Medical Emergencies.pptx

Medical Emergencies
Presented by
Abhishek Shandilya
I Year PG
Oral & Maxillofacial Surgery

Under the guidance of :
DR. SHOAIB R. TIPPU
Professor & Head
Dept. of OMFS

Contents
1. Whats an
emergency????
2. Introduction
3. Classification of
life threatening
situations
4. Prevention
5. Preparation
– BLS
– Emergency drugs
& equipments
6. Emergency
management

7. Unconsciousness
– Syncope
– Postural hypotension
– Acute adrenal insufficiency
8. Respiratory distress
– Airway obstruction
– Hyperventilation
– Asthma
9. Seizures

Webster
• A sudden, urgent, usually
unexpected occurrence or occasion
requiring immediate action.
•

Emergency situations can be broadly divided
into –
Stress
Pre-existing
condition

Introduction
• Managing emergency situation
in oral & maxillofacial surgery
office can be frightening
experience at best; however,
this experience can quickly
turn into a catastrophe if the
doctor and his staff are not
adequately prepared.

“When you prepare for an emergency, the
emergency cease to exit”

Classification of life
threatening situations

1. Based on cardiac etiology
Noncardiovascular
emergency
a. Stress related
» Vasodepressor
syncope
» Hyperventilation
syndrome.
» Acute adrenal
insufficiency
» Asthma
» Hypoglycemic
reactions.
» Epilepsy
» Thyroid crisis
b. Non- stress related.
» Orthostatic
hypotension
» Overdose
reaction.
» Hyperglycemia
» Allergy
Cardiovascular emergency
a. Stress related
» Angina pectoris
» Acute Myocardial
Infraction
» Heart failure
» Cerebral ischemia
and infraction
b. Non- stress related.
» Acute myocardial
infraction

2. Classification based
on clinical signs and
symptoms:
a. Unconsciousness
 Vasodepressor syncope
 Orthostatic hypotension
 Acute adrenal insufficiency
b. Respiratory difficulty
 Airway obstruction
 Hyperventilation
 Asthma
 Heart failure and acute pulmonary edema
c. Altered consciousness
 Hyperglycemia and hypoglycemia
 Hyperthyroidism and hypothyroidism
 Cerebrovascular accident

d. Seizure disorders
e. Drug related emergency situations
 Drug overdose reactions
 Allergy
f. Chest pain
 Angina pectoris
 Acute myocardial infarction.
g. Cardiac arrest.

Response to acute illness should
include
Anticipation based on history and clinical
situation.
A search for illness or injury likely to be
present.
Readiness to provide appropriate
treatment.

Prevention
“Never treat a stranger”

1. Physical Evaluation
• Medical history questionnaire
• Physical examination (vital signs, visual
inspection, functional tests, auscultation
of heart and lungs)
• Dialogue history (recognition of anxiety)

2. Psychological examination
• Medical history questionnaire
• Anxiety questionnaire
• Observation
 Increased BP & Heart rate
 Trembling
 Excessive sweating
 Dilated pupils

DETERMINATION OF MEDICAL RISK.
• Physical status classification system
(1962, American Society of
Anesthesiologists)
• ASA I : A patient without systemic disease, a
normal healthy patient
• ASA II : A patient with mild systemic disease
• ASA III : A patient with severe systemic disease
that limits activity but is not incapacitating
• ASA IV : A patient with incapacitating systemic
disease that is a constant threat to life.
• ASA V : A moribund patient not expected to
survive 24 hrs with or with out surgery.
• ASA VI : Clinically dead patient being maintained
for harvesting organs.

• ASA E : Emergency operation of any variety; E
precedes the number, indicating the patients physical
status( ASA E-III)

 Medical consultation
 Stress reduction protocol
 Premedication
 Appointment scheduling
 Minimized waiting time
 Psycosedation during therapy
 Adequate pain control during therapy
 Duration of dental treatment
 Postoperative control of pain and anxiety

Preparation
“More patients will do well when
you act than when you don’t act”

 Role of dentist
 Other office staff
 Emergency drugs & equipments.

