MedEmerg-Midterm-Ricker

• Stress is the most common cause of a
medical emergency
• Injections cause stress
•  Injections cause medical emergencies

• Stress predisposes anyone to a medical
emergency
• Administration of local anesthesia is the most
stressful procedure performed in the dental
office
• > 50% of medical emergencies in a dental
clinic occur during administration of local
anesthesia

Prevention!
Prevention!!
Prevention!!!

Know Your Patient!!!
Know Your Patient!!!
Know Your Patient!!!

Physical Evaluation

• Medical History Questionnaire
• Vital Signs
• Visual Inspection
• Additional (focused) evaluation
Medical History Questionnaire

• Review UNC SOD Health History Questionnaire
• Ask delving questions about any positive
response.
• I always ask:
“are you taking any medications?”
“are you allergic to anything?”
“are you under a physicians care for
anything?”
Vital Signs

• Blood Pressure
• Heart Rate and Rhythm
• Respiratory Rate
• Temperature
• Height
• Weight

• Patient seated, upright
• Patient’s arm relaxed, slightly
flexed, supported on a firm
surface, at the level of the heart
• Patient should relax in chair at
least 5 minutes before BP is
recorded
• Proper cuff size
• Cuff properly positioned


• If measuring manually
– Stethoscope positioned properly
– Lower margin of cuff 1” above antecubital
fossa
– Release pressure gradually (2-3mm
Hg/second)
– Pulse first heard, then muffled, then
disappears

Machine
• Manually
– Radial
– Brachial (infant)
– Carotid
– Femoral

Respiratory Rate
– Surreptitiously
– 30-60 sec
• Temperature
– Digital, tempa-dot, skin, ear
– Usually not done unless you suspect fever or infection
• Height and Weight
– Okay to ask patient
– Measure if patient is obviously wrong
– Measure if patient will be sedated or given a lot of drugs

• General appearance
• Level of apprehension
• Posture, body movements, speech
• Nondental odors on breath
– Diabetes, uremia, alcohol
• Skin
– Diabetes, hyperthyroid, apprehensive
– Pallor, cyanosis, flushed, jaundiced
• JVD, Clubbing, Swollen ankles, Exopthalmos

• Ask more questions about each of the
medical conditions identified in the
Medical History Questionnaire
(sometimes you can learn a lot of
medicine from a well informed patient)
• Ask more questions about each of the
medical conditions you suspect from your
physical exam

– Listen to heart and lungs
– ECG
– PFTs
– CBC, Chem 7
– UA
– CXR

• Heightened anxiety and fear of
dentistry
• Can lead to the acute
exacerbation of medical problems
– Angina, seizures, asthma
• Can lead to stress related
problems
– Hyperventilation, vasodepressor
syncope


• Medical history questionnaire
– Do you have fainting spells or seizures
– Have you had any serious trouble associated with
any previous dental treatment
• Anxiety questionnaire
• Art of observation

• In Reception Area
– Questions receptionist regarding injections,
sedation
– Nervous conversations with other patients in
area
– Hx of emergency dental care only
– Hx of canceled appointments for nonemergency
tx
– Cold, sweaty palms


• In Dental Chair
– Unnaturally stiff posture
– Nervous play with tissue or handkerchief
– White-knuckle syndrome
– Perspiration on forehead and hands
– Over willingness to cooperate with doctor
– Quick answers
– BP, P, trembling, sweat, dilated pupils

• Can pt physically and psychologically
tolerate stress of treatment in relative
safety?
• Is pt at a greater risk of morbidity or
mortality than normal during treatment?
• If pt is a greater risk, what treatment
modification should be used to minimize the
risk during the treatment?
• Is the risk too great for the patient to be
managed safely in the dental office?

Valuable to determination risk before dental procedures
ASA I: normal healthy pt without systemic ds
ASA II: pt with mild systemic ds
ASA III: pt with severe systemic ds that limits activity but is
not incapacitating
ASA IV: pt with an incapacitating systemic ds that is a
constant threat to life
ASA V: a moribund pt not expected to survive 24 hrs with or
without an operation
ASA E: emergency operation, any variety (e.g.. ASA E-III)

• Complete the pt’s dental and physical
evaluation
• Be prepared to discuss fully with the pt’s
physician the proposed dental tx
• Very important to determine the pt’s
ability to tolerate in relative safety the
stress involved in proposed dental tx



• Telephone - if in a hurry
– Receptionist: your name and pt’s name
– Physician:
• Summarize your evaluation, dx, and proposed plan of
treatment
• Ask for additional information and suggestions
• Discuss any problems
– Write a complete report of phoncon in record
– F/U with written letter

• Stress
– Physiologic: pain, strenuous exercise
– Psychologic: anxiety, fear
• Adrenal medulla  epi, norepi
• Epi, norepi  cardiovascular workload
• Cardiovascular work  angina, dysrythmia, MI
• Lungs  bronchospasm, pulmonary edema
• CNS  stroke, seizure

• Premedication?
• Appointment scheduling
– Tolerate stress best when well rested
– Usually morning
• Minimize waiting time in reception area
• Record VS
– Both preop and postop
– Compare to VS from earlier visit

• Unconsciousness - a lack of response to sensory
stimulation
• Syncope – sudden, transient (<30 minutes) LOC
• Regardless of the cause management remains the
same
• Position
• Airway
• Breathing
• Circulation
• Definitive Care

• 30+ causes
• Neurogenic, Vascular, Endocrinopathies,
Toxins/Drugs, Psychogenic, Cardiogenic, Disorders of
Oxygenation
• For you, the emergency treatment is more
important than the diagnosis

• Stress
• Primary cause in dental setting
• Impaired physical status
• ASA III or IV
• Administration or ingestion of drugs
• Analgesics
• Antianxiety agents

• Most commonly used drug in dentistry
• >1 million carpules/day in USA
• Major predisposing role in syncope
• Overwhelming majority stress induced
• Rarely overdose or allergy

• Vasodepressor syncope Most common
• Drug administration/ingestion Common
• Orthostatic hypotension Less common
• Epilepsy Less common
• Hypoglycemic reax Less common
• Acute adrenal insufficiency Rare
• Acute allergic reax Rare
• Acute MI Rare
• CVA Rare
• Hyperglycemic reax Rare
• Hyperventilation Rare

• Thorough pretreatment medical and dental
examination
• Medical disabilities
• Psychological disabilities
• Stress reduction protocol
• Patient in supine (or feet 10°) position
• Prevents cerebral anoxia

• Inadequate delivery of blood/O2 to the brain
• Acute adrenal insufficiency; Hypotension
• Orthostatic hypotension; Vasodepressor syncope
• Systemic or local metabolic deficiencies
• Acute allergic reax; Drug ingestion/administration
• [glu]; [glu]; Hyperventilation
• Direct or reflex effects on the nervous system
• CVA; Convulsive episode
• Psychic mechanisms
• Hyperventilation; Vasodepressor syncope

