LA COMPLICATIONS

1. COMPLICATIONS OF L.A
Presented by: Dr. MD MAHBUBUL HODA
Moderator : Dr Gaurav Patel.

2. SYSTEMIC COMPLICATION OF L.A

3. General Principles of Toxicology:
• 1. No drug ever exerts a single action.
2. No clinically useful drug is entirely devoid of toxicity.
3. The potential toxicity of a drug rests in the hand of the user.
Adverse Drug Reactions: Overdose
• absolute or relative over-administration of a drug which
produces elevated levels in the blood; dose related

4. Adverse Drug Reactions: Allergy
• hypersensitive state acquired through exposure to a
particular allergen, re-exposure to which brings about a
heightened capacity to react; not dose related
Adverse Drug Reactions: Idiosyncrasy
• response that cannot be explained by any known
pharmacological or biochemical mechanism

5. Causes of adverse drug reactions:
1.Toxicity caused by direct extension of the usual
pharmacological effects of the drug
• A. Side effects
B. Overdose reactions
C. Local toxic effects
• Causes of adverse drug reactions:
2.Toxicity caused by alteration in the recipient of the drug
• A. A disease process
B. Emotional disturbances
C. Genetic aberrations
D. Idiosyncrasy
3. Toxicity caused by allergic responses to the drug

6. Adverse Drug Reactions
1) Side effects
2) Overdose reactions
3) Local toxic effects (most common)
4) Allergic reactions

7. Signs and Symptoms – Toxic Reaction to Local
Anesthesia
•Talkativeness
•Slurred speech
•Dizziness
•Nausea
•Depression
•Euphoria
•Excitement
•Convulsions

8. Overdose Reactions
Clinical signs and symptoms that
develop as a result of an
over-administration of a drug

10. Overdose Contributing Factors
•Age
•Weight
•Other medications
•Presence of disease
•Genetics
•Mental well being

13. Drug Factors
•Vasoactivity
•Concentration
•Dose
•Route of administration
•Rate of injection
•Vascularity of the injection site
•Presence of vasoconstrictors

14. Allergic Reactions to Local
Anesthetic Agents
•Hypersensitive state as a result of
exposure to an allergen
•Re-exposure can heighten the initial
reaction

15. Clinical Manifestations of an Allergy
•Fever
•Angioedema
•Urticaria
•Dermatitis
•Depression of blood-forming organs
•Photosensitivity
•Anaphylaxis

16. Angioedema

17. Angioedema, also known as Quincke's edema, and
angioneurotic edema.
It is the rapid swelling (edema) of the dermis,
subcutaneous tissue, mucosa and submucosal
tissues. It is very similar to urticaria, but urticaria,
commonly known as hives, occurs in the upper
dermis

19. Urticaria (hives)

20. Definition
• Urticaria is a very common problem:
• Classically urticaria is characterised by itchy swollen areas
WHEALS/ ANGIOEDEMA ,or both
• Acute/ chronic
• Acute -<6 weeks; chronic > 6 weeks

21. Classification of urticaria
• The principal antigens capable of producing allergic asthma seasonal
allergens (tree pollen, grass pollen, ragweed and certain seasonal
molds)
• 1) "Allergic" urticarial: urticaria follows less than 30 minutes after
ingestion of contact with the sensitizing agent
Physical urticaria
• Diverse physical stimuli (heat, exercise, the sun, cold, pressure and
vibration) may provoke urticaria.

22. • "Pseudo-allergic" urticaria
Several substance labelled as "non-specific histamine liberators" (foods,
hormones, medications, etc.) can provoke urticaria. Among these agents,
the classics are: codeine, morphine, several antibiotics, radio-contrast
products used in radiology, the curares (general anaesthesia) and dextran.
• "Secondary" urticaria
Urticaria is associated with an auto-immune disease, a
hypocomplementemia, thyroid disease, cancer, or an infection (parasites,
helicobacter pylori, etc.).

