Local and systemic complications of local anesthesia administration in dentistry contents : Introduction Types of complications Localized complications with their management Generalized complications with their management

1. Local and Systemic
Complications with LA Administration
Prepared by
Mohammed Ali Shaalan

2. Seminar content :
•Introduction
•Types of complications
•Localized complications with their
management
•Generalized complications with
their management

3. Introduction
Local anesthetics allow dentistry to be practiced without patient discomfort.
However, regardless of appropriate preanesthetic patient assessment, good
patient communication, and use of proper technique according to all the
recommended guidelines and procedures prior to the administration of the
local anesthetic agent, localized and systemic responses to anesthetic
injections are uncommon but may occur.

4. Serious complications associated with the use of these
drugs are rare.
The toxicity of local anesthesia can be local or systemic.
Systemic toxicity of anesthetics most often involves the
central nervous system (CNS) or/and the cardiovascular
system.

5. Definitions :
Complications is any deviation from the normally expected
pattern during or after securing local analgesia
Localized complications occur in the region of the injection and
can be attributed to the anesthetic needle, administration
technique, and/or to the anesthetic drug administered.
Systemic complications occur in the systems of the body and
are attributed to the drug administered such as hypersensitivity
and allergy or overdosage and toxicity

6. Classifications :
According to Bennett, there are three primary categories for
local anesthetic complications :
1. Primary or secondary
2. Mild or severe
3. Transient or permanent

7. 1. Primary or secondary
Primary complication,such as burning during the injection,
is experienced by the patient at the time of the injection.
The patient experiences the burning sensation at the time of drug administration.
Secondary complicationis apparent after the injection is completed.
It is caused by the injection of the local anesthetic drug,
but experienced by the patient later.
This could occur shortly after the injection or later.

8. 2. Mild or severe
Mild complicationsresolve without requiring treatment.
For example, burning during injection is temporary and resolves shortly after
the deposition of the solution.
Severe complications require a plan of treatment to resolve the
complication.
For example, anaphylaxis requires immediate treatment and drug intervention.

9. 3. Transient or permanent
Transient complications may appear severe at the time of their
observance but will eventually resolve without any residual effect.
For example, a hematoma may cause severe swelling and bruising, but will
resolve over time without leaving any residual effects.
Permanent complications leave a residual effect.
For example, nerve damage associated with the inferior alveolar (IA) local
anesthetic block may last a few weeks, months, or indefinitely.

10. Also Complications of LA can be categorized as :
• Doctor factor (wrong technique) or administration technique
• Vasoconstrictor or the anesthetic solution
• LA Needle ( anesthetic needle )
• Patient factor
Or can be categorized as :
• Local complications
• Systemic complications

11. Local Complications
with Local Anesthesia Administration

12. LOCAL Complications
1- Pain: during and post injection
2 - Failure
• Equipment failure: (Broken needle , Cartridge failure)
• Technique failure
3-Trismus
4- Hematoma
5- Facial nerve paralysis

13. 6-Nerve injury( Persistent Paresthesia/Anesthesia)
7- Tissue sloughing
8-Self- inflicted
9- Post Anesthetic Intraoral lesions
10-Infection

14. Pain on injection
Causes :
 pH of LA(~pH 5.0) (LA with VC is acidic (3.2 Painful, LA without
VC is less acidic (6.8)
 Temperature of LA >15 – 37< is not detected by the patient
 Rapid injection technique , faster injection is painful ( a rate of
60 sec. per cartridge is ideal)
 Contamination with alcohol

15. Cont causes of pain on injection
 Touching periosteum
 Intraepithelial injection leading to ballooning
 Subperiosteal injection cause discomfort due to
injection into noncompliant tissues
 Careless technique

16. Prevention
Careful technique
 Sharp needles
 Topical anesthetic
 Slow injections(a rate of 60 sec per cartridge is ideal)
 Room temperature solutions

17. Needle breakage

18. Needle breakage
Causes :
 Unexpected movement by patient
 Needle size (small , short )
 Needle manipulation ,
i.e. bending the needle
 Defective needle

19. Prevention of Needle Breakage
Patient communication
The dentist should thoroughly explain the procedure before the injection is administered,
and continue the communication throughout the procedure, helping the patient anticipate
the dentist’s actions.
in which will help alleviate the patient’s fear of the unknown
reduce the possibility of sudden unexpected movements.
Long, large-gauge needle
Long, 25-gauge needles should be used when penetrating significant soft tissue because they
are less likely to break than thinner, smaller-gauge needles.
Documented incidences of needle breakage have been reported predominantly when 30-
gauge, and occasionally 27-gauge, needles are used.
SO Do not use 30-gauge needles for IANBs in adults or children.

20. Do not bend needle
All intraoral injections can be performed successfully
without bending the needle.
Bending the needle weakens its integrity,
increasing the possibility of breakage.
prevents the proper recapping of the needle
Which
increasing the likelihood of post exposure accidents

21. Advance needle slowly
Slow advancement of the needle results in gentle contact of the
bone, decreasing the possibility of needle breakage.
In addition,
sudden forceful bone contact may startle the patient,
causing sudden unexpected movement.
Never force needle
The needle should never be forced against significant resistance
such as bone.

22. No sudden direction changes
Changes in needle direction should never be initiated when the needle is inserted
deeply in soft tissue.
The needle should be withdrawn almost completely and then redirected.
Never insert needle to hub
The most vulnerable part of the needle is at the hub,
THIS location where most needle breakages are likely to occur.
ALSO makes it virtually impossible to retrieve the needle
if breakage occur in such area
To increase the chances of retrieving a needle fragment, a portion of the needle’s
shaft in front of the hub should always be visible during the injection.

23. Treatment
If needle breakage occurs and the needle fragment is visible,
the following are recommendations for the dentist to follow:
1. Remain calm
If the patient senses panic, he or she will close the mouth,
causing the needle fragment to embed into the tissue.
2. Keep your hands in the patient’s mouth, and ask the
patient to open widely.
3. Attempt to remove it with the hemostat or cotton pliers.

24. If the needle fragment is not visible and cannot be retrieved,
the following are recommendations for the dentist to follow:
1. Remain calm, and inform the patient of the incident in a
manner that will alleviate his or her fear and apprehension.
2. The dentist, should refer the patient to an oral maxillofacial
surgeon for consultation and possible further treatment.
3. Document the incident and sequence of events in the
patient’s permanent record. It is important to include the
patient’s reaction to the situation.
4. Keep the remaining needle fragment for structural
evaluation.