• Dilation of the peripheral arterioles
• Failure of normal peripheral vasoconstrictor
activity (orthostatic hypotension)
• A sharp drop in cardiac output (from heart ds,
dysrhythmias, or decreased blood volume)
• Constriction of cerebral vessels as CO2 is lost
through hyperventilation
• Occlusion or narrowing of the internal carotid or
other arteries to the brain
• Life threatening ventricular dysrhythmias

• Oxidation of glucose provides most energy
• 2% of body mass
• Uses 20% of O2 consumed by body
• Uses 65% of Glucose consumed by body
• Requires continuous supply of both glucose and O2
• Anoxia
• Unconscious <10 seconds
• Permanent brain damage 4-6 minutes
• Cardiac arrest 5-10 minutes

• AKA vasovagal syncope or common faint
• Frequently observed
• >50% of all medical emergencies in dental office
• Usually benign and self-limiting
• 25,000 faints, all recovered
• Potentially life threatening
• Airway obstruction
• Injury from fall

• Psychogenic factors
• Fright
• Anxiety
• Emotional stress
• Receipt of unwelcome
news
• Pain, especially sudden
and unexpected pain
• Sight of blood or surgical
instruments (e.g.. Local
anesthetic syringe)

Nonpsychogenic factors
• Upright or standing
posture
• Hunger
• Exhaustion
• Poor physical condition
• Hot, humid, crowded
environment
• Male gender
• Age 16 - 35

• Signs and symptoms usually develop rapidly
• Actual LOC does not occur immediately
• Presyncope
• Syncope
• Postsyncope (Recovery)

• Early
• Feeling of warmth
• Pale or ashen-gray skin
• Heavy perspiration
• C/O “feeling bad” or
“feeling faint”
• Nausea
• BP at baseline or lower
• tachycardia

• Late
• Pupillary dilation
• Yawning
• Hyperpnea
• Cold hands and feet
• Hypotension
• Bradycardia
• Visual disturbances
• Dizziness
• LOC

• Breathing irregular, shallow, or apnea
• Pupils dilate
• Deathlike appearance
• Convulsive movements; muscular twitching
• Bradycardia (<50 to asystole)
• BP (30/15)
• Pulse weak/thready
• Muscle relaxation airway obstruction and/or
incontinence
• Usually lasts < 5 minutes

• Rapid recovery after proper positioning
• May exhibit (minutes to hours)
• Pallor
• Nausea
• Weakness
• Sweating
• Confusion or disorientation
• Vital signs slowly return to normal
• Tendency to faint again persists for many hours

• Stress leads to “fight or flight” response
• Epi and Norepi secreted
• Changes tissue perfusion for increased muscular activity
• If muscles are used blood flows back to heart thus
maintaining BP and cerebral perfusion
• If muscles not used (e.g.. sitting in a dental chair and
“taking it like a man”) blood pools in peripheral vessels
• Compensatory mechanisms activated but rapidly
fatigue
• Baroreceptors, Carotid sinus, Aortic sinus
• Reflex bradycardia leads to CO decrease followed by BPdecrease
• BP decrease + P decrease = cerebral perfusion decrease = LOC

• Assess consciousness
• Activate office emergency system
• Position patient supine with feet elevated 10°
• A – B – C
• Initiate Definitive Care
• O2, VS, NH3,
• Atropine if bradycardia persists

• Postsyncopal Recovery
• Postpone further dental
treatment
• Determine precipitating
factors



• Delayed Recovery
• Activate EMS
• Determine precipitating
factors

• AKA postural hypotension
• 2nd leading cause of transient LOC (syncope) in a
dental setting
• Not associated with fear or anxiety
• Syncope occurs when patient assumes upright
position
• Failure of baroreceptor reflexes to mediate
peripheral vascular resistance

• Dehydration
• Drugs
• Prolonged recumbancy
• Age
• Pregnancy
• Varicose veins
• Addison’s Ds (adrenocortical insufficiency)

• Medical History questionnaire
• Medications
• Hx of fainting, seizures
• Physical Examination
• Vital signs
• Palpable pulse
• Nail beds


• Dental Therapy Considerations
• Slowly reposition patient upright
• Stand nearby as the patient stands after tx
• Wheelchair to car after sedation

• Symptoms develop when pt stands
• Standing Pincreases >30 beats/minute
• Standing systolic BP drops >25 mm Hg
• Standing diastolic BP drops >10 mm Hg
• LOC

• Normal reactions to change from supine
• Baroreceptors respond to arteriolar constriction and P increases
• Reflex venous constriction
• Muscle tone and contraction increases (legs, abdomen)
• Respiration increases - aids return of blood to right heart
• Neurohormonal secretions increases (ADH, renin, etc)
• Failure of any of the above
• Rapid BP drop + No change in P = Orthostatic Hypotension

• Assess consciousness
• Activate office emergency system
• Position: supine, feet up 10
• A – B – C
• Definitive care
• O2, VS
• Slowly reposition chair, discharge pt
• Summon EMS if episode continues

• AKA – adrenal crisis
• 1° - Addison’s Ds
• 2° - Atrophy of adrenal cortex
• Adrenal cortex – cortisol helps manage stress
• Uncommon
• Potentially life threatening
• Readily treatable
• Hypersecretion is Cushing’s Ds

• Addison’s Ds
• Sudden withdrawal of steroids after prolonged
exogenous administration
• Stress – physiologic or psychologic
• Bilateral adrenalectomy
• Sudden destruction of pituitary gland
• Injury to both adrenal glands

• Medical hx questionnaire and dialogue
• Rule of twos
• 20mg of exogenous cortisol (or equivalent)
• 2 weeks or longer
• Within the last two years

• Lethargy, extreme fatigue, weakness
• Anorexia, weight loss
• Hyperpigmentation (palms, soles, elbows, knees,
buccal mucosa, old scars)
• Hypotension (110/70)
• Nausea, vomiting


• In dental setting
• Progressive mental confusion
• Pain in abdomen/back/legs
• Cardiovascular deterioration
• Coma
• Mortality usually secondary to hypotension or
hypoglycemia

• Addison’s Ds (primary) patients have destruction of
the adrenal cortex
• Clinical manifestations usually do not develop until
90% of the cortex is gone
• Require lifelong exogenous cortisol
• Unable to respond to ACTH


• Secondary adrenal insufficiency patients receive
exogenous steroids for multiple medical therapies
• Exogenous steroids cause feedback inhibition of the
pituitary (ACTH) and adrenal gland atrophy

• Remember rule of twos
• Prevent acute problems by providing supplemental
steroid replacement of at least double the daily dose
of their normal regimen.
• Remember to taper afterwards

• A sudden, complete or partial loss of airway patency
that interferes with respiration
• Acute emergency – brain cell death in 4-5 minutes
• Dental profession lends itself to foreign objects being
lodged in the upper airway