23. • "Reflex" urticaria
Several hormones (gastrin, neurohormones) suggest that there is a
link between these substances, mastocytes and the skin. It seems,
therefore, that several "external irritants" (emotional, food, etc.)
could cause urticaria (that is often called "idiopathic").
• Hereditary angioneurotic angioedema and acquired deficiencies
in the inhibitor of C1 esterase . These very rare conditions are
associated with a non-itchy angioedema in particular that may
also manifest internally (within the intestines, etc.)

24. • Treatment of urticaria
• 1) Eliminate the allergic cause (food, medication, contact
allergen, etc.). In the same way for "pseudo-allergic"
urticaria, eliminate the provoking agent.
• 3) Treat, if possible, any disease which may be the cause of
the urticaria (secondary urticaria or angioedema).
• 4) Pharmacotherapy: above-all "symptomatic" (anti-
histamines), with new non-sedating agents with long half-
lives (cetirizine, loratadine, desloratadine, fexofenadine).

25. Latex Allergy
•The cartridge opening into which the needle
is inserted is aluminum with a very thin
diaphragm of latex in the middle
•Though patients with a latex allergy are at an
increased risk, there are no known cases or
reports of an allergic response from the latex
on a local anesthetic cartridge

26. Pregnancy
• Anesthesia crosses the placenta and could be toxic to the fetus, but is not a
known teratogen
• No drug should be administered during pregnancy especially the first trimester
• If treatment is necessary, local anesthetics with epinephrine are considered
relatively safe for use during pregnancy; check with patient’s physician
• Educate patients to the potential risks (document)

27. FDA Category of Prescription Drugs
Drug Category Use During
Pregnancy
Risk
Lidocaine B Yes -
Prilocaine B Yes -
Mepivacaine C Use with caution-
Consult physician
Fetal
bradycardi
a
Bupivacaine C Use with caution-
Consult physician
Fetal
bradycardi
a

28. TOXICITY
• Toxic overdose, due to excessive administration of a drug.
• Depends on a sufficient concentration of the drug in the blood, to
affect the CNS, R.S, CVS.
• When the drug is inadvertently administrated intravascularly 
buildup within the bloodstream is so rapid that biotransformation
and elimination can’t keep pace.

29. • In ester type, a high blood level occurs as a result of the absence of
sufficient / effective plasma cholinesterase to catalyze the hydrolysis
of the drug.
• Factors: General physical condition, Rapidity of injection, route
(inadvertant intravascular), Dose, Age of patient.

30. • “A GOOD RULE TO FOLLOW IS TO USE THE LEAST POSSIBLE
VOLUME AND CONCENTRATION NEEDED TO SECURE
SATISFACTORY ANESTHESIA”.
• Should be injected slowly.
• More vascular area, More rapid absorption, and greater is
the possibility of a toxic reaction.
• “ALWAYS ASPIRATE BEFORE INJECTING”

31. C.N.S
• Depression of inhibitory areas  excitatory action to occur unopposed
 overt manifestation of CNS stimulation.
• Hyperexcitable neurons at cortical centre  epilepsy.
• Sub-toxic doses  depress these hyperexcitable neurons (anti-
convulsant effect)

32. • Toxicity on cortical includes, talkativeness, slurred speech,
apprehension, muscle twitching, tremors, tinnitus, drowsiness.
• Medullary stimulation  increase in heart rate / B.P / R.R.

33. • Medullary depress fall in H.R / B.P / R.R.
• Development of either excitation / sedation, should alert the
practitioner to the possibility of a rising blood level and subsequent
development of seizure.
• Overt sign of stimulation (depression)  lethargy, unresponsiveness,
lack of movement, drowsiness, weakness.

34. • Following a seizures, a period of post-ictal depression occurs (severe
depression of both cortical and medullary centers).

35. C.V.S
• Stimulatory effect noted during the early stages of toxicity (reflex
mediated by CNS).
• The effect on myocardium (quinidine – like) – direct depressant  slow
the rate of impulse conduction, prolong refractory period.

36. • Acts as anti-arrythmic in low-doses (1.5 – 5.0 microgram/ml), supress
ectopic pacemaker.
• Cardiac output decreases.
• Peripheral vasodilatation.
• Cardiac standstill (asystole) – irreversible.
• “It’s a mistake to insert a needle, rapidly inject, and immediately
depart for another room, leaving the patient unobserved and
unattended”.

