1. PHYSIOLOGY
OF PAIN AND
LOCAL
ANESTHESIA

2. Pain
“ an unpleasant feeling often caused by
intense or damaging stimuli, such as
stubbing a toe, burning a finger, putting
alcohol on a cut, and bumping the "funny
bone.”
-Wikipedia

3. “Pain is the psychical adjunct of an
imperative protective reflex.”
-According to Sheringhton (1906)
“Pain as an unpleasant sensory experience
evoked by stimuli that injures”
-Mountcastle (1968)

4. “ Pain as an unpleasant sensory or
emotional experience associated with
actual or potential tissue damage or
described in terms of such damage”
-International association for the study of pain IASP
(1979)

5. ORIGIN OF PAIN:
 Pain from external sources
-from mechanical, chemicals and thermal
sources, withdrawal is possible
 Pain from internal sources
-Mainly from chemical sources, usually
dull, may be referred, last long
 Pain from lesions of nervous system
- Last long, localization may be
faulty, withdrawal is impossible
 Pain from idiopathic sources
-It’s associated with psychological, social &/or
environmental factors

6. PURPOSE OF PAIN
 It warns against tissue damage
 The negative effects associated with pain
serve as an effective re-inforcement for
learned avoidance.
 Deep pains (e.g. joint sprains, muscle stress)
tell us that it is time to rest
 As useful as pain may be, the extreme pain
suffered by people with chronic illnesses such
as cancer is a protective mechanism gone
awry- Patton et al,

7. PAIN TERMINOLOGIES

8.  Somatogenic pain
o Nociceptive
 caused by stimulation of peripheral nerve fibers that
respond only to stimuli approaching or exceeding harmful
intensity (nociceptors)
o Neuropathic
 caused by damage or disease affecting any part of the
nervous system involved in bodily feelings
(the somatosensory system)
 Hyperpathia
• A painful syndrome characterized by an
abnormally painful reaction to a stimulus,
especially a repetitive stimulus, as well as an
increased threshold.

9.  Allodynia
• Pain due to a stimulus that does not normally
provoke pain.
 Analgesia
• Absence of pain in response to stimulation which
would normally be painful
 Hyperalgesia
• Increased pain from a stimulus that normally
provokes pain.
 Phantom
• pain felt in a part of the body that has been lost
or from which the brain no longer receives
signals

10.  Psychogenic
• also called psychalgia or somatoform pain, is
pain caused, increased, or prolonged by mental,
emotional, or behavioral factors
 Breakthrough pain
• pain that comes on suddenly for short periods of
time and is not alleviated by the patients' normal
pain management.
 Incident pain
• pain that arises as a result of activity, such as
movement of an arthritic joint, stretching a
wound, etc.

11.  Referred pain
• Pain experienced at a site far away from the site of
injury.
 Neurogenic pain
• Sharp, burning and intense. Maybe constant or
intermittent
 Vascular pain
• Difficult to localize; diffuse
 Muscle pain
• Dull and limited to area of origin; movement of the
affected part worsens the pain.

12. THEORIES ABOUT PAIN
1. Specific Theory (Rene Descartes in 1644)
 Transmission of pain via “straight through” channels
from the skin to the brain
 Modified by:
a. Johannes Muellens- via sensory nerve
b. Maximillian Von Frey- specific cutaneous
receptors for the mediation of
touch, pain, pressure, heat, cold.
- also postulated about the idea of pain
“center” w/in the brain.

13. 2. Pattern theory ( Golddscheider in 1894)
• Proposed that stimulus intensity and
central summation are critical
determinants of pain.
• Suggested that particular patterns of
impulses that evoke pain are produced
by a summation of sensory input w/in the
dorsal horn of the spinal cord. Pain results
when total output exceeds a critical level.
• E.g. TOUCH + PRESSURE + HEAT= PAIN

14. 3. Gate Control Theory (Ronald Melzack and
Patrick D. Wall in 1965)
 Postulated the following:
a. The transmission of the nerve impulses
from afferent fibers to spinal cord
transmission (T) cells is modulated by a spinal
gating mechanism in the dorsal horn.