• Self evident
• Usually aspiration into the right mainstem bronchus
• May lodge in the larynx (narrowest) and cause
complete obstruction
• Respiratory arrest  cardiac arrest  cerebral
ischemia  death

• Universal choking sign
• Can’t speak, breath, cough
• Panic
• Cyanosis, costal and sternal retractions
• Crowing noise in partial obstruction
• In 3-4 minutes respiratory effort, BP, and heart
rate drop; LOC
• In 8-10 minutes full cardiac arrest

• Rubber dam
• Gauze throat screen
• Attach floss to instruments that can be aspirated
(e.g. rubber dam clamp)
• Alert dental assistant
• Good suction
• Patient position
• Magill forceps, Russian forceps

When object falls back into the oropharynx and
airway is compromised
• Tilt patient back into a head down position
• Retrieve it if you can see it
• Finger sweep (not in infants)
• Encourage coughing
• Back blows, manual thrusts
• Heimlich maneuver
• Head tilt, jaw thrust
• Surgical airway (call EMS)


• Surgical airway
• Tracheostomy performed in OR or ED
• Cricothyrotomy is fastest way into the airway
• Contraindicated in children
• Puncture through the cricothyroid membrane to restore
ventilation


• When object disappears into oropharynx and airway
is not compromised
• Immediately send patient for CXR and KUB
• Appropriate medical consults
• F/U radiographs in 2-3 days to insure the object has
passed completely through GI tract

• Ventilation in excess of what is required to maintain
normal PaO2 and PaCO2
• Produced by an increase in frequency and/or depth of
respiration
• AKA Vapors, effort syndrome, soldier’s heart
• Commonly as a result of extreme anxiety in the dental
office

• Anxiety (fight or flight)
• Respiratory alkalosis (decrease in CO2)
• increased catecholamines (chest tightness)
• decreased ionized calcium = neuromuscular irritability

• Anxiety prone
• Fear of dental therapy

• Unaware of hyperventilation
• Complaints of chest tightness, lightheadedness,
palpitations, tingling or paresthesia of the extremities
or peri-oral areas
• Muscular twitching
• Syncope

• Reduce anxiety
• Stop procedure, sit patient upright, control breathing
• Cup hands on face to rebreathe air (increase CO2)
• Do not give O2 (may worsen condition)
• Administer benzodiazepines if necessary (rarely
required)

• Talk to your patients about their fears of dental tx
• Reduce anxiety and stress
• Check VS before starting dental tx

• Reactive airway ds
• Constriction of the distal airway in response to atopic
challenge
• Most chronic ds of childhood
• Almost 10% of children have the ds and the incidence
is rising

• In most cases a type 1 immune reaction which is IgE
mediated (extrinsic)
• Causes mast cell degranulation with release of
inflammatory mediators and subsequent
bronchoconstriction
• Intrinsic asthma usually in adults caused by
environmental pollution, respiratory infection
• Status Asthmaticus / bronchospasm

• History of the disease
• Stress
• Psychological factors
• Drug reaction ( PCN)

• May occur gradually or rapidly
• Thickness in chest followed by coughing
• Sputum production with wheezing and muscle
retraction
• Air hunger and apprehension/anxiety rise
• BP and P rise, dyspnea increases
• Termination heralded by intense coughing and
expectoration of mucous plug followed by relief

• Stop procedure, sit pt upright with arms forward
• Reduce anxiety, remove kids from tx room
• Administer patient’s bronchodilator
• Administer B2 agonist drugs (epinephrine,
isoproterenol, albuterol) by inhalation
• In severe attack: O2, epi injection IM/SC (0.3mg), EMS

• Good medical hx and dialogue
• Reduce anxiety
• Sedation
• Nitrous Oxide is safe in asthmatic patient, does not
irritate the respiratory mucosa

• Most common cause of acute pulmonary edema is
congestive heart failure
• Left ventricular failure leads to right ventricular
failure and CHF
• Pulmonary edema is marked by an excess of serous
fluid in the alveolar/interstitial spaces of the lungs
which causes extreme difficulty in breathing

• An increase in afterload (e.g. HTN) causes
hypertrophy, progresses to dilation as failure
continues
• Dyspnea on exercise, hypervolemia secondary to
decreased GFR and sodium retention
• Hypervolemia increases capillary hydrostatic
pressure and edema of the extremities starts
• In the supine position fluid is forced centrally
causing increased atrial pressures which increases
pulmonary pressure and fluid escapes into the
alveoli

• Physical stress
• Psychological stress
• Salty meals
• Noncompliance with medications
• Infection
• Orthopnea is positional dyspnea

• Onset is acute
• Dyspnea and orthopnea present
• Feeling of suffocation and anxiety
• Chest pressure, tachypnea, cough
• Cyanosis, frothy bloody saliva, panic
• Respiratory arrest, cardiac arrest, death

• Stop procedure
• Position patient upright, EMS
• Reduce anxiety, monitor airway
• Bloody, bloodless phlebotomy with 3 tourniquets
• Use vasodilator (e.g. NTG) to reduce preload

• Inappropriate hypergylcemia from absolute
deficiency or reduced effectiveness of insulin
• Approximately 6% of U.S. population
• Incidence is increasing
• Disease process is primarily microangiopathic
with end organ damage
• Type 1 and Type 2

-after eating meal blood glucose rises
-blood glucose remains elevated in the diabetic
-glucose appears in urine after 180mg/dl
(glycosuria)
-through osmosis, loss of water and electrolytes
-dehydration ensues (polyuria,polydipsia)
-weight loss as a result of water loss and
skeletal muscle breakdown
-elevated glucose is unusable and free fatty
acids are broken down to ketones for fuel
(ketoacidosis – fruity smell on breath)
-as ketogenesis continues, metabolic acidosis
ensues (cardiac depression)
-metabolic acidosis causes compensatory
respiratory alkalosis (Kussmaul’s breathing –
slow deep breaths)
-hypergylcemic coma ensues (time =48hrs)

-most common acute complication
-blood glucose below 50mg/dl in adults (40mg/dl)
in children
-as blood glucose drops this alters normal
functioning of the cerebral cortex
-increased epinephrine secretion causes elevated
blood pressures, sweating, tachycardia
-hypoglycemic coma

-genetic disorder
-iatrogenic causes (surgery,cancer,etc.)

-generally diagnosed by FBG
-florid appearance, hot and dry skin (dehydration)
-polydipsia, polyuria, polyphagia
-Kussmaul’s respirations
-fruity odor to breath (ketoacidosis)
-tachycardia, hypotension, coma

-much more common
-diminished cerebral function, lethargy
-hunger, nausea
-sweating, tachycardia, piloerection, anxiety
-cold, wet skin
-loss of consciousness and seizure activity
-irreversible cerebral damage

-stop procedure
-supine position with legs elevated
-support airway, breathing
-EMS
-start IV NS (D5W if not sure), O2
-do not give insulin!