25. 5. Surgical procedures are indicated if the needle
fragment is not deeply embedded in tissue and easily
located by radiographic or clinical examination.
6. If the needle is deeply embedded in tissue, the
maxillofacial surgeon may recommend that the needle
remain in the tissue without further attempt for removal.

26. Surgical removal
• A variety of methods have been described to locate a broken
needle in the pterygomandibular space.
• locating the retained fragment through panoramic and
computed tomographic (CT) scanning are often the
investigation of choice.
• CT scan should be the imaging investigation of choice, as it
accurately relays the position of the needle to recognizable
anatomical landmarks, especially with 3D reformatting
• Plain radiographs taken at right angles to each other are used
The most frequent combinations employed are a panoramic
radiograph and posterior anterior view of the mandible(PA) .

27. Preoperative radiographic image illustrating
the broken needle:
(A) 3D computerized tomography

28. (B) lateral skull view (C) posterior-anterior skull view

29. (D) panoramic view.

30. The incision
• The incision and site of exploration can be determined
from the information available on the CT scan,
• Most reports have suggested the use of a vertical
mucosal incision often on the medial aspect of the
mandible in the area penetrated by the needle, followed
by blunt supra-periosteal dissection to identify the
needle.

31. In the previous case
• Blunt dissection was used medially along the ramus to
expose the pterygomandibular space.
• A malleable retractor was used to protect the lingual and
inferior alveolar nerves.
• Further exploration of the pterygomandibular space was
performed using a microscope.
• The tip of the needle fragment was identified under the
microscope.
• The broken needle was removed using a hemostat forcep

32. TRISMUS
(limited mouth opening)
Causes
• IM Injection (Med. Pterygoid, temporalis)
• Hemorrhage
• Barbed needle
• Contamination by alcohol or sterilant
• Bacterial infection from the site of injection

33. This happens when the needle is inserted unintentionally
through the muscles resulting in its spasm.
This can happen to almost anyone regardless of their age
because dentists will have to depend on imagination to get
to the nerve correctly and start administering local
anesthesia.
Due to different location of bony landmarks and nerves in
individuals, a needle might be inserted through a muscle
accidentally

34. Trismus Prevention
• Sharp needles
• Proper care and handling of cartridges
• Aseptic technique and clean injection site
• Atraumatic insertion
• Minimal injections and volume

35. Treatment
Moist towel 20mins/hr
Management of trismus will require the patient to place a hot moist towels at
the site for approximately 20 minutes every hour
Physiotherapy
the patient should gradually open and close the mouth as means of physiotherapy.
R/O Infection
Muscle relaxants
Analgesics
analgesics might be prescribed
depending on the severity of pain.

36. Hematoma
Hematoma due to needle accidentally penetrate a b.v.
leading to effusion of blood into extravascular spaces

37. A hematoma develops when a blood vessel, particularly an artery,
is punctured or lacerated by the needle.
This is observed as asymmetrical swelling and discoloration of the
tissue resulting from the effusion of blood into extravascular spaces .
Hematomas particularly result after administration of a posterior
superior alveolar (PSA) block.
However, the inferior alveolar and mental nerve blocks also commonly
cause hematomas.
Hematomas less often occur after an infraorbital (IO) block,
because pressure is applied to the foramen immediately following the
injection.
Hematomas are least likely to develop following palatal blocks.

38. A, Hematoma producing initial swelling from administration of the right
posterior superior alveolar nerve block
B, Progression of hematoma one week following initial swelling.

39. Although hematomas may appear serious, they are more a
cosmetic nuisance. Trismus and mild pain may also occur.
A hematoma resulting from a PSA block is usually the largest
due to the infratemporal fossa being able to accommodate large
volumes of blood, and clinically appears as extraoral bruising.
Hematomas resulting from an IA block appear as intraoral
bruising.

40. Prevention
Although hematomas can occur even when proper technique is
used,
to decrease the risk the dentist should follow these guidelines:
1. Know your anatomy.
2. Use a short needle and modify the needle penetration depth for
the PSA block for children, petite adults, and patients with small
facial characteristics.
3. Minimize the number of needle insertions.
4. Follow all recommended injection techniques for all local
anesthetic injections.

41. Management of Hematoma
1. At the first sign of swelling, apply pressure directly to the area for a minimum of
2 minutes.
This involves the medial aspect of the mandibular ramus for the IA block, the
mental foramen for the mental/incisive block, and because it is difficult to locate
the blood vessels for the PSA block, pressure should be applied as far distally as
possible without producing a gag reflex.
2. Apply ice to the region of the developing
hematoma to reduce the swelling.
Ice will constrict the blood vessels,
decreasing the effusion of blood into the
extravascular spaces,
and also provide some analgesic effects
for the patient.

42. 3. Inform the patient that soreness and limited movement of their jaw may occur.
Instruct the patient to use warm moist towels applied to the region the next day for 20
minutes every hour to assist in the resorption of blood.
Heat application (>6 hours post injection vasodilatory) should be avoided .
4. Inform the patient that there are no serious complications associated with
hematomas,
and that swelling and discoloration should disappear after 7–14 days.
5. Do not dismiss the patient until bleeding has stopped.
Document the incident in the patient’s record including instructions presented to the
patient, and the patient’s response.
6. When hematoma is large prescribe antibiotics to prevent infection
7. Analgesics and follow up as indicated.

43. Temporary facial nerve paralysis

44. Temporary facial nerve paralysis is caused by the
inadvertent deposition of local anesthetic solution
during the inferior alveolar (IA) block into the parotid
gland, anesthetizing the facial nerve that runs through
the parotid gland
This is due to over insertion of the needle penetrating
the parotid gland.
This produces a unilateral loss of motor function
to the facial expression muscles.

45. The patient might not
be able to smile,
or close the eyelid,
when they are asked to do so,
on the affected side
A, Inability to close eyelid.
B, Drooping of lip on affected
side (patient’s left).

46. Treatment
1. Reassure the patient
At the point of muscle weakening, the patient will be alarmed
and immediate reassurance is necessary to alleviate the
patient’s fears.
Reassure the patient that the paralysis is only temporary and
will last only a few hours.
Explain that weakness in the muscles will resolve as soon as the
anesthetic action fades.