15. b. The spinal gating mechanism is
influenced by the relative amount of activity in
larger diameter (L) and small diameter (S) fibers.
Activity in large fibers tend to inhibit transmission
(close the gate) while small fiber activity tends to
facilitate transmission (open the gate)
c. The spinal gating mechanism is
influenced by nerve impulses that descends from
the brain.
d. a specialized system of large
diameter, rapidly conducting fibers (central
control trigger) activates selective cognitive
processes that then influence, by way of
descending fibers, the modulating properties of
the spinal gating mechanism.

16. e. When the output of the spinal cord
transmission (T cells) exceed critical level, it
activates the action system those neural
areas that underlie the complex, sequential
patterns of behavior and experience he
characteristics of pain.

17. SUBSTANCIA GELATINOSA
 The control system composed of lamina II
and III.
 Intentional stimulation of fast conducting
large diameter fibers result in inhibition
transmission of pain by small nerve fibers.
 Trnsmission of impulses is prevented from
reaching the T cells (2nd order neurons that
transmit impulses to higher nervous system
centers)
 When T-cells stimulation succeeds a critical
level, the action system is activated.

18. ACTION SYSTEM
 Subserver emotions
 Involves the RAS, limbic system, thalamus
and hypothalamus.
a. Sensory Discriminative Components
 It knows where the pain is coming from.
 Rapidly transmit spatiotemporal information
about the stimuli
 Responsible for the phantom limb

19. b. Motivational- affective system
 Associate pain with misery/ suffering
 Regulates vasomotor and autonomic functions
 Can be altered with the effects of narcotics.
c. Activation of motor mechanism
 Responsible for individual’s overt reaction to pain
 An affective aspect of painful experience
 Its is a series of responses seen in an individual.

20. 1. Startle response 6. Evocation of past
2. Flexion response experiences
3. Postural 7. Prediction of the
readjustment consequences
4. Vocalization 8. Other patterns of
5. Reorientation in behavior aimed in
an individual reducing the
sensation.

21. d. Descending control
 Facilitates neural transmission location
within PAG (periaqueductal Gray matter)
of the midbrain.
 Results in profound analgesia
 Can be activated by pharmacological and
psychological factors.

22. TYPES OF PAIN

23.  Based on where in the body the pain is felt:
 Somatic
 Visceral
 Neuropathic
• Pain of all three types can be either acute or chronic.
• Somatic, visceral, and neuropathic pain can all be felt
at the same time or singly and at different times.
 The different types of pain respond differently to
the various pain management therapies.
 Somatic and visceral pain are both easier to
manage than neuropathic pain.

25. Nociceptive Pain
 arises from the stimulation of specific pain
receptors.
 These receptors can respond to heat,
cold, vibration, stretch and chemical
stimuli released from damaged cells.

26. Non Nociceptive Pain
 arisesfrom within the peripheral and
central nervous system.
 Specific receptors do not exist here, with
pain being generated by nerve cell
dysfunction.

27. Somatic Pain
 Caused by the activation of pain receptors in either
the cutaneous (body surface) or deep tissues
(musculoskeletal tissues).
 Deep somatic pain
 When it occurs in the musculoskeletal tissues
• Common causes of somatic cancer pain include
metastasis in the bone (an example of deep somatic
pain) and postsurgical pain from a surgical incision (an
example of surface pain).
• Deep somatic pain is usually described as dull or aching
but localized.
• Surface somatic pain is usually sharper and may have a
burning or pricking quality.