-stop procedure
-sit upright (or whatever makes pt comfortable)
-support airway, breathing
-administer oral carbohydrates
-if loss of consciousness, notify EMS and start
IV/IM glucagon or 50% dextrose

-No modifications usually necessary with Type 2
-Advise Type 1 patients to eat normal meals and use
insulin as prescribed for minor procedure
-Consult physician for procedures that impair
inability to eat post-operatively to modify the insulin
regimen (e.g. full mouth extraction, denture related
procedures)
-Antibiotics

• Produces and secretes three essential hormones for
regulation of biochemical activity
• Thyroxin (T4), Triiodothyroxine (T3), calcitonin
• Hypothyroid/hyperthyroid/euthyroid
• Hypothyroidism – deficient state of thyroid
hormones (cretinism in children, myxedema as an
adult) Myxedema coma mortality 50%
• Hyperthyroidism – excess state of thyroid hormones
(thyrotoxicosis, Grave’s disease) Thyroid storm is life-
threatening, high mortality

-in effect body functions and metabolism slow
down
-mucopolysaccarides and mucoproteins infiltrate
the skin leading to puffy non-pitting edema
(myxedema)
-cardiac enlargement, leads to effusions, cardiac
and pulmonary failure
-coma is the end point secondary to hypothermia,
hypoglycemia, CO2 retention, hypotension,
hypoxia

-elevation of body basal metabolic rate and
increased energy consumption
-increased heart rate and cardiac irritability
-liver dysfunction is also present, jaundice may
appear, use medications cautiously
-thyroid storm characterized by hyperpyrexia (>
105 degrees F), dysrythmia, CHF, pulmonary
edema

a. Hypothyroidism- usually as a result of idiopathic
atrophy (autoimmune?), more common in females,
careful with CNS depressants (e.g. sedation)
b. Hyperthyroidism- Grave’s disease most common,
antibodies against fractions of the gland
(autoimmune), more common in females,
progression to storm is rare

-in children (cretinism) retarded physical and
mental development, flat nose, broad puffy face,
enlarged tongue
-in adult, cold intolerance, weight gain, fatigue,
non-pitting edema, hoarse voice, bradycardia
-myxedema coma: hypothermia, bradycardia,
hypotension, loss of consciousness

-nervousness, irritability, insomnia
-intolerance to heat, tremors, sweating, weight
loss with increased appetite, exopthalmos, staring
(Grave’s)
-increased blood pressure and tachycardia
-thyroid storm severe hypermetabolism with
hyperpyrexia (agitation, psychotic behavior)

-stop procedure
-position supine
-support airway/breathing
-EMS
-start IV with D5W
-hospitalization for management

-stop procedure
-position supine
-support airway/breathing
-EMS
-start IV D5W
-hospitalization for management

-euthyroid patients do not require modification
-hypothyroidism consult physician, careful with
CNS depressants
-hyperthyroidism consult physician, do not use
atropine (vagolytic), watch epinephrine dosage, do
not use gingival retraction cords that have been
treated with racemic epinephrine

• AKA “stroke”
• Third leading cause of death
• Most common form of brain disease
• Two major types hemorrhagic and occlusive
• Incidence is decreasing, but mortality is
increasing
• Rare in children but can occur

-cannot store O2 or glucose
-an occlusive event disrupts blood flow
-ischemia causes lactate to form which alters
vascular permeability and edema forms
-edema (causes headache) may force cerebral
hemispheres inferiorly and cause herniation into
the brain stem
-may cause ischemia and infarction of medulla
(brain stem and leads to death)

-rapid, more intense, higher mortality
-two pathways, aneurysms (dilated vessels) and
weakened vessel walls (HTN), both rupture
-once rupture occurs blood fills the cranium and
causes a mass effect and can cause herniation into
brain stem
-edema also develops and makes bad situation
worse

-HTN is the single most important risk factor
(Framingham)
-other factors include diabetes, cardiac
disease, hypercholesteremia
-dental office good model for elevated blood
pressure

-In TIA onset is abrupt and recovery rapid,
paresthesias and monocular blindness are
hallmarks
-In Infarction gradual onset, usually preceded by
TIA, mild headache, neurologic deficits
-In Hemorrhage, abrupt onset, violent headache
with vomiting, confusion, coma, and death (50%
lose consciousness 50% mortality)

-stop procedure
-position with head and chest up (decrease
intracranial blood flow and pressure)
-support airway/breathing
-notify EMS
-Start IV D5W, hospitalization

-management of hypertension
-post CVA patients should not have elective
dental therapy for 6 months
-watch for blood thinners
-judicious epinephrine use (retraction cord)
-dialogue with physician

• Transient alteration in brain function
characterized by abrupt onset of motor,
sensory and psychic symptoms
• Not usually a life threatening event except in
status epilepticus
• Have many underlying causes
• Prevention of injury to patient and supportive
therapy are essential

-epilepsy is not a disease but a symptom of brain
dysfunction
-increased neuronal permeability of Na+ and K+
-these hyperexcitable neurons have recurrent, high
frequency episodes of activity
-the action potential is propagated along neural
pathways and neighboring neurons are stimulated
to discharge (recruitment)
-the action potential then travels to the
subcortical areas or the thalamus and if the
discharge remains localized a partial seizure
develops, if it spreads additional neurons are
recruited and it becomes generalized
-increased cerebral blood flow and O2 use

a. Partial – involve specific area of brain, may have
illusions, hallucinations, motor activity, conscious
level is disturbed, amnesia
b. Grand Mal – AKA generalized tonic clonic seizure
- most common form of epilepsy
-lasts 2-3 minutes, post-ictal phase 5-15mins,
complete recovery several hours
c. Psychomotor – AKA temporal lobe epilepsy
essentially a partial seizure
-automatisms, apparently purposeful movement
(e.g. lip smacking)
d. Status epilepticus – unbreaking seizure
-in convulsive form 10% mortality
-most common precipitating factor is non
compliance with medication
e. Petit Mal – AKA absence seizure
-most common in children, usually progresses to
grand mal
-lasts up to 30 seconds, no movement
-multiple daily episodes
f. Jacksonian Seizure – A partial marching seizure
-loss of consciousness after midline crossed

- generalized metabolic/toxic disturbance
which increases neuronal excitation
-Cerebrovascular insufficiency
-triggers: sleep, menstrual cycle, fatigue,
flickering lights, stress

a. Partial – simple when consciousness is
unaltered, complex when it is altered
-aura (bad taste) followed by automatisms
-mild confusion amnesia
b. Petit Mal – sudden immobility and blank
stare, blinking and amnesia (lost time)
c. Grand Mal – prodromal phase of changes in
emotion reactivity (depression/anxiety)
-aura heralds seizure (taste, hallucination, visual
disturbance)
-loss of consciousness, falls (injury), jerking
movements, increase in blood pressure and heart
rate
-tonic/clonic activity
-in post ictal phase consciousness returns, muscular
flaccidity (bowel/bladder), amnesia, confusion