47. 2. Protect cornea
Ask the patient to remove contact lenses if applicable and to manually close his or
her eye.
Although the corneal reflex remains functional, this will assist in keeping the
cornea lubricated.
The eye on the affected side should therefore be protected
and covered by an eye-shield or eye-pad.
A drops of sterile paraffin or (Saline Eye Drops )
might be administered to help protect the cornea

48. 3. There are no contraindications to completing the scheduled
treatment.
However, it may be advisable to reschedule treatment for a different
time.
This should be determined on an individual basis and predominantly depends on
the patient’s reaction to the situation.
If treatment is to be continued, the IA block must be completed
reinjected because the target site was missed during the first
injection.
4. Document the incident and the patient’s reaction in the patient’s
chart.
5. Follow-up as indicated.

49. Persistent Paresthesia/Anesthesia
Injury to a nerve where the patient experiences
a sudden sharp and electrical pain.
This happens most frequently where the injection was very accurate and the
needle has touched the nerve.
If the nerve is damaged in any case, the anesthetic effect might persist for weeks
or even months or permanent loss of sensation if the impact has resulted in a
permanent damage to the nerve.

50. Causes :
Trauma to nerve sheath OR Intraneural injection
paresthesia may be caused by trauma to the nerve sheath resulting
from the needle contacting the nerve during its insertion or
removal from the tissues.
This occurs most commonly with the lingual nerve producing
a sensation of an electrical shock when it occurs.
Hemorrhage around neural sheath
Hemorrhage around the nerve sheath may also contribute to
paresthesia by creating excessive pressure on the nerve

51. Neurolytic agents (alcohol, phenol)
Paresthesia may be a result of irritation to the nerve following the
administration of a contaminated local anesthetic solution with
alcohol or other disinfectants.
Edema caused by the irritation places pressure on the nerve, resulting
in prolonged anesthesia.
The observed frequencies of paresthesia following the administration
of articaine (p < 0.002) or prilocaine (p < 0.025) were significantly
greater than the expected.
These results are consistent with the suggestion that local anesthetic
formulations may have the potential for mild neurotoxicity.

52. To prevent paresthesia
To prevent paresthesia, local anesthetic cartridges should be
stored properly in their original containers.
• Cartridges should never be placed in disinfecting solution,
• Injection techniques should be used as recommened
Most paresthesia is not serious and will typically resolve within
8 weeks.
It most commonly occurs with the lingual and inferior alveolar
nerve and produces only minimal sensory deficit. Fortunately,
permanent nerve damage rarely occurs

53. Management
1. Reassure the patient.
The patient will typically call the dental office the day after the procedure
concerned about the prolonged numbness.
Reassure the patient that paresthesia is not uncommon following the
administration of local anesthetics.
2. Arrange for the patient to be examined
to determine the extent of paresthesia.
• Instruct the patient that paresthesia may last up to 2 months and perhaps
longer.
• Inform patient of normal signs of nerve recovery
-Tingling
-Intermittent burning or sharp pain

54. 3. A vitamin B12 complexes might be prescribed to fasten the
time of healing.
4. Re-evaluate patient in 2 weeks
5. Document degree and extent
6. If symptoms persist, refer to OMFS
7. The patient should be examined by the dentist every 2
months until normal sensation returns.
8. Avoiding injections to the traumatized nerve.
Alternative pain control measures should be taken.

55. Self- inflicted

56. This happens after anesthesia where the patient is not
instructed not to bite on his/her lips for 2-3 hours
to compensate for duration of the anesthesia
as the patient will not have any kind of sensation in
his/her lips and might unintentionally bite on it for a
long period of time leading to an ulcer
Children and MR at high risk
• Use short-acting LA
• Instructions
• Close observation

57. Treatment
• The mistake here lies back to the dentist of not
informing the patient or instructing not to bite in
his/her lips.
• If this incident occurs however, the ulcer will heal by
itself in 10-15 days.
It might take longer depending on the severity of the
ulcer but, in general, it heals by itself
Analgesics might be prescribed to alleviate pain and
inflammation.

58. Post Anesthetic Intraoral lesions

59. • Resemble HSV outbreak
• Appears after 2 days from LA administration
Causes :
• Local tissue trauma/hypoxia/necrosis
• Activation of HSV
Treatment
• Reassure patient
Self limiting 10-14 day course
• Analgesics

60. Epithelial Desquamation

61. Cause
• Prolonged use of topical anesthetic
• High concentration of vasoconstrictors
Predominantly in palatal mucosa
Treatment
• Resolution in 7-10 days
• Analgesics
• Saline rinses or Peridex
• Petrolatum can be used to
coat the area to minimize
discomfort

62. Failure anesthesia
Causes :
• Wrong technique
• Anatomical variations: Bifid MC (double nerve supply)
and Retromolar canal
or Nerve anastomosis Secondary supply by a soft tissue
nerve: LN, LBN & GPN
• Inadequate dose or Sepsis acidity
• Anxiety reduced patient pain threshold (Patient
immaturity)

63. Management of failed local anesthesia
• Check anatomical landmarks
• Repeat injection
• Consider alternate or additional technique
• Consider whether anxiety may be contributory
factor for pain and try again about a week later

64. Infection
Infection around the area of needle penetration
Or deep in the tissue
Causes :
• Contamination of the anesthetic needle before injection
• Improper handling of local anesthetic
• Administration of contaminated solution
• Administering local anesthetics through areas of dental
infection
Treatment
• Antibiotics should be prescribed
• Analgesics for pain

65. Systemic Complications
with Local Anesthesia Administration

66. • Systemic toxicity of local anesthetics can occur after
administration of an excessive dose, with rapid absorption, or
because of an accidental intravenous injection. The
management of local anesthetic toxicity can be challenging,
and in the case of cardiac toxicity, prolonged resuscitation
efforts may be necessary.
• Therefore, understanding the circumstances that can lead to
systemic toxicity of local anesthetics and being prepared for
treatment is essential to optimize the patient outcome.