28. Somatic Pain
 Source - tissues such as skin, muscle, joints, bones,
and ligaments - often known as musculo-skeletal
pain.
 Receptors activated - specific
receptors (nociceptors) for heat, cold, vibration,
stretch (muscles), inflammation (e.g. cuts and
sprains which cause tissue disruption), and oxygen
starvation (ischaemic muscle cramps).
 Characteristics - often sharp and well localised,
and can often be reproduced by touching or
moving the area or tissue involved.
 Useful Medications - may respond to combinations
of Paracetamol, Weak Opioids OR Strong Opioids,
and NSAIDs

29. Visceral Pain
 "Viscera" refers to the internal areas of the
body that are enclosed within a cavity.
 It is caused by activation of pain receptors
resulting from infiltration, compression,
extension, or stretching of the thoracic
(chest), abdominal, or pelvic viscera.
 Common causes of visceral pain include
pancreatic cancer and metastases in the
abdomen.
 It is not well localized and is usually described
as pressure-like, deep squeezing.

30. Visceral Pain
 Source - internal organs of the main body cavities. There
are three main cavities - thorax (heart and lungs),
abdomen (liver, kidneys, spleen and bowels), pelvis
(bladder, womb, and ovaries).
 Receptors activated - specific receptors (nociceptors) for
stretch, inflammation, and oxygen starvation (ischaemia).
 Characteristics - often poorly localised, and may feel like a
vague deep ache, sometimes being cramping or colicky in
nature. It frequently produces referred pain to the back,
with pelvic pain referring pain to the lower back,
abdominal pain referring pain to the mid-back, and
thoracic pain referring pain to the upper back.
 Useful medications - usually very responsive to Weak
Opioids and Strong Opioids.

31. Acute pain
 Sudden onset, lasting for hours to days and
disappears once the underlying cause is treated.
 Acute pain has a clear cause. It could result from
any illness, trauma, surgery or any painful medical
procedures.
 It is beneficial to the patient because if there’s no
pain, the individual will ignore his illness resulting in
complications and even death.
 Acute pain signals that there is something wrong
and motivates the person to get help.

32. Acute Pain
 Short lasting and usually manifests in ways
that can be easily described and
observed.
 It may, for example, cause sweating or
increased heart rate. It can last for several
days, increasing in intensity over time
(subacute pain), or it can occur
intermittently (episodic or intermittent
pain).

33. Chronic pain
 Starts as an acute pain and continues
beyond the normal time expected for
resolution of the problem or persists or recurs
for various other reasons It is not
therapeutically beneficial to the patient.
 In acute pain, attention is focused to treat the
cause of pain whereas in chronic
pain, the emphasis is laid upon reducing the
pain to give relief, limit disability and improve
function.

34.  Chronic pain is defined as pain lasting for
more than 3 months. It is much more
subjective and not as easily described as
acute pain. Effectively treating chronic
pain poses a great challenge for
physicians. This kind of pain usually affects
a person's life in many ways. It can
change someone's personality, ability to
function, and quality of life.

35. SPECIAL TYPES
OF PAIN

36. Neuropathic
 Results from damage or disease affecting
the somatosensory system.
 It may be associated with abnormal
sensations called dysesthesia, and pain
produced by normally non-painful stimuli
(allodynia).
 May have continuous and/or episodic
(paroxysmal) components.
 Common qualities include burning or
coldness, "pins and needles"
sensations, numbness and itching.

37. Cause
 Central neuropathic pain is found in spinal cord
injury, multiple sclerosis, and some strokes.
 Aside from diabetes and other metabolic
conditions, the common causes of painful
peripheral neuropathies are herpes
zoster infection, HIV-related neuropathies,
nutritional deficiencies, toxins, remote
manifestations of malignancies, immune mediated
disorders and physical trauma to a nerve trunk.
 Neuropathic pain is common in cancer as a direct
result of cancer on peripheral nerves (e.g.,
compression by a tumor), or as a side effect
of chemotherapy radiation injury or surgery.