1. Staff training should include:
• Basic life support training for all members of dental
office staff
• Training in the recognition and management of
specific emergency situations
• Emergency “fire drills”
2. Office preparation should include:
• Posting emergency assistance numbers
• Stocking emergency drugs and equipment

Check for Unresponsiveness
Unrespond
Check for unresponsiveness
---”Are you all right?”
Call for help
---108

Open Airway
Upper airway obstruction by the tongue &
epiglottis
“Head tilt-
chin life”

Fingers of one hand under the mandible,
lifting the chin anteriorly, whilst the
thumb in the mouth depresses the lip
and opens the mouth

If suspected
head trauma
“Jaw thrust”

Grasp the angles of the jaw on each side
with the fingers and displace the
mandible forwards , the heels of the
hand may simultaneously hold a face
mask in place for assisted ventilation

Oropharyngeal
airway
Nasopharyngeal
airway
Airways:

Oropharyngeal airway: often termed the
Guedel airway. It is designed to sit over the
back of tongue. Once sized it is inserted
upside down and rotated into position on
contacting the soft palate.

Nasopharyngeal airway: inserted in one nostril
and providing an airway to the oropharynx,
should be easy to insert when lubricated via
either nostril. Preferred in awake patient as it
is better tolerated.

Endotracheal tube intubation:
Layngoscope:
Check light
Endotracheal tube:
Male: 7.0, 7.5, 8.0
Female: 6.5, 7.0, 7.5
Test cuff
“sniffing” position
Oral-pharyngeal-tracheal axis

Vocal cord
Lift forward & upward
Sellick maneuver
Length: 19~23cm
Cuff
Check position: stethoscope, CXR
Endotracheal tube intubation:

Assess airway patency & Breathing

Atmospheric air ventilation (Bag – valve – mask device
like Ambu bag)

Positive pressure ventilation
- Deliver positive pressure ventilation
- “Leak-proof” seal
- “OK” signal
- Squeeze Ambu bag slowly: >2sec
- Observe chest rise
- Deliver 2 initial breaths
- Sellick maneuver (cricoid pressure)
- Preventing gastric inflation

- Locate the trachea
Keep head tilt
position
- Gently feel the carotid pulse
Slide to the groove between
trachea & SCM

Chest
compressions
∆ It consists of rhythmic
application of pressure
over the lower half of
sternum.
∆ This increases blood flow
by increased intra
thoracic pressure & direct
compression of heart.

Locate the margin of the rib
- Follow the rib
margin to xiphoid
process
- Put hand above
fingers
Put another hand
directly over the hand

- Lock the elbow in position, with the
arms straightened
- “Shoulder over hand” position
- Depress the sternum about 4~5cm
- Complete release the pressure but
keep in contact with the victim’sternum
- Rate: 100/min
- Compression : Ventilation = 15 : 2

Initial assessment Check for unresponsiveness
Access airway
Signs of airway obstruction?
Access breathing
Signs of inadequate breathing?
Access pulse
Pulse absent?
Check BP
Recovery position
Open airway
Positive ventilation
Administration oxygen
Chest compression
Ready for defibrillation
Follow ACLS protocol
Yes
No
Yes
No
Yes
No

Administration routes for drugs:
(by rate of onset)
1. Endotracheal (when available):
Epinephrine, lidocaine, atropine and naloxone only
2. Intravenous
3. Sublingual or intralingual
4. Intramuscular
a) Vastus lateralis
b) Mid-deltoid
c) Gluteal region

Module one - basic emergency kit (critical drugs and
equipment)
Module two - noncritical drugs and equipments
Module three- advanced cardiac life support
Module four - antidotal drugs

In each module
a) Injectable drugs
b) Noninjectable drugs

Module one:-
• Injectable drugs
1. Epinephrine – 1: 1000
2. Antihistamine – CPM(chlorpheniramine maleate)
• Noninjectable drugs
1. Oxygen – E- Cylinder
2. Vasodialator – NTG, Amyl nitrite
• Emergency equipments
1. Oxygen delivery system
2. Suction & suction tips
3. Tourniquets
4. Syringes
5. Magill intubation forceps