-stop procedure remove dental appliances
-position supine/floor
-EMS
-support airway/breathing
-soft suction as appropriate
-remove equipment/instruments
-pad head
-hold feet/hands
-reassure patient and monitor vitals
-IV/IM benzodiazepines in status (10mg valium)

-caring and discussing fears (embarrassment,
social rejection, higher rate of suicide)
-anxiety reduction
-sedation (nitrous) or oral (benzodiazepines)

• Signs and symptoms that result from overly
high drug concentration in the blood and
tissue
• In dentistry most commonly from local
anesthesia and epinephrine (also opioids and
sedatives)
• Carefully separate out “allergy” to local
anesthesia

- in the cardiac system local anesthesia is used to
manage arrhythmias
-in mild doses shortens action potential and
refractory period
-in moderate doses it decreases contractility,
decreases cardiac output and blood pressure
-in excessive doses causes massive peripheral
vasodilatation, and cardiac depression with cardiac
arrest

-extremely sensitive readily crosses blood brain
barrier (Na+ channels)
-possesses anticonvulsant property at mild dosages
-paresthesias of peri-oral tissues and agitation in
moderate doses from blockade of nerves
-as drug levels increase seizures develop followed
by CNS depression, respiratory arrest and cardiac
arrest

-age
-body weight (calculate)
-liver disease
-dose
-route of administration
-rate of injection
-vascularity at injection site
-use of vasoconstrictors (reduced toxicity)

-usually as a result of too large of a dose or rapid
intra-vascular injection
-in minimal to moderate cases usually excitatory –
confusion, slurred speech, tremor, nystagmus, blood
pressure, heart rate and respiratory rate increase,
tinnitus, numbness, drowsiness
-in severe cases, seizures, loss of consciousness,
respiratory depression, cardiac depression, death

-stop procedure
-position comfortably/O2
-support airway/breathing
-if seizure may give IV anticonvulsant
(diazepam), same protocol for seizure
-EMS, cardiac support if arrest

-almost all cases of overdose preventable
-calculate drug dose
-aspirate before injection
-beware of patients with extensive liver
disease
-use the minimal dose necessary to
adequately perform the procedure

-less commonly from local anesthesia
preparations than from gingival retraction
cord with racemic epinephrine
-anxiety, elevated blood pressure, rate,
palpitations,
-may precipitate arrhythmia or myocardial
infarction

• Hypersensitive state after exposure to an
allergen, re-exposure causes a heightened
capacity to react
• Type I (anaphylaxis), acute and life
threatening
• Type IV (delayed) local reaction through
chronic exposure

-sensitizing dose by initial exposure to allergen,
lymphocytes form IgE specific antibodies which
attach to mast cell and basophils
-challenge dose of allergen causes cross linking and
degranulation of mast cells and basophils which
release chemical mediators into the blood like
histamine (major) which cause capillary
permeability and vasodilatation = hypotension,
bronchoconstriction is also caused
-transudation of fluid and proteins causes
laryngeal edema, angioedema, mucous
secretion and dyspnea
-decreased vasomotor tone and peripheral
pooling of blood cause hypotension and
shock

-antibiotics (penicillin)
-analgesics (aspirin)
-antianxiety (barbiturates)
-local anesthetics (esters, paraben
preservative, sulfites)
-acrylic (dentures)

-the more intense the reaction, the more rapid the
onset of symptoms
-angioneurotic edema from topical anesthesia -
includes urticaria, erythema, swelling (may obstruct
airway)
-conjuctivitis, rhinitis, abdominal pain
-wheezing, coughing, dyspnea, hoarseness
-tachycardia, hypotension, cardiac arrest

-stop procedure
-position supine
-support airway/breathing
-EMS/O2
-Administer IM epi (0.3ml 1:1000)
-Administer histamine blocker/steroid

-obtain good history
-physician consultation
-formal allergy testing
-modify drug regimens for cross reactivity
-choose different route of administration

• AKA ischemic heart disease
• Angina meaning suffocating pain or choking
feeling
• Indicates significant coronary artery disease
• Indicates inadequate oxygen supply to the
myocardium
• Risk of adverse cardiac event greater

-transient inability of the coronary arteries to
provide adequate oxygenated blood to the
myocardium
-ischemic myocardium produces chemical
mediators which act on the spinal cord to produce
pain
-the pain causes increased blood pressure and
tachycardia which increase oxygen demand further
(feedback loop)

2. Predisposing Factors
-genetics, sex, age, race
-smoking, HTN, diabetes, high cholesterol
-stable (returns to baseline after activity
stopped)
-unstable (no activity required,
spontaneous)

-All local anesthetics vasodilate (procaine most
potent) with one exception (cocaine – binds to NE
sites with resultant free NE)
bupivicaine > lidocaine > mepivicaine
-oral route ineffective due to hepatic first-pass and
significant biotransformation to inactive
metabolites
-intratracheal uptake almost as fast as IV
(emergencies)
-IV use for ventricular dysrythmias

-once absorbed in blood distributed to all
areas of the body especially vascular areas
(brain, liver, spleen, kidneys etc.)
-one half life of drug is the time to when
there is a 50% drop in blood level
bupivicaine > mepivicaine > lidocaine
-all local anesthetics cross the blood brain
barrier and the placental barrier

-prototypical drug is procaine
-hydrolyzed in the plasma by
pseudocholinesterase
-rate of hydrolysis affects toxicity (longer
hydrolysis phase increases toxicity
-procaine is hydrolyzed to PABA prior to
excretion in urine
PABA causes allergic reactions
-Atypical pseudocholinesterase deficiency is a hereditary condition in which there is impaired biotransformation of drugs like procaine and succinylcholine which leads to prolonged and toxic concentrations of the drugs (“difficulty” during general anesthesia)

-prototypical drug is lidocaine
-biotransformation occurs primarily in the liver (hepatic disease)
-prilocaine also metabolized partially in lungs
-prilocaine and articaine can induce methemoglobinemia via metabolite orthotoluidine
- lidocaine metabolites lead to sedative effect

-primarily in the kidneys
-esters more secreted in metabolite form
-amides more secreted in parent compound
form
-kidney disease may interfere with drug
excretion and lead to toxicity

-crosses blood brain barrier
-low drug levels anticonvulsant
-high drug levels seizures
“inhibition of inhibition”

– Slurred speech
– Shivering
– Muscular twitching
– Tremor in muscles of
face and distal
extremities

• Subjective
– Bilateral perioral numbness
– Warm, flushed feeling
– Pleasant dreamlike state
– Light-headedness
– Dizziness
– Inability to focus eyes
– Tinnitus
– Drowsiness
– Disorientation

-cardiac depression and vasodilation
-decreased cardiac output and hypotension
-generalized vasodilation with the exception
of cocaine

• After 2 carpules for intraoral local anesthesia:
0.5 – 2 micrograms/ml
• Antidysrhythmic therapeutic levels: 1.8 – 6
micrograms/ml
• Toxicity: > 6 micrograms/ml
– Circulatory collapse
• CO decrease, peripheral vasodilitation, BP decrease