38. Neuralgia
 Pain in one or more nerves caused by a
change in neurological structure or
function of the nerves rather than by
excitation of healthy pain receptors.
 Neuralgia falls into two categories:
 central neuralgia - the cause of the pain is
located in the spinal cord or brain
 peripheral neuralgia.

39. Neuralgia
• This unusual pain is thought to be linked to
four possible mechanisms: ion channel
gate malfunctions; the nerve fibers become
mechanically sensitive and create an ectopic
signal; signals in touch fibers cross to pain
fibers; and malfunction due to damage in the
brain and spinal cord.

40. Pain Receptors
 The pain receptors in the skin and other
tissues are all free nerve endings.

42. Stimuli
 Mechanical
 Thermal
 Chemical
 Bradykinin, serotonin, histamine, potassium ions,
acids, acetylcholine, proteolytic enzymes,
substance P, prostaglandin

43. Pain Fibers
 A-delta or Aδfibers
 C-fibers

44. A-delta fibers C-fibers
 Thinly myelinated  Unmyelinated
 1-5 µm in diameter  0.2-1.5 µm in diameter
 Stimulation is  Stimulation is
interpreted as fast interpreted as slow
pain pain
 Respond to stimuli  React to stimuli that
such as cold and are thermal,
pressure mechanical, and
chemical in nature

45. 4 Distinct Processes of Pain
1. Transduction
2. Transmission
3. Modulation
4. Perception

46. 1. Transduction
• Noxious stimuli are translated into
electrochemical impulses at sensory nerve
endings
• Afferent nerve endings participate in
translating noxious stimuli
2. Transmission
3. Modulation
4. Perception

47. 1. Transduction
2. Transmission
• Impulses are sent to the dorsal horn of
the spinal cord, and then along the
sensory tracts to the brain
3. Modulation
4. Perception

48. 1. Transduction
2. Transmission
3. Modulation
• Process of dampening or amplifying
the pain related neural signals
• Transmission is altered by the
influence of discreet pathways
containing analgesic
neurotransmitters
4. Perception

49. 1. Transduction
2. Transmission
3. Modulation
4. Perception
• Conscious awareness of the
experience of pain
• Subjective and emotional experience
of pain is created

50. Limbic forebrain To cerebral cortex
Cerebrum
Thalamus
Hypothalamus
Paleospinothalmic pathway
Brain Stem Neospinothalmic pathway
Spinal Nerve
Spinal cord
Pain receptors

51. Thalamus (sensation) Limbic cortex*
Somesthetic nuclei (emotional experience)
Neospinothalmic tract
Paleospinothalmic tract
(sharp, bright pain)
(dulll, aching pain)
Nociceptive A-delta
stimuli (fast)
Spinal cord and dorsal horn*
C-fiber Pain modulating circuits
(slow)
Primary touch fibers

52. Pharmacologic and non
pharmacologic Treatment
of Pain

53. Pharmacological Therapy
(Medication)
• Nonopioid pain relievers (e.g. aspirin and
ibuprofen)
• Opioids (e.g. vicodin and morphine)
• Adjuvant medications (drugs whose
primary purpose is not for pain but rather
for other conditions; e.g. antidepressants
and anticonvulsants)
• Topical treatments (drugs that are
applied directly to the skin)

54. Non-Pharmacological
Treatment
Less invasive options:
• Physiatric Approaches
• Non-invasive Stimulatory Approaches
• Psychological Approaches
• Alternative Approaches
More invasive options:
• Anesthesiologic Approaches
• Invasive Stimulatory Approaches
• Surgical Approaches

55. Physiatric Approaches:
1. Therapeutic Exercise options help:
 Strengthen weak muscles
 Mobilize stiff joints
 Restore coordination and balance
 Promote a sense of well-being
 Decrease anxiety and stress
 Maintain an appropriate weight

56. 2. Heat Therapy
• Heat therapy reduces pain, especially pain from
muscle tension or spasms. Heat helps with pain
because heat increases the blood flow to the
skin, dilates blood vessels, increasing oxygen and
nutrient delivery to tissues, and decreases joint
stiffness by increasing muscle elasticity.
3. Cold Therapy
• Cold therapy constricts blood vessels near the skin
and helps relieve the pain of muscle tension or
spasms. It also helps reduce the swelling of an injury.