Module two:-
• Injectable drugs
1. Anticonvulsant – Midazolam, Diazepam
2. Analgesic – Morphine
3. Vasopressor – Methoxamine, Phenylephrine.
4. Antihypoglycemic – 50% dextrose, Glucogon.
5. Corticosteroid – Hydrocortisone, Dexamethosone
6. Antihypertensive – Lebetalol, Propronolol
7. Anticholinergic – Atropine

• Noninjectable drugs
1. Respiratory stimulant – Aromatic Ammonia
2. Antihypoglycemic – Sugar
3. Bronchodilator – Albuterol, Metaproterenol.
• Emergency equipments
1. Device for cricothyrotomy
2. Artificial airways
3. Laryngoscope & endotracheal tubes

Module three:-
Essential ACLS drugs include
1. Epinephrine
2. Oxygen
3. Lidocaine
4. Atropine
5. Dopamine
6. Morphine sulphate
7. Verapamil

Module four:-
1. Narcotic antagonist – Naloxone,
Nalbuphine
2. Benzodiazepine antagonist –
Flumazenil
3. Antiemergence delirium drug –
Physostigmine
4. Vasodilator – Procaine

The most important emergency drug.
Indications



Available both as a Spray & Tab.
In management of Angina & early
MI 0.4mg tab sublingually or 0.4mg
sublingual spray.
Trade name: Nitrocontin,
Nitrolingual spray.

Potent Bronchodilator.
Trade name

Antiplatlet action.


Trade name

 Anticonvulsant.
Alternative drug


Trade name

Anticholinergic.
Trade name

δ High suction device & suction tips.

Magill intubation forceps
Blunt ended scissors
with right angle bend

Automated external defibrillator

EMERGENCY MANAGEMENT
• Primary survey:
1. ABCDE: Airway, Breathing,
Circulation, Disability, Expose.
2. Purpose: identification &
treatment of immediately life-
threatening problems

• Secondary survey:
1. Head to toe examination
2. Purpose: identification & treatment of
immediately life-threatening problems
3. History: find quick source information
(physician)
4. System-specific tests and therapy
5. Reevaluation
6. Definitive care.

Possible causes of
unconsciousness
1. Vasodepressor syncope
2. Drug administration
3. Orthostatic hypotension
4. Epilepsy
5. Hypoglycemic reaction
6. Acute adrenaline insufficiency
7. Acute allergic reaction
8. Acute MI
9. CVA
10. Hyperglycemic reaction
11. Hyperventilation

General Considerations
• Predisposing factors
1. Stress
2. Impaired physical status
3. Administration or ingestion of drugs
• Prevention
1. Through pretreatment medical evaluation of the
patient both physiologically and psychologically
2. Sedation techniques: either pharmacological or non
pharmacological.
3. Sit-down dentistry, with patients treated while they lie
supine.

• Clinical manifestations
An unconscious patient is incapable of
responding to sensory stimulation and
has lost protective reflexes along with
an attendant lack of ability to maintain
a patent airway.

• Pathophysiology
Engle in his classic test on fainting classified
4 mechanisms
1. Inadequate cerebral circulation
2. Reduced cerebral metabolism due to general
or local metabolic changes
3. Direct or reflex effects on that part of CNS
concerned with regulation of consciousness
4. Psychic mechanisms

• The human brain, accounts for only 2% of body
mass but uses 20% of oxygen and 65% of total
glucose.
• Approx 20% of circulation per minute must reach
brain
• At any moment of time blood circulation of brain
contains 7mL of oxygen, an amount sufficient to
supply the brain’s requirement for 10 seconds

• With loss of consciousness there is
generalized decreased skeletal muscle
tone, same occurs with tongue which
looses tone , falls back into
hypopharynx, producing airway
obstruction.
• Relief of this obstruction will thus
become the primary objective of
resuscitation of the unconscious patient.