-neuromuscular blockade when combined with
general anesthesia
-drug interactions potentially prolonging other
CNS depressants
-Malignant Hyperthermia (Hyperpyrexia to 108
degrees, muscle rigidity, hypotension, acidosis and
death) Ca++ release in myoplasm. Can happen
with amides not esters

• Oppose the vasodilating property of local
anesthetics
• Decrease perfusion to site of injection
• Decrease absorption into the vascular
system–lower blood levels decrease toxicity
• Increase the duration of anesthesia
• Decrease bleeding at the site of injection


• For use in dentistry, they are all direct acting
sympathomimetic amines
• Act on alpha and beta adrenergic receptors to
varying degrees
• Alpha receptor activation causes
vasoconstriction by acting on smooth muscle
in vessel walls

• The dilution is commonly referred to as a
ratio 1:1 = 1gram/1ml
1:1000 = 1g in 1000ml or 1mg/ml
1:10,000 = 0.1mg/ml
1:100,000 = 0.01mg/ml
*In a 1.8cc (ml) solution of 1:100,000 you
would have 0.018mg (18 micrograms)
*1cc of 1% solution = 10mg of solute

-acts on both alpha and beta receptors; beta effects
predominate; AKA Adrenalin
-large doses to a specific area leads to a high tissue
concentration and the alpha effects take over
-sodium bisulfite (anti-oxidation) used as preservative
(shelf-life about 18 months); may cause allergy
-BP increases, P increases, CO increases
-max dose healthy 0.2mg (11 cartridges 1:100000)
-max dose cardiac 0.04mg (2 cartridges 1:100000)

-AKA Levophed, not routinely used or
recommended in dentistry
-one fourth as potent as epinephrine
-acts almost exclusively on alpha receptors
-increases blood pressure, decreases heart rate
and cardiac output
-max dose healthy 0.34mg (10ml 1:30000)
-max dose cardiac 0.14mg (4ml 1:30000)

-AKA neo-cobefrin
-15% as potent as epinephrine
-acts primarily on alpha receptors
-less cardiac and CNS side effects
-all patients max dose 1mg (20ml of a
1:20,000 – 11 cartridges)

• Only epinephrine and levonordephrine are available
in the US
• With epinephrine there is a rebound vasodilation, as
the alpha effect ceases beta receptors are stimulated
• Use with caution in patients with significant cardiac
disease, sulfite sensitivity, taking MAO inhibitors or
tricyclic antidepressants or phenothiazines

• Individual variation to drug
• Accuracy of administered drug
• Status of tissue (vascularity, pH)
• Anatomical variation
• Type of injection administered
(supraperiosteal vs. nerve block)

• Manufacturer – see drug insert
• Malamed uses the more conservative dosage
regimen suggested by the Council on Dental
Therapeutics of the American Dental
Association

• Ester AKA Novocain
• Used as the sole local anesthetic agent in US for
many years; introduced in 1904
• Historically significant
• Produces the most vasodilation
• Used now to break ateriospasm
• Now only used in combination in dentistry

• Combination of two esters
• Useful when amides absolutely
contraindicated
• Removed from the US in 1996 officially
• Max dose is 6.6mg/kg

• AKA Xylocaine
• Amide introduced in 1948 - “gold standard”
• Onset 2-3 mins T1/2 1.6hrs
• May be used as topical in 5% concentration
• Lidocaine without epi is not clinically useful pulpal
anesthesia 5-10 mins
• 2% lidocaine with epi 1:50,000 is used for
hemostasis
• 2% lidocaine with epi 1:100,000 is the most
common

-pulpal anesthesia 5-10mins soft tissue 60-
120mins
-max dose 4.4mg/kg absolute max 300mg

-pulpal anesthesia 60mins soft tissue 3-5hrs
-max dose 6.6mg/kg absolute max 500mg

-this is what you will use most
-pulpal anesthesia 60mins, soft tissue 3-5hrs
-max dose 6.6mg/kg, absolute max 500mg
-cartridge is 1.8cc = 36mg of lidocaine and
0.018mg of epi in one cartridge

• Amide, AKA Polocaine/Carbocaine
• Onset 1-2mins T1/2 1.9hrs
• 3% mepivicaine plain is useful for patients who are
unable to receive a vasoconstrictor
-pulpal anesthesia 20-40mins soft tissue 2-3hrs max
dose 6.6mg/kg; absolute 400mg
• 2% mepivicaine with levonordefrin 1:20,000
-pulpal anesthesia 60min; soft tissue 3-5hrs
-max dose 6.6mg/kg; absolute max 400mg
-not as good for hemostasis

• Amide, AKA Citanest
• Onset 2-4mins T1/2 1.6hrs
• May cause methemoglobin formation
• 4% prilocaine plain
-pulpal anesthesia 40-60mins soft tissue 2-4hrs
-max dose 6.0mg/kg absolute max 400mg

• Citanest Forte
• 4% prilocaine with epi 1:200,000
-pulpal anesthesia 60-90mins soft tissue 3-
8hrs
-max dose 6.0mg/kg absolute max 400mg

• Amide, AKA Marcaine
• Used for lengthy or painful procedures
• Onset 6-10mins T1/2 2.7hrs
• 0.5% bupivicaine with epi 1:200,000
-pulpal anesthesia 90-180mins soft tissue 4-9hrs
-max dose 1.3mg/kg, absolute max 90mg

• Amide, AKA Duranest
• Lengthy, painful procedures
• Onset 2-3mins T1/2 2.6hrs
• 1.5% etidocaine with epi 1:200,000
-pulpal anesthesia 90-180mins soft tissue 4-
9hrs
-max dose 8mg/kg absolute max dose 400mg

• Lidocaine – standard
• Mepivicaine – heart patients
• Prilocaine – alternative
• Articaine – alternative
• Bupivicaine – long acting
• Etidocaine – long acting

• Penetrates the mucous membrane 2-3mm
• Provides relief of pain from needle penetration
• Usually in higher concentration than injectable local
anesthesia
• Many names/brands benzocaine (hurricaine),
butacaine, cocaine (not desirable), Dyclonine (is a
ketone and useful in allergic patients), lidocaine,
tetracaine (cetacaine)

• Use atraumatic injection technique
• Use topical anesthesia
• How long do you need the patient anesthetized?
• Use the minimal amount of drug required to allow
you and the patient to complete the procedure
comfortably
• Think about post-operative pain and use a longer
lasting drug to achieve better pain control


• Be concerned about self-mutilation/burns in
your patients
• If you need hemostasis choose the
appropriate anesthetic
• Be mindful of the medical status of your
patients

• 25 gauge RED
• 27 gauge YELLOW
• 30 gauge BLUE

• Short 20mm
• Long 32mm

Place Needle on Syringe
Pull Back on Thumb Ring to Insert
Carpule into Syringe
Slowly slide carpule forward to
penetrate diaphragm
Put in needle puncture guard
Engage harpoon into stopper