57. Non-Invasive Stimulatory
Approaches:
1. Transcutaneous Electrical Nerve
Stimulation (TENS): a method of applying
a gentle electric current to the skin to
relieve pain. It is a small box-shaped
device that patients can put in their
pocket and it transmits electrical impulses
through wires to electrodes taped to the
skin in the painful area. However, TENS
can become less effective at relieving
pain over time.

58. Psychological Approaches:
1. Cognitive Behavioral Techniques
• Deep breathing – the patient focuses on
breathing deeply. This may shift attention away
from the pain.
• Progressive muscle relaxation – patients contract,
then relax, muscles throughout the body, group by
group. This helps patients relax the muscles in their
body.
• Imagery – patients focus on pleasant thoughts,
such as waves crashing onto a beach. The patient
may also be told to think of an image that
represents pain and then imagine it changing into
an image representing a pain-free state.

59. • Meditation – the individual aims to empty the mind
of thoughts and focus on breathing and the
rhythms of the body.
• Biofeedback Therapy – individuals learn to reduce
their body’s unproductive responses to stress which
decreases their sensitivity to pain.
• Distraction – a pain management technique in
which patients focus their attention on something
other than their pain and negative emotions, by
doing thing such as singing, listening to music,
watching TV, or talking to friends.

60. Psychotherapy and Social
Support
• Psychotherapy: a one-on-one approach that may
be useful for anyone whose pain is difficult to
manage, who has developed clinical depression, or
who has a history of psychiatric illnesses. The goals of
psychotherapy include teaching new coping
skills, establishing a bond to decrease patient’s sense
of isolation, and fostering a sense of self-worth.
• Group Approaches: an approach where individuals
with the same conditions get to together for support.
This approach helps the patient maintain a social
identity and shows the patient how others are
coping.

61. Alternative Approaches
1. Acupuncture: an ancient method for
relieving pain and controlling disease. Thin
metal needles that are gently twirled for ten
to twenty minutes can be used to stimulate
acupuncture points, which relieve pain in
specific parts of the body. It is effective for
some patients with chronic pain.
2. Massage: works by stimulating blood flow,
relaxing muscles that are tight or in spasm,
and promoting a feeling of well-being.
Massage should not be used on swollen tissue.

62. Local
Anesthesia

63. TERMINOLOGIES
 ANESTHESIA – It is a condition wherein
there is loss modalities of sensation.
 ANALGESIA – It is the deadening or
absence of the sense of pain without loss
of consciousness.

64.  LOCAL ANESTHESIA – It is an anesthesia
without the involvement of the CNS and a
condition wherein the patient remains
conscious.
 GENERAL ANESTHESIA – It is an anesthesia
wherein there is an elimination of all the
sensations, accompanied by the loss of
consciousness.

65.  LOCAL ANESTHETICS – These are agents
that are used to eliminate the different
modalities of sensation.
 GENERAL ANESTHETICS – These are agents
that produces loss of sensation and loss of
consciousness.

66. Local anesthesia
 lossof sensation in a circumscribed area
of the body by a depression of excitation
in nerve endings or an inhibition of the
conduction process in the peripheral
nerves.
 In clinical practice a localized loss of pain
sensation is desired. Although the terms
dental anesthesia and dental analgesia
are used synonymously in dentistry, local
analgesia is more accurate.

67.  Local anesthesia can be achieved by a
number of mechanisms including
mechanical trauma, anoxia, and use of
neurolytic agents in addition to traditional
local anesthetic drugs. However, clinically
only reversible local anesthetic agents
and other reversible techniques such as
temperature reduction or electronic
stimulation are useful to prevent pain.

