(wt. 15-30 kg)-3-4 times per day for 2-3 days.
-Severe patient diphenhydramine iv (few minutes for action)
-or im (10-30 mins).
 FOR RAPID ONSET OF SKIN REACTION-diphenhydramine iv or im .give o2
and find iv line.
-administer epinephrine via im (1:1000)
>15 kg-0.075ml of 1:1000 epinephrine
15-30kg-0.15ml
>30kg- 0.03ml
- If iv -Administer epinephrine (1:10000)-0.1 mg over 3-4 mins.
Repeat after15-30 mic only to max dose of 5ml
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129. MANAGEMENT
 FOR RESPIRATORY REACTION-
BRONCHOSPASM-these patient either will be asthmatic or allergic to
aspirin.
-epinephrine can be given in dose as discussed earlier.
-In case of hypertensive patient albuterol is the drug of choice.
-diphenhydramine in same dose as discussed
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130. MANAGEMENT
 LARYNGEAL EDEMA- diagnosed when little or no air movement is
seen, heard or felt
 SIGNS-respiratory distress
-Exaggerated chest movement
-High pitched crowing sound
-Cyanosis
-Loss of consciousness
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131.  DEFINATIVE TREATMEN T- position the patient. Lift chin or give jaw
thrust
-administer oxygen
-give diphenhydramine
-cricothyrotomy(for total obstruction)
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132. SEIZURE
 A paroxysmal disorder of cerebral function characterized by an attack
involving changes in the state of consciousness, motor activity, or sensory
phenomena; a seizure is sudden in onset and especially of short durations.
 TYPES-1) partial seizure
 2)generalized seizure -grandmal epilepsy
-absence seizure
-jacksonian
-psychomotor
-status epilepticus
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133. PREVENTION
 NONEPILEPTIC CAUSES-physical evaluation before the treatment and
proper use of local anaesthesia
 EPILEPTIC CAUSES-1)dialogue history
 2)physical examination- observe patient between the epileptic attack. No
physical signs as such appear but there may be variation in
electroencephalogram
 3)psychological implication on patient
 4)dental therapy consideration- minimal or moderate sedation
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134. CLINICAL MANIFESTATION
1)PARTIAL SIEZURE- limb jerks for several seconds
Fumbling of hands
Smacking of lips
patient gets reoriented in 1 min ,but feels lethargy after 3min
Patient experiences postictal confusion and amnesia for ictal activity.
2)ABSENCE SEIZURE-onset between 3 and 15 yrs.
Complete suppression of mental function, manifested by sudden immobility and
blank stare
Minor facial clinic movement
Blinking at 3 cycles / sec
Attacks last for 5-30 sec
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135.  3)TONIC CLONIC SEIZURE- phases
 A)PRODORMAL PHASE-it is subtle to obvious emotional change.
Phase of aura occurs-patient is not aware of aura because of amnesia
 B)PREICTAL PHASE-occurs after aura, patient looses consciousness,
falls. epileptic cry occurs-bilateral myoclinic jerk. BP&HR-↑, bladder
pressure increases, piloerection, hypersecretion occurs
 C)ICTAL PHASE-Tonic phase: 10 to 20 sec
-Clonic phase:2-5 mins
 D)POSTICTAL PHASE-patient becomes normal, sleep deeply. If the
seizure is for long period patient becomes comatose. Full recovery takes
2 hour
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137. 4)TONIC-CLONIC SEIZURE STATUS(grand mal status)-it is a life threatening
condition. continuous seizure of repetitive recurrence without recovery between
attacks.
May persist for hours and days
CLINCAL FEATURES-
Attack lasting for more than 5 mins
Unconscious patient
Cyanotic, diaphoretic
Hyperthermia
Tachycardia
Dysrhythmias
High blood pressure
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138. MANAGEMENT
Lie the patient if possible on the floor
Suction between the teeth and cheek
Head tilt and chin lift –to maintain airway
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139.  DEFINATIVE TRATMENT-for paediatric patient intranasal midazolam
 For adult-iv midazolam 1ml(1mg)/min until the seizure stops
 Intranasal dosage of 0.2mg/kg of midazolam
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140. CHEST PAIN
Angina pectoris
Acute myocardial infarction
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141. ANGINA PECTORIS
 Discomfort in the chest or adjacent areas caused by myocardial ischemia. It
is usually brought by exertion and associated with a disturbance in
myocardial function, but without myocardial ischemia.