67. • Systemic toxicity is typically manifested as central nervous system (CNS)
toxicity (tinnitus, disorientation, and ultimately, seizures) or
cardiovascular toxicity (hypotension, dysrhythmias, and cardiac arrest).
• The dose capable of causing CNS symptoms is typically lower than the
dose and concentration result in cardiovascular toxicity. This is because
the CNS is more susceptible to local anesthetic toxicity than the
cardiovascular system. However, bupivacaine toxicity may not adhere to
this sequence, and cardiac toxicity may precede the neurologic symptoms.
• Although less common, cardiovascular toxicity is more serious and more
difficult to treat than CNS toxicity.

68. These complications may caused by:
• direct extension of the usual pharmacological effects of
the drugs :
1. Side effects
2. Overdose
3. Local toxic effect
• caused by alteration in recipient of the drug
1. Disease process ( hepatic dysfunction ,CHF, renal
dysfunction )
2. Emotional disturbance
3. Genetic aberrations (Atypical plasma cholinesterase )
• caused by allergic response to the drug

69. Systemic Complications Of Local Anesthesia are :
1. Toxicity due to overdose
2. Allergy Anaphylactic reactions
3. Idiosyncrasy
4. Syncope
5. Drug interaction
6. Serum hepatitis
7. Respiratory arrest
8. Cardic arrest
9. Hyperventilation
10.Infection to more distant areas

70. local anesthetic toxicity
While generally safe, local anesthetic agents can be
toxic if administered inappropriately, and in some cases
may cause unintended reactions even when properly
administered. Adverse effects are usually caused by high
plasma concentrations of the agent, which may result
from one of the following:
• Inadvertent intravascular injection
• Excessive dose or rate of injection
• Delayed drug clearance
• Administration into vascular tissue

71. Predisposing factors
Patient factor Drug factor
1. Vasoactivity
2. Concentration
3. Dose
4. Route of administration
5. Vascularity of injection site
6. Presence of vasoconstrictor
7. Rate of injection
1. Age
2. Weight
3. Other drug
4. Sex
5. Genetics
6. Mental attitude and
environment

72. Predisposing factors to toxic reactions to
the local anesthetic itself include:
Age a Patients under 6 years and over 65 years of age
- Absorption, metabolism, and excretion are not fully
developed before age 6, and these functions diminish
after age 65.

73. Patient’s weight
Underweight patients, especially those with little
muscle mass –
Drugs are calculated on mg of drug/per kg, or pound
of weight
The less an individual weighs and the less muscle
mass he has, the lower the tolerance to the drug.

74. Liver disorders
Liver damage causes local anesthetic to build up in the blood.
Most local anesthetics are biotransformed in the liver and
broken down to products that can be eliminated from the body
by the kidneys.
patients with reduced hepatic function may exhibit an
abnormally decreased rate of metabolism of amide local
anesthetics, resulting in potentially toxic blood levels.
Dosage levels must therefore be reduced for these patients

75. For example, because lidocaine is hepatically
metabolized,
liver dysfunction increases the risk of toxicity.
Because lidocaine is also protein bound, low protein
states may also increase risk
In such cases, local anesthesia should be used
judiciously and in consultation with the patient`s
physician.

76. Genetic factor
Pseudocholinesterase deficiency:
• Pseudocholinesterase deficiency is an inherited blood plasma
enzyme abnormality in which the body's production
of butyrylcholinesterase ( pseudocholinesterase) is impaired.
• People who have this abnormality may be sensitive to certain
anesthetic drugs, including the muscle relaxants
succinylcholine and mivacurium as well as other ester local
anesthetics.
local anesthetics of the ester type (eg, procaine) should be
avoided in patients who have this rare familial enzyme defect .

77. • Dentists should be aware of the importance of
avoiding ester local anesthetics in patients with
pseudocholinesterase deficiency.
• Although ester local anesthetics are not commonly
used in clinical practice, they are often employed
when a patient has a suspected allergy to amide
local anesthetics or where vasoconstrictors are
contraindicated.

78. • A personal or family history of an adverse drug reaction to
one of the choline ester compounds, such as succinylcholine,
mivacurium, or cocaine, may be the only clue suggesting
pseudocholinesterase deficiency.
• This condition is recognized most often when respiratory
paralysis unexpectedly persists for a prolonged period of time
following administration of standard doses of
succinylcholine.
• The mainstay of treatment in these cases is ventilatory
support until diffusion of succinylcholine from the
myoneural junction permits return of neuromuscular
function of skeletal muscle.
• The diagnosis is confirmed by a laboratory assay
demonstrating decreased plasma cholinesterase enzyme
activity.

79. Acid-base status
Acid-base status plays an important role in the setting of local anesthetic toxicity
Acidosis and hypercarbia amplify the CNS effects of local anesthetic overdose and
exacerbate cardiotoxicity.
Hypercarbia enhances cerebral blood flow; consequently, more local anesthetic is
made accessible to the cerebral circulation.
Diffusion of carbon dioxide across the nerve membrane can cause intracellular
acidosis, and as such, it is promoting the conversion of the local anesthetic into the
cationic, or active, form. Because it is impossible for the cationic form to travel
across the nerve membrane, ionic trapping occurs, worsening the CNS toxicity of the
local anesthetic.
Hypercarbia and/or acidosis also reduce the binding of local anesthetics by plasma
proteins, and as a result, the fraction of free drug readily available for diffusion
expands

80. Interactions with other drugs (eg, cimetidine, beta-
blockers) can also affect lidocaine drug levels
• There are interactions between epinephrine and
other drugs. The action of catecholamines is
potentiated by some drugs, e.g. tricyclic
• antidepressants, MAO inhibitors, antiparkinson
drugs, methyldopa, guanethidine. In patients, taking
those drugs, dose of epinephrine must be reduced.

81. Cardiovasculardisease
patientswithischemicheartdisease(anginapectoris,previous
myocardialinfarction)orwhohavehadpreviouscardiac
surgeryorcirculatorydysfunctionsuchascardiacfailure,show
higherplasmalevelsoflidocainewhencomparedwithhealthy
subjectsgiventhesamedose.
Thereforeitisrecommendedthatthemaximumsafedosebe
halvedinsuchpatients.

82. Kidney disorders - If the kidneys can not eliminate the
byproducts of local anesthetics, there can be toxic
accumulations in the blood.
Pregnancy - During pregnancy, renal function can be
disturbed. This can impair excretion and result in an
increased blood level of the local anesthetic.
• Bupivacaine has been shown to have increased
cardiotoxicity in pregnant women resulting in a
decreased CC/CNS dose ration.