68. Properties of an ideal local
anesthetic
 Specific action
 Reversible action
 Rapid onset of action
 Suitable duration of action
 Active whether applied topically or injected
 Nonirritant
 Causes no permanent damage
 No systemic toxicity
 High therapeutic ratio
 Chemically stable and a long shelf life
 Ability to combine with other agents without loss of
properties
 Sterilizable without loss of properties
 Nonallergenic
 Nonaddictive

69. Local anesthetic agents can be classified
in several ways:
 Chemical structure
 local anesthetics are classified usually as
either esters or amides.
 Duration of action
 local anesthetics maybe classified as short
acting, intermediate-acting, or long-acting.

70. General constituents of a dental
cartridge of anesthetic solution
 Local anesthetic agent
 Vasoconstrictor
 this is sometimes included to delay the removal
of the anesthetic from the tissues by decreasing
the blood flow through adjacent blood vessels.
A vasoconstrictor produces the following
advantages: (a) longer duration of local
anesthetic action, (b) reduced bleeding of a
surgical site, and (c) reduced systemic effects.
The most commonly used vasoconstrictors are
epinephrine (adrenaline) and octapressin
(felypressin). Only epinephrine is available in the
United States.

71.  Reducing agent
 this prevents oxidation of the vaso constrictor and acts
by competing with the vasoconstrictor for oxygen
available in the solution. The most commonly used
reducing agent is sodium metabisul-fite.
 Preservative
 a bacteriostatic preservative prolongs the shelf life of
the solution, but since preservatives can provoke
allergic reactions, they are no longer contained in
dental local anesthetic cartridges in the United States.
The typical shelf life of an anesthetic without
preservative is approximately 18 months to 2 years.

72.  Fungicide
 Thymol is used occasionally as a fungicide.
 Carrier solution
 an acidic aqueous solution dissolves the
local anesthetic salt and maintains it at an
acceptable pH.

73. The injectable local anesthetics used in
dentistry have a common core structure
consisting of
 Hydrophilic amino terminal
 Intermediate chain
 Lipophilic aromatic terminal

74. Hydrophilic portion
 consists of a substituted secondary or
tertiary amine.
 Solubility in water is essential for 2 reasons
 to allow for the dissolution in a solvent to
permit injection
 to allow penetration through interstitial fluid
following administration.

75. Intermediate chain
 Consists of either an amide or ester linkage.
 Allows spatial separation of the hydrophilic
and lipophilic components of the molecule.
 The older agents, procaine and cocaine, are
ester-based drugs but are no longer widely
used as dental anesthetics due to their
unwanted side effects, such as toxic or
allergic reactions

76. Lipophilic part
 an aromatic residue that is essential for its
ability to penetrate fatty tissue such as the
lipid sheath of nerves in order to gain
access to the nerve cell membrane to
reach its site of action.

77. Theories of regional anesthesia
 Acetylcholine Theory
 Calcium Displacement Theory
 Surface Charge Theory
 Specific Receptor Theory
 Membrane Expansion Theory

78. Acetylcholine theory
 Acetylcholine, aside from its role as a
neurotransmitter at nerve synapses, is also
involved in nerve conduction
 There is no evidence that proves that
acetylcholine is involved in neural
transmission along the body of the neuron

79. Calcium Displacement Theory
 Localanesthetic nerve block is produced
due to displacement of Calcium ions that
control the membranes permeability to
sodium

80. Surface charge theory
 “repulsion theory”
 Local anesthetics acted by binding to the
nerve membrane and changing the
electrical potential at the membrane surface
 The electrical potential at the membrane
surface becomes more positive, decreasing
the excitability of the nerve by increasing the
threshold potential
 This theory cannot explain the activity of
uncharged LA such as benzocaine in
blocking nerve impulses