Management - BLS
Step 1: Recognition of unconsciousness - 3
criteria
1. Lack of response to sensory
stimulus (AVPU).
2. Loss of protective reflexes.
3. Inability to maintain patent
airway.
Step 2: Call for assistance
Step 3: Position patient
 Supine position with feet 10-15
degree angle
 Avoid Trendelenburg position -
restricts respiratory movements.
 In pregnants left lateral position.

Step 4: Assess and open airway.
1. Remove pillow or any head
support
2. Head tilt
 Head tilt
 Head tilt – neck lift
 Head tilt – chin lift
3. Jaw thrust (If needed)

Step 5: Assess airway patency and
breathing
 Determined by looking,
listening, and feeling
Remove foreign material in the
airway.

Step 6: Artificial ventilation (If
needed)
 May be provided by one of 3
ways
1. Exhaled air ventilation
2. Atmospheric (ambient) air
ventilation
3. Oxygen- enriched ventilation
 Exhaled air ventilation - 16% to
18%inspired oxygen
Mouth to mouth breathing
Mouth to nose breathing
Pocket mask breathing
Adults 12 times per minute ( once
every 5 seconds)
Child 15 times per minute (once every
4 seconds)
Infants 20 per minute ( once every 3
seconds)

Atmospheric air ventilation - 21%
of oxygen
Self inflating bag-valve-mask
devices
Ambu bag
Pulmonary manual resuscitator
Artificial airways.

Oxygen- enriched ventilation
Demand-valve mask

Step 7: Assess circulation
Monitoring
BP
Heart rate

Step 8: Definitive management of
unconsciousness
According the cause for
unconsciousness

• A sudden, transient loss of consciousness
that is usually secondary to a period of
cerebral ischemia.
Synonyms:
Atrial bradycardia
Benign faint
Neurogenic syncope
Psychogenic syncope
Simple faint
Swoon
Vasodepressor syncope
Vasovagal syncope
Prick shock

 Predisposing factors:
1. Psychogenic factors – fright, anxiety,
stress, unwelcome news, pain, sight of
blood or surgical instruments etc
2. Nonpsychogenic factors – sitting
upright, standing, hunger, missed meal,
exhaustion, poor physical condition and
hot, humid, crowded environment.
 Men have higher incidence

 Prevention:
Proper positioning of the patient
Relief of anxiety
Medical history questionnaire

• Clinical manifestations:
 3 definite phases
1. Presyncope
2. Syncope
3. Postsyncope

Presyncope: signs and
symptoms
Early
 Feeling of warmth
 Pallor
 Heavy
perspiration
 Feeling “bad” or
“faint”
 Nausea
 BP approx at
baseline
 Tachycardia
Late
 Pupillary dilation
 Yawning
 Hyperpnea
 Coldness of hands
 Hypotension
 Bradycardia
 Visual disturbances
 Dizziness
 Loss of consciousness

 Syncope:
• Breathing irregular, jerky and gasping; may be
shallow, and scarcely perceptible; or it may
cease entirely (respiratory arrest).
• Pupils dilate; death like appearance.
• Convulsive movements or muscle twitching of
the hands, legs or facial muscles.
• Bradycardia continues, a heart rate of less
than 50 beats per minute is not uncommon.
• In severe episodes periods of complete
ventricular asystole have been recorded even
in normal healthy persons.

• BP drops extremely low (30/15 mm of Hg)
• Pulse weak and thready.
• With loss of consciousness – generalized
muscular relaxation → partial or complete
airway obstruction.
• Fecal incontinence may occur, particularly
with systolic BP below 70 mm of Hg.
• If unconsciousness persists more than 5
minutes after management, or complete
clinical recovery is not got in 15-20 min other
cause should be considered

Postsyncope:
• Pallor, nausea, weakness and sweating
for few minutes to many hours.
• Short period of mental confusion or
disorientation.
• BP and heart rate returns to normal
slowly.
• Tendency for an second episode if
allowed the patient to stand or sit too
soon.