83. Drug factors
• Various factors lead to toxic reactions to local anesthetics.
Local anesthetics have vasodilating properties, which increase
the possibility of overdose.
Low doses of local anesthetics may cause vasoconstriction, where as, moderate or high
doses result in vasodilation and decreased SVR. Cocaine is the only local anesthetic
thatcausesvasoconstrictionatalldoses.
• The amount of drug given should not be more than 1.1 dental
cartridges of 2 percent lidocaine per 20 pounds of body
weight.
More than that amount increases the chances of toxic overdose.

84. The rate of injection
The rate of injection is the most important factor in
preventing overdose. A rapid injection (30 seconds or
less) causes rapid blood levels, which increases the
chance of overdose.
So , Injections should be administered slowly
(60 seconds or more for administration of a 1.8 mL cartridge).
This produces a low blood level, which decreases the
chance of overdose

85. Anothercauseoftoxicoverdoseisintravascularinjection
• which occurs when the anesthetic is unintentionally injected directly
intoabloodvessel.Bothinterarterialandintravenousinjections may
produceoverdosereactions.
• Intravascular injection is usually prevented by using an aspirating
syringe. A return of blood into the dental cartridge is considered a
positive aspiration. Even if there is no return of blood into the dental
cartridge, there is still a risk of intravascular injection if the injection
isadministeredrapidlyandincloseproximitytoacapillarybed.

86. Vasoconstrictorsareimportant
• The mouth is highly vascular, making absorption of local anesthetic into
the blood more rapid than at other sites. This is why the presence of a
vasoconstrictorinlocalanestheticsissoimportant.
• The vasoconstrictor counteracts the vasodilating properties of blood
vesselsanddecreasestherateofsystemicabsorption.

87. • The most common vasoconstrictor is epinephrine. Epinephrine should
not be used on patients who take a variety of medications; however,
there is a greater risk of medical emergency if local anesthesia is
administeredwithoutit.
• The most common adverse drug reaction with local anesthesia is not a
reaction or drug interaction with epinephrine - it is local anesthesia
toxicity.
• If epinephrine is contraindicated for a patient, the local anesthetic
mepivicaine (Carbocaine) is a good alternative. It is slower to dissipate
fromtheinjectionsiteanddoesnotcontainavasoconstrictor.

88. Maximum safe dose

89. Minimum Intravenous Toxic Dose of Local
Anesthetic in Humans
Agent Minimum Toxic Dose (mg/kg)
Procaine 19.2
Tetracaine 2.5
Chloroprocaine 22.8
Lidocaine 6.4
Mepivacaine 9.8
Bupivacaine 1.6

90. CNS toxicity
• CNS toxicity is biphasic.
• The earlier manifestations are due to CNS excitation,
with problems such as seizures.
• Subsequent manifestations include CNS depression with
a cessation of convulsions and the onset of
unconsciousness and respiratory depression or arrest.

91. Toxicity mechanisms
CNS toxicity from local anesthetics manifests initially as CNS
excitation, followed by CNS depression.
This biphasic effect occurs because local anesthetics first block
inhibitory CNS pathways (resulting in stimulation) and then
eventually block both inhibitory and excitatory pathways
(resulting in overall CNS inhibition).

92. Cardiovascular effects
• Cardiovascular effects occur at higher serum concentrations of
local anesthetics.
• These effects may include arrhythmias ,acceleration of the
ventricular rate has been reported in patients with atrial
arrhythmias
• Cardiovascular effects occur because these agents block sodium
channels through a fast-in, slow-out mechanism that affects
impulse conduction through the heart and nerve tissue.
• In the heart, this depresses Vmax (ie, the rate of depolarization
during phase 0 of the cardiac action potential) and may lead to
reentrant arrhythmias. Additionally, conduction through the sinus
and atrioventricular nodes is suppressed

93. History
• Manifestations of local anesthetic toxicity typically appear 1-5 minutes
after the injection, but onset may range from 30 seconds to as long as 60
minutes.
• Initial manifestations may also vary widely. Classically, patients experience
symptoms of central nervous system (CNS) excitement such as the
following:
• Circumoral and/or tongue numbness
• Metallic taste
• Lightheadedness
• Dizziness
• Visual and auditory disturbances (difficulty focusing and tinnitus)
• Disorientation
• Drowsiness
Although cardiac toxicity classically does not occur without preceding CNS
toxicity, numerous published case reports describe episodes limited to
cardiovascular manifestations. In these cases, onset of symptoms was delayed
by 5 minutes or more. [1]

94. Physical Examination
• After the use of local anesthetic agents, consider the
appearance of new signs or symptoms as a possible sign of
toxicity.
• The manifestation of toxicity depends on the organ system
or systems that are affected. Toxicity manifestations can
be categorized as follows:
• CNS
• Cardiovascular
• Hematologic
• Allergic
• Local tissue

95. Central nervous system manifestations
• With higher doses, initial CNS excitation is often followed by
a rapid CNS depression, with the following features:
• Muscle twitching
• Convulsions
• Unconsciousness
• Coma
• Respiratory depression and arrest
• Cardiovascular depression and collapse

96. • With progression of toxicity, the patient may experience tonic-
clonic seizures and, eventually, unconsciousness and coma.
• CNS symptoms may be masked in patients premedicated with
anticonvulsants such as benzodiazepines or barbiturates. The
first sign of toxicity in these premedicated patients may be
cardiovascular depression.
• When blood levels are high enough to block inhibitory and
excitatory pathways, convulsions cease and the patient may
experience respiratory depression or arrest and cardiovascular
depression.
• Large bolus injections may increase peak anesthetic levels to the
point where the CNS and cardiovascular system are affected
simultaneously.

97. Cardiovascular manifestations
• Risk of cardiovascular toxicity is somewhat greater with
lipophilic local anesthetics such as bupivacaine.
• Risk of cardiac toxicity is greatest in those patients with
underlying cardiac conduction problems or after myocardial
infarction.
• Toxic doses of local anesthetic agents can cause myocardial
depression (tetracaine, etidocaine, bupivacaine), cardiac
dysrhythmias (bupivacaine), and cardiotoxicity in pregnancy.
• Several anesthetics (eg, lidocaine) also alter vascular tone, with
low doses having vasoconstrictive effects and higher doses
causing relaxation of vascular smooth muscle, possibly leading
to hypotension.