Resheath needle after injection

1. Use a sterilized sharp needle
2. Check the flow of local anesthetic solution
3. Solution at room temperature
4. Position the patient – supine if tolerated
5. Dry the tissue
6. Apply topical antiseptic (optional)
7. Apply topical anesthetic


8. Communicate with the patient – explain
superficial numbness, minimize discomfort
9. Establish a firm hand rest
10. Make the tissue taut
11. Keep the syringe out of patient’s sight
12. Insert the needle into the mucosa – bevel
towards bone
13. Watch and communicate with the patient –
never say that it won’t hurt
14. Inject several drops (optional)


15. Slowly advance needle towards target
16. Aspirate
17. Slowly deposit the local anesthetic solution
18. Communicate with the patient – explain why
you are injecting slowly
19. Slowly withdraw the syringe and cap the
needle using safe technique
20. Observe the patient after the injection
21. Record the injection in the patient’s chart

1. Posterior Superior Alveolar
(PSA)
2. Infraorbital
3. Maxillary
(2nd Division Block)
5. Greater Palatine
6. Nasopalatine

Advantages


• Fewer injections (pain)
when anesthetizing
several sites
• Less total volume of
anesthetic solution and
less chance of overdose
• Lasts longer and more
profound

• Lasts longer
• Greater chance of
complication
– Hematoma
– Intravascular injection
– Slightly lower success
rate
– Trismus
– Anesthesia more wide
spread than desired

ASA - canine to canine and anterior soft tissue
MSA - premolars, ant soft tissue, and ML cusp of 1st molar
PSA - molars, ant soft tissue
GP - hard palate through canines

less likely to penetrate
periosteum and cause pain
and bruising

• Anesthetizes
– Maxillary 3rd, 2nd, and 1st molars; (MB root of 1st molar
not anesthetized = 28%)
– Buccal periodontium and facial bone
• Indications
– Treating >1 maxillary molar
– Infection in site
– Infiltration not effective
• Contraindication: risk of hemorrhage too great

• Atraumatic
• 95% success rate
• Less injections when
treating multiple teeth
• Less total volume

• Hematoma
• No bony landmarks
• 2nd injection usually
required for 1st molar

PDL injections, infiltrations, V2
Block

• Anesthetrizes
– ASA nerve: pulps of incisors and canine
– MSA nerve: 72% pulp of premolars, MB root of 1st
– Infraorbital nerve
• Inferior palpebral
• Lateral nasal
• Superior labial
– Facial bone and periodontium of effected teeth
• Indications
– Multiple teeth
– Infection
– Infiltrations not effective
• Contraindications
– 1 or 2 teeth
– Bleeding disorders, anticoagulants


• Advantages
– Simple
– Minimal volume of solution
– Minimal punctures
• Disadvantages
– Lack of confidence in operator – fear of injury to
eye
– Landmarks usually difficult to palpate

• Anesthetizes posterior portion of hard palate
and its overlying soft tissues, anteriorly as far
as the 1st premolar and medially to the
midline.
• Indications: pain control during restorative,
periodontal, or oral surgical procedures
• Contraindications
– Inflammation in site
– Smaller area of therapy (1 or 2 teeth)


• Advantages
– Minimizes needle penetrations and volume of
solution
– Minimizes patient discomfort – mucosa at site of
injection not attached
• Disadvantages
– No hemostasis except at site of injection
– Potentially traumatic/painful
• Alternatives: infiltration, V2 block

• Anesthetizes nasopalatine nerves bilaterally
anterior portion of hard palate (soft and hard
tissues) from mesial of right 1st premolar to
the mesial of the left 1st premolar
• Indications: restorative, periodontal, or oral
surgery procedures on multiple teeth
• Contraindications
– Inflammation or infection in area
– Smaller area of therapy


• Advantages
– Fewer needle penetrations
– Less volume of solution
• Disadvantages
– Hemostasis only in area of injection
– Potentially the most painful intraoral injection
• Alternatives
– Local infiltrations
– Maxillary nerve (V2) block

• Contraindications
– Inexperienced operator
– Pediatric patient
– Uncooperative patient
– Inflammation or infection at injection site
– When hemorrhage is risky
– Bony obstructions in canal (5-15%)
• Anesthetizes
– Pulpal anesthesia in hemimaxilla
– Soft tissue and bone in hemimaxilla
– Skin of lower eyelid, side of nose, cheek, upper lip
• Indications
– Extensive restorative, periodontal, or oral surgery
procedures
– Inflammation or infection precluding other blocks
– Diagnosis or treatment of neuralias or tics of V2 nerve
• Advantages
– High success rate – 95%
– Minimizes needle penetrations (1 vs 4) and volume
of anesthetic (1 vs 2 carpules)
– Usually atraumatic
• Disadvantages
– Risk of hematoma
– Lack of hemostasis at surgery site
– Discomfort
– Arbitrary landmarks
• Alternatives - other blocks, infiltrations

ANTERIOR
– Muscles of mastication
• Temporalis
• Masseter
• Lateral pterygoid
– Buccal nerve
POSTERIOR
– Auriculotemporal
– Lingual
– Inferior Alveolar
• Mylohyoid

• AKA mandibular nerve block
• Most commonly used
• Highest rate of failure (15-20%)
• Useful in quadrant dentistry
• Try to avoid bilateral mandibular blocks
(uncomfortable to the patient)
• Most difficult block to master


1. Nerves Anesthetized
-Inferior alveolar, mental,
incisive, lingual (usually)
2. Indications
-procedures on multiple
teeth in one quadrant
-buccal and lingual soft
tissue required

-infection or acute inflammation
-tongue and lip biters (children, mentally
handicapped)

-One injection provides a wide area of
anesthesia

-sometimes not necessary for localized
areas/procedures
-high block failure rate
-intra-oral landmarks not consistent
-high rate of positive aspiration (10-15%)
-lingual and lip anesthesia (biters/hot
beverages)

6. Insertion
-mucosa on medial aspect of the mandibular
ramus
7. Target
-Inferior alveolar nerve before it enters the
foramen

-coronoid notch (greatest
concavity on the anterior
border of the ramus)
-pterygomandibular raphe
-occlusal plane of the
mandibular posterior
teeth

-deposition of anesthetic below mandibular
foramen
-deposition of anesthetic too far anteriorly
-accessory innervation of the mandibular teeth
(mylohoid nerve posteriorly and
mylohoid/overlapping fibers of contralateral IAN)
-bifid inferior alveolar nerve (lower)

-Hematoma (hold pressure)
-Trismus
-Facial Paralysis (anesthetic in parotid)