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142. precipitating factor of angina pectoris
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143. SIGN AND SYMPTOMS
 Characteristics of the Pain :-
 1)Levine sign
 2)Dull, aching, heavy pain than a searing hot or knife like pain.
 3)It is generalized
 4)Commonly in the middle of sternum.
 5)Radiating type – commonly to the left shoulder, left side of neck,
distally down the medial surface of the left arm.
 Complain of heavy weight in chest.
 Heart rate – 200/150 mmhg
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144. DENTAL CONSIDERATION
 1)LENGTH OF APPOINTMENT
 2)SUPPLEMENT OF OXYGEN-nasal hood (3-5L/min)
 -nasal cannula (5-6L/min).
 3)PAIN CONTROL-LA with adrenaline for pain control.
 4)SEDATION—inhalation sedation with N2O &O2.
 5)ADDITIONAL COSIDERATION-vital sign monitor before treatment.
 Nitroglycerin premedication-should be given 5 mins before the start of
treatment. Onset of action 2-3mins,Duration of action 30 mins
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145. MANAGEMENT
Termination of dental procedures
Position – allowing patient to position themselves in the most
comfortable manner.
C –A – B
Oxygen administration – nasal cannula. Max 6l/min -24-44% O2
delivered
Nitro-glycerine spray sublingually
Tab Nitroglycerin :- 0.3- 0.6 mg every 5min as needed, with not
more than 3 tab per 15 mins.
If patient is not recovered after 2nd dose of nitroglycerin then it is
suspected to be MI.
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146. ACUTE MYOCARDIAL INFARCTION
 It is a clinical syndrome caused by deficient coronary
 Arterial supply to region of myocardium that results in
 cellular death and necrosis.
 PREDISPOSING FACTORS –obesity
male
5th -7th decade of life
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147. DENTAL THERAPY CONSIDERATION
 TREATMENT ONLY AFTER 6TH MONTH OF MI
 MEDICAL CONSULTTION FOR ASPRIN THERAPY
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148. SIGN AND SYMPTOMS
SYMPTOMS
 1)Pain :- Severe to tolerate
 Prolonged to 30 mins even hours
 Crushing, choking
 Radiates to the left arm, hand, epigastrium, shoulders
 2)Weakness, Dizziness, Palpitations & Cold perspiration
SIGNS
 1)Restlessness
 2)Acute distress
 3)Skin – cool, pale , moist
 4)Heart rate – initially bradycardia later tachycardia
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149. MANAGEMENT
 DEFINATINE TREATMENT(MONA)
 M-morphine-To relief pain – morphine sulphate 2 to 5 mg can be
administered in every 5 to 30 min. If respiratory rate is below 12 beats
per min , morphine is contraindicated.
 O-oxygen-nasal cannula. Max 6l/min -24-44% O2 delivered
 N-nitroglycerine-0.3-0.6mg
 A-aspirin- to relive pain
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150. CARDIAC ARREST
 Angina pectoris, MI and heart failure represents clinical manifestation of
ischemic heart disease.
 CHAIN OF SURVIVAL
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151. EARLY CPR
 1)RECOGNITION OF UNCONSCIOUSNESS-
 (PCAB)
 P-Position . Patient is supine, with elevated by 10 degree
 C-circulation. rescuer should not take more than 10 sec to check pulse.
 A-assessment and maintenance of airway. Head tilt chin lift
 B-breathing. Assessment and ventilation. Rescuer should start chest
compression immediately when the patient dose not respond.
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152. Cardio Pulmonary Resuscitation
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153. Automated external defibrillator
 Place AED on victim side
 Attach the electrode pad
 Attach the electrode cable to AED
 Analyse, if required press the analyse button
 Deliver the shock
 Start CPR immediately after shock
 If, no shock is indicated , then continue with CPR.
 Injection adrenaline 1:1000 iv as soon as possible
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