81. Specific Receptor Theory
 Local anesthetics act by binding to
specific receptor binding site present on
the sodium channels. Specific receptor
sites are present on either the external or
internal surface of the sodium channels
 Nerve conduction is interrupted once the
local anesthetics gain access to the
receptors

82. Specific Receptor Theory
 External receptor site
 Two naturally occurring biotoxins, tetrodotoxin
and saxitoxin block sodium influx by acting on
the external receptor
 Internal receptor site
 Local anesthetics may act by competitive
action with calcium for the same receptor

83. Displacement of calcium ions from the sodium channel receptor site
Binding of the local anesthetic molecule to the receptor site
Blockade of the sodium channel
Decrease in sodium conductance
Depression of rate of electrical depolarization
Failure to achieve threshold potential level
Lack of development of propagated action potentials

84. Classification of Local Anesthetics
according to biological site and
mode of action
 Agent acting at receptor site on external
surface of nerve membrane
 Agents acting on receptor site on internal
surface of nerve membrane
 Agents acting by a receptor independent
physic-chemical mechanism
 Agents acting by combination of
receptor and receptor-independent
mechanism

85. Membrane Expansion Theory
 Statesthat local anesthetic agents
penetrate the lipid portion of the cell
membrane which causes its expansion
and decreases the diameter of sodium
channels. This causes the inhibition of flux
of sodium ions and nerve impulse
generation

86. Na+
Na+
+ + + + + +

87. Mechanism of Action
 Itsmechanism of action is related to the
ion channels, nerve, and depolarization
 Local anesthetics block the conduction of
impulse in peripheral nerves that inhibits
the nerves from being excited and thus
create anesthesia

88. Factors Affecting the Reaction
of Local Anesthetics
1. Lipid solubility
 All local anesthetics have weak bases.
Increasing the solubility leads to faster nerve
penetration, block sodium channels, and
speed up the onset of action
 The more tightly local anesthetics bind to the
protein, the longer the duration of onset of
action
 2 forms of local anesthetics:
 Ionized
 Non-ionized

89. 2. pH influence
 Decrease in pH shifts equilibrium towards
the ionized form, delaying the onset of
action
 Lower pH : more acidic : slower onset of
action
3. Vasodilation
 Lower rate of vasodilation leads to a
slower absorption of local anesthetics
agent, and longer duration of its action

90. Duration of Local Anesthetics
 Long-acting
 180 minutes or more
 0.5% Bupivacaine with 1:200,000 epi
 0.5% to 1.5% Etidocaine with 1:200,000 epi
 Medium-acting
 90 to 150 minutes
 4% Prilocaine with 1:200,000 epi

91. Duration of Local Anesthetics
 Short-acting
 45to 75 minutes
 4% Prilocaine when used for nerve block
 2% Procaine with 0.45 Ppropoxycaine used as a
vasoconstrictor
 Ultra-short acting
 Less than 30 minutes
 Procaine w/o a vasoconstrictor
 2% Lidocaine w/o a vasoconstrictor

92. Procedures requiring local
anesthesia
 Root canal treatment
 Removal of teeth
 Deep dental fillings
 Periodontal gum surgeries
 Cosmetic dentistry procedures
 Crown and bridge work
 Implants
 Oral surgical procedure

93. Groups of Local Anesthesia
 ESTER GROUP  NON-ESTER GROUP
 Benzoic acid esters  Anilide
 Cocaine  Bupivacaine
 Benzocaine
(Marcaine)
 Etidocaine
 Para-aminobenzoic (Duranest)
acid esters  Mepivacaine
 Procaine (Carbocaine)
 Tetracaine  Lidocaine
 Propoxycaine (Xylocaine)
 2-chloroprocaine  Prilocaine (Citanest)

94. Amides
 Amide link between secondary or tertiary
amine and aromatic ring
 Undergoes biotransformation primarily in
the liver by microsomal enzymes
 End products of metabolism are excreted
by the kidneys