37. MANAGEMENT
• Most instant – immediate, mild, transient – NO SPECIFIC TREATMENT.
• If the patient, is suddenly talkative, apprehension – REASSURANCE.
• In severe – generalized tonic-clonic seizures (sudden and short)  stop
dental procedure, padded tongue blade, suction to remove excess saliva,
patency of airway (by extending the neck).

38. • Depression phase is more critical, more time for support and
evaluation, ABC’s of resuscitation, extend the head, airway cleared by
suction, semi-recumbent position (to increase venous return),
ventilation.
• Monitor pulse, B.P.
• Episode becomes self-limiting as the drug undergoes redistribution
and biotransformation.

39. For CNS stimulation:
• If there is progressive development of CNS stimulation – 50-100 mg
phenobarbitol, prevent the development of seizures. The drug must be
given at the earliest signs of toxicity, since these agent will potentiate
the degree of post-stimulatory depression.
• Diazepam – 5-10 mg – doesn’t compound post-stimulatory depression.
• Artificial ventilation – prevents the development of hypoxia,
hypercarbia, and acidosis – factors that tend to extend the duration of
the seizures.

40. • Corrected by positional change + infuse 5% dextrose with R.L.
• Vasopressors.
• For bradycardia – 0.5 mg atropine or 0.2 mg glycopyrrolate

41. For CNS depression
• For MILD – mechanical means are sufficient.
• For severe – mechanical + pharmacological.
• Maintain airway, respiration.
• Dilation of microcirculation results in hypovolemia  pooling of blood
 fall in venous return  decrease in cardiac output / B.P.
• .

42. PREVENTION
• Adequately evaluated before injection.
• Least possible volume.
• Inject slowly.
• ASPIRATION must be done.
• Vasoconstrictor should be used (if not contraindicated).

43. VASOCONSTRICTORS
• Useful adjunct.
• It slows the absorption (reduce toxicity).
• Prolongs the action.
• Permits smaller volume.
• Increases the efficiency of the drug.
• All L.A are vasodilators, are rapidly absorbed into systemic  toxic
overdose. Stronger the concentration, the greater the vasodilating
effect.

44. IDIOSYNCRASY
• Bizzare type of reaction that cannot be classified as toxic or allergic.
• Unusual symptoms.
• Unrelated to drug, possibly being psychogenic or having some
underlying pathology.

45. • It has to be differentiated from toxic / allergic reaction.
• Maintain airway, oxygen, fluids, position.
• Psychotherapy, and premedication are useful (by taking preoperative
history).

46. Allergic and Anaphylactoid reaction
• 1% of all reactions.
• Antigen unit with antibody  release of histamine. (hypersensitivity)
• Asthma, rhinitis, angioneurotic edema, urticaria, rashes.

47. • Capillaries are more permeable, extravasation of plasma into
surrounding tissues  angioedema.
• Spasm of bronchioles and vasodilation of arterioles  pool of blood.
• Better to have the patient tested before proceeding.
• Solutions contain methylparaben, germicide / preservative – produce
allergy.

48. • Most common Immediate reactions: urticaria, angioedema.
• Second most common – asthma (R.S distress of expiratory type –
prolonged expiration).
• Angioedema of pharynx, larynx  R.S distress.
• In generalized anaphylaxis – sudden CVS collapse, severe R.S distress.
• Pruritis, erythema, urticaria, wheeze, dyspnea, cyanosis,
hypotension, unconscious, cardiac arrest.

49. Localized immediate reaction
• Urticaria, pruritis, angioedema.
• Diphenhydramine 50mg.
• Epinephrine 0.3 – 0.5 mg (0.3 to 0.5 ml of 1:1000 adrenalin).
• Dexamethasone 8mg.
• Ventilation.
• Cricothyrotomy.

50. Asthmatic attacks
• Aerosol inhaler.
• Isoproterenol or epinephrine  relaxation of bronchiole smooth
muscles.
• Slow I.V aminophylline 250 to 500mg.