98. The sequence of cardiovascular events is ordinarily as follows:
Low blood levels of local anesthetic usually generate a small increase in
cardiac output, blood pressure, and heart rate, which is most likely due to a
boost in sympathetic activity and direct vasoconstriction.
As the blood level of local anesthetic rises, hypotension ensues as a result of
peripheral vasodilation due to relaxation of the vascular smooth muscles.
Further rise of local anesthetic blood levels leads to severe hypotension,
resulting from the combination of reduced peripheral vascular resistance,
reduced cardiac output, and/or malignant arrhythmias.
Eventually, extreme hemodynamic instability may lead to cardiac arrest.

99. The range of signs and symptoms of cardiovascular
toxicity include the following:
• Chest pain
• Shortness of breath
• Palpitations
• Lightheadedness
• Diaphoresis
• Hypotension
• Syncope

100. • Effects on cardiac conduction include widened PR
interval, widened QRS duration, sinus tachycardia,
sinus arrest, and partial or complete atrioventricular
dissociation.
• Cardiac arrest has been reported after intraurethral
administration of lidocaine.
• Cardiac toxicity is potentiated by acidosis, hypercapnia,
and hypoxia, which worsen cardiac suppression and
increase the chance of arrhythmia.
• This is important to consider since seizure makes this
metabolic picture more likely.

101. Overdose
Overdose can be defined as those clinical signs and
symptoms that result from an overlay high blood level of
the drug in varous target tissue and organs

102. CLINICAL MANIFESTAIOTNS OF OVERDOSE
minimal to moderate overdose level :
Signs: Symptoms:
• Talkativeness
• Apprehension
• Slurred speech
• Excitability
• Stutter ‫بالكالم‬ ‫تلعثم‬
• Euphoria
• Nystagmus‫اراديا‬ ‫ال‬ ‫العين‬ ‫مقلتي‬ ‫تذبذب‬
• Muscular twitching / tremors
• Elevated BP
• Sweating
• Elevated heart rate
• Nausea/vomiting
• Elevated resp. rate
• Disorientation
• Failure to follow commands /
reason
• Lack of response to painful stimuli
• Restless
• Visual disturbances
• Nervous
• Auditory disturbances
• Numbness
• Metallic taste
• Light-headed and dizzy
• Drowsy and disoriented
• Losing consciousness
• Sensation of twitching (before
actual twitching is observed)

103. Moderate to High overdose level :
Generalized tonic-clonic seizure activity
followed by
• Generalized CNS depression
• Depressed BP, heart rate
• Depressed respiratory rate

104. Pathophysiology
Local anesthetics cross blood-brain barrier, producing CNS depression as level rises
eg. LIDOCAINE
Blood Level Action Produced
• < .5 ug/ml
• 0.5-4 ug/ml
• 4.5-7.5 ug/ml
• > 7.5 ug/ml
• - no adverse CNS effects
• Anticonvulsant
• - agitation, irritability
• - tonic-clonic seizures
Local anesthetics exert a lesser effect on the cardiovascular system
eg. LIDOCAINE
Blood Level Action Produced
• 1.8-5 ug/ml
• 5-10 ug/mlx
• >10 ug/ml
• treat PVCs, tachycardia
• - cardiac depression
• - severe depression,
bradycardia, vasodilatation,
arrest

105. MANAGEMENT of OVERDOSE
Mild Reaction -slow onset
• Reassure patient
• Administer O2
• Monitor vital signs
• Consider IV anticonvulsant
• Allow recovery or get medical help
• Get medical consultation, esp. if possibility of metabolic or
renal dysfunction

106. Severe Reaction - rapid onset
• Stop all treatment
• Place patient in supine position, feet up
• Establish airway, give O2
• If convulsions, protect patient
• Call for emergency medical help
• Administer anticonvulsant drugs
• Consider vasopressors
• Get medical consultation, esp. if possibility of metabolic
or renal dysfunction

107. Vasoconstrictor Overdose Epinephrine Overdose
Clinical manifestations:
• Fear, anxiety
• Tenseness
• Restlessness
• Tremor
• Weakness
• Throbbing headache
• Dizziness
• Pallor
• Respiratory difficulty
• Palpitations
• Sharply elevated BP (systolic)
• Increased heart rate
• Cardiac tachyarrhythmias
Management :
• Stop dental treatment
• Sit patient up
• Reassure patient, administer O2
• Monitor BP and pulse until fully
recovered

108. Allergic Reactions
Can be of 2 types :
• Antigen induced occurs in sec/min(Angioedema,Anaphylaxis )
Or
• IV Cell mediated 48 hrs (Contact dermatitis)

109. Allergens in LA :
Esters - usually to the Para-amino-benzoic-acid product
Na bisulfite or metabisulfite - found in anesthetics as perservative for
vasoconstrictors
Methylparaben - no longer used as perservative in dental cartridges
Amino amides are not associated with PABA and do not produce
allergic reactions with the same frequency. However, preparations
of amide anesthetics may sometimes contain methylparaben, which
is structurally similar to PABA and thus may result in allergic
reactions.

110. Allergy - signs/symptoms
Dermatologic:
• Urticaria - wheals, pruritis
• Angioedema
• Minor rash
Respiratory:
• Laryngeal edema
• Bronchospasm
• distress anxiety
• wheezing
• diaphoresis
• dyspnea
• cyanosis or flushing
• tachycardia
• use of accessory
muscles

111. Anaphylaxis
Typical progression
• Skin reactions
• Smooth muscle spasms (GI, GU, respiratory)
• Respiratory distress
• Cardiovascular collapse
may occur rapidly, with considerable overlap

112. Management of Allergic Reactions
Delayed skin reaction
Benadryl - 50 mg stat & Q6H X 3-4 days
Immediate skin reaction
Epinephrine 0.3 mg IM or SC
Benadryl - 50 mg IM
Observation, medical consultation
Benadryl - 50 mg Q6H X 3-4 days