95. Esters
 Esterlink between secondary or tertiary
amine and aromatic ring
 Inactivated by hydrolysis which occurs in
the plasma
 Catalyzed by the enzyme plasma
cholinesterase

96. Factors in selecting the
method of induction
 Area to be anesthetized
 Profoundness required
 Duration of anesthesia
 Presence of infection
 Age of patient
 hemostasis

97. Indications and contraindications
for regional anesthesia
 Indication: when it is necessary for the patient
to remain in the conscious state
 Contraindications:
 Fear or apprehension on the side of the patient
 Presence of infection
 Allergy to various local anesthetics
 Patient is below age of reason
 Mental deficiencies
 History of major oral surgery
 Presence of anomalies

98. TOXICITY
 Is the peak circulation levels of local
anesthetics
 Levels of LA concentration administered to
patients are varied according to age, weight
and health
 Maximum dose for an individual is usually
between 70mg to 500mg
 The amount of dose also varied bassed on
the type of solution used and the presence of
vasoconstrictor

99. Common toxic effects
 Light headedness
 Shivering or twitching
 Seizures
 Hypotension
 Numbness

100. COMPLICATIONS OF LOCAL
ANESTHETICS
 Arising from drugs/ chemical used
 Soft tissue injury
 Sloughing of the tissue
 Toxicity
 Allergy
 Infection caused by contaminated
solution

101.  Arising from injected technique
 Needle breakage
 Hematoma
 Failure to obtain local anesthesia
 Post- injections herpetic lesions

102.  Arising from both  Infection
 Pain on injection  Persistent pain
 Burning of the  Neurological
injection symptoms
 Trismus facial paralysis
 Blanching of the skin visual disturbances
 Edema
 Persistent paresthesia

103. Soft tissue injury
 Self inflicted trauma to lips and tongue while still
numb
 Seen in children which are mentally and
physically disabled.
 Soft tissue anesthesia last longer than the pulpal.
Sloughing of tissue
i. Epithelial desquamation
 Topical anesthetic for prolong period
 Hightened sensitivity of tissue to LA reactions in
area of topical anesthetics.
ii. Sterile abscess prolonged
 Ischemia due to vasoconstrictions
 Develops on hard palate

104. Needle breakage
 PRIMARY CAUSE: unexpected movement of the patient
 SECONDARY CAUSE:
 Inaapropriate thickness of the needle
 Previously bent
 Redirection of needle once inserted inside tissue
 Manufacture defect (rare)
 Forcing needle against resistance
 Needle engaging the periosteum
PREVENTION:
o Inform the patient
o Avoid multiple penetration
o Use proper gauze needle
o Use presterilized disposable needle
o Entire length should not be inserted
o Stabilization of the jaw

105. Hematoma
 effusion of blood into extravascular space can
result from inadvertently nicking of blood vessels
during the insertion of LA
• CAUSE:
Nick blood effusion from the vessels until extravascular
pressure exceeded intravascualar clotting occurs
• PREVENTION:
 Use the appropriate length of the needle
 Minimize no. of penetration
 Do not use needle as probe

106. Failure to obtain local anesthesia
 CAUSES:
o Operator dependent
 LA agent (type, dose)
 Improper surgical technique
 Injection of wrong solution
o Patient dependent
 Anatomical- additional innervation
 Psychological- uncooperative movement
 Pathological- infection

108. Pain on injection
• Careless technique
• Blunt needle
• High temperature of solution
• Rapid insert of LA solution
Burning sensation
• Rapid injection
• Contaminated needle cartridge
• High temperature of LA solution can alter the ph of
solution

109. Infection
• Contamination of needle
• Improper preparation of the site
• Needle passing through an area of infection
• LA solution deposited under pressure.
Edema
• Trauma
• Infection
• Hemorrahage
• Allergy
Injection of irritating solutionTissue blanching
• Trauma to blood vessels by needle
• I.V administration
Trismus