Pathophysiology
Stress
Release of catecholamines
Changes in tissue blood perfusion; decreased peripheral vascular
resistance, increased blood flow to tissues (skeletal muscle)
leads to pooling of blood
↓circulatory volume
↓cerebral blood flow
syncope

↓BP
Compensatory mechanisms are activated
• Baroreceptors – constrict peripheral vessels
• Carotid and aortic reflexes – ↑Heart rate
↑ venous return to heart, ↑ CO and ↑ heart rate
(during early presyncopal period)
These mechanisms soon fail due to fatigue – reflex Bradycardia
Further ↓BP

Management:
• Presyncope
• Stop the procedure
• Patient placed supine with legs slightly elevated
• Muscular movements, aids the return of blood from
periphery
• If thought necessary, oxygen may be administered,
using full-face mask or nasal hood.
• An ammonia ampule may be crushed and held
under patient’s nose.
• Postponement of dental procedure.

Syncope
• Should follow the basic management
steps
Step 1 to step 7
• Definitive management
1. Loosening of binding clothes ties, collar, belts
etc)
2. Respiratory stimulant aromatic ammonia
crushed and held near nose.
3. Cold towel can be placed on the patient’s
forehead
4. Blankets can be placed over the patient if they
complain of feeling cold or is shivering.

5. If bradycardia persists, an
anticholinergic atropine (0.5 – 1.0 mg
IM or IV) may be administered and
repeated if needed after 5 minutes to a
maximum of 3 mg..
6. It may not be prudent to allow patient
to leave the office unescorted.

Differential
Diagnosis
 Anxiety attacks
 Hyperventilation syndrome
 Hypoglycemia
 Epilepsy

• Also called as orthostatic hypotension, is the second
leading cause of transient loss of consciousness.
• Def: fall in systolic pressure of 20mm of Hg or
more upon standing.
Postural Hypotension results from a failure of
baroreceptor –reflex -mediated increase in
peripheral vascular resistance in response to
positional changes.

Predisposing Factors
 Drug administration
 Prolonged periods of recumbancy and
covalescence
 Inadequate postural reflexes
 Pregnancy (later stages)
 Advanced age
 Venous defect in the legs
 Postsympatectomy for “essential
hypertension”
 barre syndrome or multiple sclerosis

 Addison’s disease
 Physical exhaustion
 Starvation
 Chronic Postural Hypotension [Shy –
Drager syndrome (multi system
atrophy)]
 CNS lesions
 Demyelination of small fibers as in
Guillian-

• Criteria for postural hypotension.
1. Symptomology develops on standing
2. Increase in standing pulse atleast 30
beats per minute
3. Decrease in standing systolic BP atleast
25 mm of Hg
4. Decrease in standing diastolic BP
atleast 10 mm of Hg

• Prevention:
• Proper medical history questionnaire
• Physical examination
Recording both supine and standing BP
• In pregnant, simply turning the
patient to her left is enough: by
placing a pillow under the right
buttock when on dental chair.

Management
• Should follow the basic management steps
• Definitive management
Usually resolve with the above steps.
If these does not elevate the BP to acceptable levels,
Establish IV line and administer rapid infusion of 500 ml
of Ringer’s lactate
If the heart rate is less than 60 ATROPINE is given
If heart rate normal but BP reduced EPHEDRINE, a
vasopressor which acts both on α & β adrenergic receptors
is preferred
It is important that changes in position from supine to the
erect be made slowly.
Recheck the BP before the patient leaves the office.

• Differential Diagnosis
 Hemorrhagic shock
 Renal failure and dialysis (altered
sympathetic regulation)
 Acute congestive cardiac failure
 Cardiogenic shock

• A condition first recognized by Addison
in 1844.It is an uncommon, potentially
life threatening and readily treatable
condition
• Cortisol one of the glucocorticoid a
product of the adrenal cortex helps the
body adapt to stress and is thereby
extremely vital to survival.