113. Bronchial constriction
Semi-erect position, O2 - 6 L/min
Inhaler or Epinephrine 0.3 mg IM or SC
Benadryl - 50 mg IM
Observation, medical consultation
Benadryl - 50 mg Q6H X 3-4 days
Laryngeal edema
Place supine, O2 - 6 L/min
Epinephrine 0.3 mg IM or SC
Maintain airway
Benadryl - 50 mg IV or IM
Hydrocortisone - 100 mg IV or IM
Perform Cricothyrotomy

114. Anaphylaxis
1. Place supine, on flat surface
2. ABCs of CPR, call for medical help
3.Epinephrine 0.3 mg IV or IM (Q 10 mins)
4. O2 - 6 L/min, monitor vital signs
If no improvement give Epinephrine 0.3 mg IV or IM again in 10
mins
• Histamine blocker -50mg
• Diphenhydramine (Benadryl, 25-50 mg for adults, 1 mg/kg for
pediatric patients).
• OR 10 mg Chlorpheniramine corticosteriod
• Hydrocortisone 100mg IM/IV vi)
CPR After clinical un improvement, Benadryl and Hydrocortisone

115. Hematologic manifestations
Methemoglobinemia is a condition caused by elevated levels of methemoglobin in
the blood.
Methemoglobin is a form of hemoglobin that contains the ferric [Fe3+] form of iron.
The affinity for oxygen of ferric iron is impaired.

116. • Methemoglobinemia has been frequently reported in association with
benzocaine use;
• however, lidocaine and prilocaine have also been implicated. O-toluidine, the
liver metabolite of prilocaine, is a potent oxidizer of hemoglobin to
methemoglobin.
• At low levels (1-3%), methemoglobinemia can be asymptomatic, but higher
levels (10-40%) may be accompanied by any of the following complaints:
• Cyanosis
• Cutaneous discoloration (gray)
• Tachypnea
• Dyspnea
• Exercise intolerance
• Fatigue
• Dizziness and syncope
• Weakness

117. Adverse effects of topical
application
Topical anesthesia can produce systemic toxicity

118. • A variety of anesthetics are available for topical or
mucosal application (eg, tetracaine, benzocaine,
lidocaine, cocaine).
• Adverse effects from these agents typically occur
when they are applied to abraded or torn skin,
resulting in systemic absorption and high plasma
concentrations of the agent.
• Similarly, absorption of oral viscous lidocaine may
cause systemic toxicity, particularly with repeated
use in infants or children.

119. The following systemic reactions may occur with
topical anesthetics:
• CNS: High plasma concentration initially produces CNS stimulation (including
seizures), followed by CNS depression (including respiratory arrest); CNS
stimulatory effects may be absent in some patients, particularly with amides
(eg, tetracaine); epinephrine-containing solutions may add to the CNS
stimulatory effect
• Cardiovascular: High plasma levels typically depress the heart; effects may
include bradycardia, dysrhythmias, hypotension, cardiovascular collapse, and
cardiac arrest; epinephrine-containing local anesthetics may cause
hypertension, tachycardia, and myocardial ischemia
• Suppression of the gag reflex with oral administration
Other adverse effects include the following:
• Transient local burning or stinging sensation
• Skin discoloration
• Swelling
• Neuritis
• Tissue necrosis and sloughing
• Methemoglobinemia with prilocaine

120. Fainting or syncope
Fainting or syncope frequently occurs because
of patient frightened at the thought of
receiving an injection

121. Predisposing factors:
1-Psychogenic factors: fear , anxiety and sight of
unpleasant object as blood or surgical instrument
2-Non-psychogenic: factors as pain especially sudden
unexpected, sitting in waiting area for a long period,
hunger causing low glucose supply or exhaustion ,poor
physical condition

122. Clinical features
1-Pre-syncope period :
The patient feels faint and may feel nauseating. Paleness and coldness of hand,
cold sweating over the forehead and hands, hypotension , tachycardia and deep
irregular respiration Loss of consciousness: Hypotension , bradycardia and
shallow irregular respiration. Possible muscular twitches (tremors) or convulsive
movements of the extermities. Progression may occur into muscular relaxation
and apnoea
2-Post-syncope period After regaining consciousness the patient feels weak,
nauseating and mentally confused for few minutes.

123. Pathophysiology
Stress causes the secretion of adrenalin into the circulation
this cause
peripheral vascular resistance and blood flow to the
muscle to prepare body to response to this stressful
condition

124. Treatment
1-Stop any dental procedure
2-Place patient in supine or trendelenberg position to facilitate
venous return to the heart
3-Maintain patient airway , respiratory stimulants by aromatic
spirit of ammonia
4-Oxygen administration might be needed
5-Keep the patient in this position under observation 6-For
persistent bradycardia give atropine 0.4 mg i.v

125. Regional or systemic infection:
spread of infection within the perioral tissues can be
potentially spread through planes of the head and neck by
passage of a needle through an infected area.
* Endocarditis risk: injections such as the intraligamentary
injection can force bacteria into the systemic circulation
and cause bacterial endocarditis

126. Hepatotoxicity
(bupivacaine):
probable cause of clinically apparent liver
injury).

127. Mechanism of Injury
• The mechanism by which bupivacaine might cause liver
injury is unknown, but is most likely due to an idiosyncratic
hypersensitivity reaction. The amide local anesthetics are
metabolized locally and do not affect the activity of
cytochrome P450 enzymes.
Management
• The liver injury linked to exposures to amide anesthetics has
largely been limited to use of bupivacaine given by infusion
or multiple injections over a period of 1 to 3 days.
• The injury was invariably self-limited, and no instance of
chronic liver injury, vanishing bile duct syndrome or acute
liver failure has been linked to bupivacaine or other local
anesthetics.

128. Local Anesthetic Toxicity Treatment & Management
• In the patient with suspected local anesthetic toxicity,
the initial step is stabilization of potential threats to life.
If the signs and symptoms develop during administration of the local anesthetic,
stop the injection immediately and prepare to treat the reaction.
Ensure adequate oxygenation, whether by face mask or by intubation.
• Attention to impending airway compromise, significant hypotension, dysrhythmias, and
seizures takes precedence.
• Once other possible etiologies of the patient's new symptoms have been excluded,
management of the specific symptoms can begin.