-place index finger or thumb on the coronoid notch,
pull tissue tight
-6 to 10mm above the occlusal plane of the mandible
or the middle of finger thumb determines the height
of injection
-the anteroposterior point of the injection is then ¾
the distance to the pterygomandibular raphe
-align the barrel of the syringe across the
contralateral premolars
– Height of injection
• Coronoid notch
• 6-10 mm above the occlusal plane
– A-P site of injection
• Into base of “V” formed by pterygomandibular raphe
and ramus of mandible
– Penetration depth
• 20-25mm, 2/3 to ¾ the length of a long needle
– Height of injection
• Coronoid notch
• 6-10 mm above the occlusal plane
– A-P site of injection
• Into base of “V” formed by pterygomandibular raphe
and ramus of mandible
– Penetration depth
• 20-25mm, 2/3 to ¾ the length of a long needle

-retract tongue to midline, then inject at
the apical area of second molar on the
lingual surface of the mandible

-supraperiosteal injection technique
across the midline of the anterior
mandibular teeth (buccal surface)

-deposit 0.1 to 0.2 ml of anesthetic when
withdrawing needle from inferior alveolar
block

-tingling or numbness of lip
and chin to midline
-tingling or numbness of the
ipsilateral anterior two thirds
of the tongue
-anesthesia of teeth and
gingiva ipsilaterally (except
buccal nerve distribution)

• AKA long buccal nerve block
• Anesthetizes soft tissues and
periosteum buccal to the
mandibular molars
1. Indications
-buccal soft tissue anesthesia for
procedures on the mandibular
molars
2. Contraindications
-infection/inflammation in the
area

3. Advantages
-easy, high success rate
4. Disadvantages
-potentially painful if periosteum is torn

5. Insertion
-mucosa distal and buccal to the most
posterior mandibular molar


6. Target
-buccal nerve as it passes
over the anterior border of
the ramus
7. Landmarks
-mandibular molars
-mucobuccal fold
8. Failures
-rare

9. Complications
-rare (hematoma)
10. Technique
-penetrate mucosa about 2mm contact bone
-aspirate and inject

• AKA mandibular block
• Blocks entire distribution of V3
• Anesthesia of inferior alveolar, lingual,
mental, incisive, mylohoid, buccal and
auriculotemporal nerves
• Difficult learning curve
• More successful than inferior alveolar block

1. Indications
-procedures on multiple teeth
-soft tissue anesthesia
-failed inferior alveolar block
2. Contraindications
-infection/inflammation
-lip/tongue biters
-patients who are unable to open mouth wide

-only one injection
-high success rate (95%)
-minimal complications
-successful anesthesia of bifid inferior
alveolar nerves

-tongue/lip anesthesia
-longer time to onset of anesthesia
-high learning curve

5. Insertion
-mucosa on the mesial of ramus in line of
tragus and commissure distal to the
maxillary second molar


6. Target
-lateral surface of condylar
neck, below insertion of
lateral pterygoid
7. Landmarks
-tragus and commissure
-just below the
mesiopalatal cusp of the
maxillary second molar

-Insufficient volume of anesthetic (bigger
nerve)
-anatomical difficulties (do not deposit
anesthetic unless bone is contacted)

-hematoma (rare)
-trismus (rare)
-paralysis of cranial nerve III, IV, VI (eye
paralysis, diplopia)

-have patient open wide, point of
insertion below mesiopalatal cusp of
maxillary second molar aiming to
tragus of ear (considerably higher
than occlusal plane)
-advance needle 20-25mm until
bone is contacted aspirate and inject
-have patient stay open 1-2 minutes
after injection

• AKA closed mouth block
• Useful when dental therapy required in
patients with limited mouth opening
(trismus)
1. Indications
-limited mouth opening
-inability to visualize landmarks for
conventional block

-infection or acute inflammation
-lip/tongue biters
-inability to gain access to the lingual aspect of
ramus

3. Advantages
-no mouth opening required
-works on patients with bifid inferior alveolar
nerves
-lower aspiration rate/atraumatic


4. Disadvantages
-difficult to visualize path of needle and
depth of insertion
-no bone contact

5. Insertion
-soft tissue overlying medial border of ramus
adjacent to maxillary tuberosity at the
mucogingival junction height
6. Target
-soft tissue of the medial
ramus (below Gow-gates
and above Inferior alveolar
block)
7. Landmarks
-mucogingival junction of
maxillary (second/third
molar)
-maxillary tuberosity/
coronoid notch

8. Failures
-must stay in line with flare of the mandible or
injection will be too lateral
-needle insertion too low
-under/overinsertion of the needle
9. Complications
-Hematoma/trismus
-facial nerve paralysis (overinsertion into parotid
gland)

-bevel of needle away from bone
-advance needle 25mm
-aspirate
-inject

• The mental nerve leaves the mental
foramen and provides sensory
innervation to the lip and chin area
• The incisive nerve continues forward
to provide sensory innervation to the
anterior mandibular teeth
• Both have limited usefulness on a
routine basis for dental therapy

1. Indications
-buccal soft tissue
anesthesia for procedures
anterior to the mental
foramen (biopsy)
2. Contraindications
-inflammation and
infection in the areas

3. Advantages
-high success rate
-easy/atraumatic
4. Disadvantages
-hematoma (5%)

. Insertion
-mucobuccal fold anterior to foramen


6. Target
-mental nerve as it exits the mental foramen
7. Landmarks
-mandibular premolars
-mucobuccal fold

-rare
-miss the foramen



9. Complications
-hematoma

10. Technique
-locate foramen with finger in mucobuccal
fold
-insert needle anterior to foramen (5mm)
-aspirate and inject

1. Indications
-dental procedures which require pulpal
anesthesia of the mandibular anterior teeth
-used instead of bilateral inferior alveolar
blocks for treatment limited to the anterior
mandible
2. Contraindications
-inflammation or infection

3. Advantages
-pulpal anesthesia of the anterior mandibular teeth
without lingual anesthesia (uncomfortable)
-high success rate
4. Disadvantages
-no lingual anesthesia
-cross innervation from contralateral inferior
alveolar nerve may require additional
supraperiosteal injections for pulpal anesthesia

5. Insertion
-mucobuccal fold anterior to mucobuccal fold
6. Target
-mental foramen (incisive nerve lies in this)
7. Landmarks
-mandibular premolars
-mucobuccal fold

8. Failure
-Inadequate volume of anesthetic
-Inadequate pressure after injection
9. Complications
-rare
-hematoma

10. Technique
-same as for
mental block
-hold pressure for
two minutes after
injection to force
anesthetic into the
foramen and reach
the incisive nerve

• Useful for supplemental anesthesia of anterior
mandibular teeth when getting crossover fibers from
contralateral inferior alveolar nerve
• Thin cortical plate allows for supraperiosteal
injection technique to be successful for mandibular
incisors only in most patients
• Technique exactly the same as for maxillary teeth
with deposition of anesthetic at root apex to block
dental plexus

• Always recap needle after injection
• Be confident
• Understand the anatomy
• Always aspirate
• Always use a finger rest for stabilization
• If the patient complains of an electric shock
after the needle is positioned, reposition the
needle as you are likely in the nerve itself