• Hypersecretion of cortisol leads to
Cushing's syndrome characterized by
“buffalo hump” on the back ,raised BP,
eosinopenia, lymphopenia. Its not a
life-threatening situation
• Cortisol deficiency on the other hand,
may lead to relatively rapid onset of
clinical symptoms, quite possibly
patient’s death.

• Primary adrenocortical insufficiency
is called Addison’s disease, an
insidious and usually progressive
disease.
• Secondary form of the disease is
usually produced by administration
of exogenous glucocorticosteroids to a
patient with functional adrenal
glands.

• In development of acute adrenal crisis,
secondary adrenal insufficiency is
today a much greater potential treat
than is Addison's disease.
• Acute adrenal insufficiency is a true
medical emergency . Death is usually
the result of peripheral vascular
collapse (shock) and ventricular
asystole (cardiac arrest).

Predisposing factors
• The major predisposing factor in all cases is the lack of
glucocorticosteroid hormones, which develops through
the following mechanisms.
1. Sudden withdrawal of steroid in patient with Addison's
disease.
2. Sudden withdrawal of steroid in a patient with normal
adrenal cortices but on exogenous steroid administration.
3. Following stress, such as physiologic or psychologic stress.
4. Following bilateral adrenalectomy.
5. Sudden destruction of pituitary gland.
6. Injury to both adrenal gland by trauma, hemorrhage,
infection, thrombosis or tumor.

Prevention
Acute adrenal insufficiency is best
managed by its prevention which
is based on
1. Medical history questionnaire.
2. Dialogue history.
RULE OF TWOS
1. In a dose of 20 mg or more of
cortisone or equivalent daily.
2. Via the oral or parental route for
a continuous period of 2 weeks
or longer.
3. Within 2 years.
1. Steroid used in the management
2. Dose of steroid
3. Route of administration
4. Frequency of administration
5. Length of time elapsed since
the drug therapy was terminated

Clinical Manifestation
CHRONIC
Weakness and fatigue
Anorexia
Weight loss
Hyperpigmentation
Nausea vomiting
Salt carving
Constipation
Vitiligo
Auricular calcification
ACUTE
Syncope
Diarrhea
Musculoskeletal complaints
Abdominal pain, cramping
Hypotension
lethargy
Confusion
Psychosis

Acute episode will be marked most notably by
 Progressively severe mental confusion
 Intense abdominal pain
 Low back pain
 Progressive deterioration of cardiovascular system
 Loss of consciousness
 Onset of coma
 If unmanaged - death

Management
• The patient with acute adrenal
insufficiency is an immediate
danger because of
Glucocorticoid deficiency
Depletion of extracellular fluid
Hyperkalemia
• Treatment is based on the prompt
correction of these conditions.

• Conscious patient
1. Terminal dental therapy
2. Position the patient ( supine )
3. Monitor vital signs
4. Summon medical assistance ( patients physician )
5. Oxygen
6. Administer glucocorticosteroids
i. If a known adrenal insufficiency patient
administer 100 mg of hydrocortisone sodium
succinate (IV or IM) and repeat every 6 – 8 hours
ii. If no prior history, dexamethasone phosphate 4 mg
IV every 6 – 8 hours until diagnosis is confirmed
by ACTH stimulation test.

Additional management
1. 1 liter of normal saline infused in first
hour
2. 5 % dextrose added next to help combat
hypoglycemia
3. If absence of IV line 1 – 2 mg of
glucagon should be administered IM

• Unconscious patient
1. Recognize unconsciousness
2. Position the patient
3. Provide BLS

Definitive management
1. Oxygen
2. There will be no response by
patient to ammonia
3. Administer 100 mg hydrocortisone
IV or IM should be injected over
30 seconds
4. 1 liter of normal saline infused in
first hour
5. 5% dextrose added next to help
combat hypoglycemia

Chest thrust:
- for responsive pregnant or obese
victim
- hand position and technique:
same as
chest compression

Finger sweep & tongue-jaw lift:
- for unresponsive/unconscious victim
- not indicated for responsive or seizure
patient
-“tongue-jaw lift” maneuver

EMERGENCY
CRICOTHYROIDOTOMY
• DEFINITION -
– An emergency surgical procedure where an
incision is made through the skin and
cricothyroid membrane which allows for the
placement of an endotracheal tube into the
trachea when airway control is not possible by
other methods.