129. • Benzodiazepines are the drugs of choice for seizure
control.
• Propofol can be used to control seizures but has the risk
of potentiating cardiovascular toxicity.
• Refractory seizures may require neuromuscular blockade
(eg, with succinylcholine).
• In severe reactions, monitor the cardiovascular system
and support the patient with intravenous fluids and
vasopressors as required. Small bolus doses of
epinephrine are preferred. Vasopressin is not
recommended.

130. • Hypoxemia and metabolic acidosis may potentiate the
cardiovascular toxicity of lidocaine and other local anesthetics.
Early control of seizures and aggressive airway management to
treat hypoxemia and acidosis may prevent cardiac arrest.
 Use of sodium bicarbonate may be considered to treat severe
acidosis.
• Cardiac arrest due to local anesthetic toxicity is a rare but well
recognized complication that may occur in cases of large
overdose, especially those involving inadvertent intravascular
injection. These patients have a favorable prognosis if circulation
can be restored before hypoxemic injury occurs. Aggressive
resuscitation is therefore indicated in most cases.
Cardiopulmonary bypass has been used effectively to treat
cardiac arrest due to local anesthetic toxicity.

131. • Increasing evidence suggests that the intravenous (IV)
infusion of lipid emulsions can reverse the cardiac
and neurologic effects of local-anesthetic toxicity.
Although no blinded studies have been conducted in
humans, studies in animal models and multiple case
reports in human patients have shown favorable results.
Indeed, case reports support the early use of lipid
emulsion at the first sign of arrhythmia, prolonged
seizure activity, or rapid progression of toxic
manifestations in patients with suspected local
anesthetic toxicity.

132. • Infrequently, local anesthetics may provoke an allergic
or hematologic reaction. Allergic reactions can be
treated with diphenhydramine or, for more serious
reactions, epinephrine or corticosteroids.
• Methemoglobinemia should initially be treated
symptomatically.
Subsequent treatment is guided by blood levels of
methemoglobin; methylene blue and hyperbaric oxygen
may be required in severe cases.

133. • Local ischemic or nerve toxicities may occur, particularly in the
extremities with prolonged anesthesia or use of agents
containing epinephrine. Suspected nerve damage should prompt
neurologic consultation for urgent peripheral nerve studies. If
vascular compromise, such as limb ischemia, is suspected,
consult a vascular surgeon immediately. Therapy for
extravasation (eg, warm compresses, phentolamine,
nitroglycerin cream) should be initiated for localized vascular
toxicity.
• Patients with persistent or unresolved significant reactions
require admission to a monitored bed for observation, further
evaluation, and treatment. Patients who are stable and have
minor or easily controlled adverse reactions can be discharged
and monitored on an outpatient basis.

134. • Finally, the prevention of local anesthetic toxicity
should always be the primary consideration.
• Although all adverse reactions cannot be anticipated,
complications can be minimized by strict adherence to
the guidelines of anesthetic dosing, identification of
patients at increased risk, and implementation of
appropriate anesthetic application techniques to avoid
unintentional intravascular injection.

135. Prevention of local anesthetic toxicity
• The following suggestions may help avoid complications related to local
anesthetic use, especially in emergency department patients:
• Consider obtaining and documenting informed consent in individuals with a prior history of
anesthetic reactions
• Document the amount and type of anesthetic used during the procedure
• Always obtain an adequate history and physical examination to identify risk factors and allergies
• Do not use class IB antidysrhythmics (including phenytoin) for seizures or dysrhythmias believed to
be due to cocaine toxicity
• Consider changes in neurologic signs or symptoms as a possible manifestation of anesthetic toxicity
• Admit patients with serious or unresolved symptoms
• Know the toxic dose of the local anesthetic being used. Use the lowest concentration and volume of
local anesthetic that still produces good results. Add epinephrine at a ratio of 1:200,000 to slow
vascular uptake through vasoconstriction.

136. • Describe the early symptoms of local anesthetic overdose
to patients and instruct them to inform the physician if
they experience any of these effects. Be sure that patients
understand the effects of local anesthetics and that they
should tell the physician if symptoms occur.
• A careful injection method may help prevent toxic
reactions. Perform high-volume (>5 mL) injections
slowly, in 3-mL increments. Stop to aspirate and observe
for blood in the syringe after every 3 mL injected.
(Injecting local anesthetic in this manner reduces the
chances of a large-volume intravascular injection.)

137. • Maintain verbal contact with the patient during the
procedure. This helps detect subtle symptoms, such as
dysarthria, as well as more severe ones, such as
changes in mental status.
• Because benzodiazepines raise the threshold for CNS
symptoms but not for cardiovascular symptoms, heavy
benzodiazepine premedication is likely to result in a
patient progressing directly to cardiovascular toxicity
without showing preliminary signs of CNS toxicity

138. In general
prevention of systemic complications :
Prior to Treatment
1. Complete review of medical status (including vital
signs)
2. Anxiety / Fear should be assessed and managed
before administering anesthetic

139. • Administration of Anesthetic
1. Place pt. supine or semi-supine position
2. Dry site, apply topical X 1 min
3. Select appropriate drug for treatment (time)
4. Vasoconstrictor unless contraindicated
5. Weakest anesthetic in the minimum volume
(compatible with successful anesthesia)

140. 6. Inject slowly (minimum of 60 sec / 1.8 ml)
7. Continually observe –
Never leave patient alone after injection
8. Use only aspirating syringe
9. Aspirate in two planes, before injecting
10. Use sharp, disposable needles of adequate
diameter and length

141. Dosage guidelines
Lower concentrations of local anesthetics are typically
used for infiltration anesthesia.
• Variation in local anesthetic dose depends on the
procedure, the degree of anesthesia required, and
individual patient circumstances. Use of a reduced dose
is indicated in the following patients:
• Debilitated or acutely ill patients
• Very young children or geriatric patients
• Patients with liver disease, atherosclerosis, or occlusive
arterial disease

142. The table below lists maximum recommended doses and toxic limits for
the most common anesthetics (from Malamed Handbook of Local
Anesthetics)
Drug Toxic Limit Maximum
2% Lidocaine
(Xylocaine)
2 mg/lb 300 mg
3%
Carbocaine(Mepivacaine
)
2 mg/lb 300 mg
4% Citanest (Prilocaine) 2.7 mg/lb 400 mg
1.5% Duranest
(Etidocaine)
3.6mg/lb 400 mg
0.5% Marcaine
(Bupivacaine)
0.6mg/lb 90 mg