ADVANTAGES OF EMERGENCY
CRICOTHYROIDOTOMY
• Provides a definitive airway for ventilating
the patient
• Can be performed quickly and has few
complications associated with the procedure

For an emergency cricothyroidotomy the laryngeal
prominence and cricoid cartilages are palpated and
entry is made through the median cricothyroid
ligament.
This procedure is preferable to a tracheotomy as there
are no large midline vessels in front of the median
cricothyroid ligament whereas there are in front of the
superior part of the trachea.

ANATOMICAL LANDMARKS AND
STRUCTURES-Closeup

Anterior view of the larynx to show the median
cricothyroid ligament.
1. Thyroid lamina.
2. Arch of cricoid cartilage.
3. Median cricothyroid ligament (cut here)

Required Equipment
• #10 or 11 Scalpel
• Endotracheal Tube
• 10 cc Syringe
• Stethoscope
• Curved Kelly
Hemostat, Straight
will work
• Ambu-bag
• Sterile Dressing
• Vaseline /
Petroleum Gauze
• Betadine or
Alcohol Wipes

PROCEDURAL STEPS FOR EMERGENCY
CRICOTHYROIDOTOMY
• Locate the cricothyroid membrane
• Stabilize the thyroid cartilage using your
non-dominant hand
• Swab the incision site with alcohol or
betadine swabs

• Make a vertical incision through the skin
approximately 2-5 cm (1 inch+) long over
the cricothyroid membrane
• Visualize the cricothyroid membrane

• Make a transverse
incision into the
cricothyroid
membrane
– DO NOT make the
incision more than
1/2 inch deep or
you may perforate
the esophagus

• Insert the Curved Kelly Hemostat into the
incision and blunt dissect the incision (turn
the Curved Kelly Hemostat 90 degrees to
open up the incision)
• If you only have a straight hemostat, use it.

• Insert the endotracheal tube (adult 6.5 or
smaller, Ped ? whatever will fit), into
the incision, directing the tube distally
down the trachea

Correction of respiratory alkalosis.
Not to administer O2.

Adm O2 and Albuterol inhaler.
Hydrocortisone sodiumsuccinate 100mg
IV.

• Paroxysmal disorder of cerebral
function characterized by an attack
involving changes in the state of
cosciousness , motor activity or
sensory phenomena.
• Convulsion and seizure are
synonymous

• Epilepsy: a chronic brain disorder of
various etiologies characterised by
recurrent seizures due to excessive
discharge of cerebral neurons
• Status epilepticus: condition in which
seizures are so prolonged that
recovery does not occur in between
attacks

• Tonic: a sustained muscular contraction;
patient appears rigid or stiff during the
tonic phase of a seizure
• Clonic: intermittent muscular
contractions and relaxation; the clonic
phase being the actual convulsive
portion

• Although all seizures are significant,
generalised are clinically more
dangerous in the dental office due to
their greater potential for injury and
post seizure complications

Predisposing
factors:
• Anxiety
• Hunger
• Menstruation
• Alcohol
• External stimuli, flashing lights etc
• Non compliance with medications

Signs & Symptoms (Grand mal)
Warning cry
Immediate loss of consciousness
Rigid (tonic phase)
Widespread jerking (clonic
phase)
Vomiting
Flaccid after a few minutes
Consciousness is regained after a
variable period
Patient may remain confused

References
•Medical Emergencies in Dental Office – Stanley F Malamed
•Contemporary Oral & Maxillofacial Surgery- Peterson
•Trauma Skills Course Manual from IDST Ghaziabad
•Internet references – Google . com

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