51. Generalized immediate reaction
• Sudden, complete collapse and LOC, with absence of pulse and
respiration, cyanotic.
• Establish airway with ventilation.
• Place the victim in a position to allow gravity to aid venous return, I.V
fluids, vasopressors, steroid.
• DELAYED REACTION:
• Occurs more than 48 hours.
• Localized edema / joint pain, tenderness, malaise.

52. Allergy testing
• Patients who have a history of asthma / hay fever may be allergic
types (atopic) and thus more likely to have an allergic reaction.
• Intradermal and mucous membrane tests may be of little value in
determining the allergic sensitivity.

53. Pharmacogenetic disorder
• Malignant hyperpyrexia  excessive calcium ion release release from
the sarcoplasmic reticulum of muscle  rapid development of
metabolic and respiratory acidosis.
• Tachycardia, unstable blood pressure, cyanosis, high fever, rigidity.
• Nonester type of L.A – provoking agents.
• Treat – dantrolene.

57. SYNCOPE
• Most frequent complication associated with L.A in dental office.
• Neurogenic shock – due to cerebral ischemia secondary to vasodilation
OR an increase in the peripheral vascular bed, with decrease in B.P.
• When patient in dental chair, the brain is placed in a superior position
and is most susceptible to reduce blood volume.

58. • Discontinue the procedure, lower the chair back, legs are elevated
(semireclining position)  aids venous return + weight of viscera is
not thrown onto the diaphragm, which impairs respiration.
• Provide oxygen + deep breaths.

59. Clinical manifestation of syncope can be
divided in to two phases
1. Pre syncope
• Feeling of warmth in face and neck
• Loss of color : Pale
• Heavy perspiration
• Nausea
• Rapid heart rate
• Pupillary dilation
• BP depressed

60. 2. Syncope
• Pupillary dilation
• Hyperpnea
• Hypotension
• Bradycardia
• Visual disturbances
• Dizziness
• Convulsive movement and muscular twitching
• Loss of consciousness

63. AIRWAY:
 The instant conscious is lost, pt. also loses the ability to
maintain the patency of airway
 Patency of airway is maintained by head tilt chin lift
procedure
 Triple airway maneuver –
 Maximum head extension
 Protrusion of the mandible
 Slight opening of the mouth
 Oropharyngeal and nasopharyngeal tubes can also be used

65. Clearing the airway of foreign objects :
• Apply four blows with clenched fist to victims back in rapid
succession
• Hamlickes maneuver - Four inward & upward thrusts in the epigastric
area
• cricothyrotomy

67. BREATHING
Various methods
• Mouth to mouth
• Pt. nose is closed
• Mouth to nose
• Ambu bag
• Anesthetic machine
• Lung inflations should be provided once every 5 sec
• In cases of respiratory arrest – 4 full lung inflations without allowing
for full exhalation

69. CIRCULATION
 Victim must alwaya be on his back on a firm surface in horizontal
position
 The heel of the hand should be placed on the long axis of the
sternum with fingers elevated away from the chest wall
 One rescuer –
 80 compressions/min
 15:2
 Two rescuers –
 60 compressions/min
 Lung inflation on upstroke of fifth compression

72. LOCAL COMPLICATIONS OF
LOCAL
ANAESTHESIA

73. • An “Anaesthetic complication” may be defined as any deviation from
the normally expected pattern during or after securing of regional
analgesia.
These complications may be classified into:
• Local.
• Systemic.

74. LOCAL COMPLICATIONS
NEEDLE BREAKAGE
PROLONGED ANESTHESIA /
PARESTHESIA
FACIAL NERVE PARALYSIS
TRISMUS
SOFT TISSUE INJURY
HEMATOMA
PAIN ON INJECTION
INFECTION / EDEMA / SLOUGHING OF
TISSUES
POST-ANESTHETIC INTRAORAL
LESIONS

75. NEEDLE BREAKAGE
• Long dental needles most likely have broken during injection, but
some portion of the needle would remain visible in the patients
mouth.
• The fragment of the needle can be removed very easily,
using haemostat.
• Since the introduction of non-reusable, stainless
steel needles, needle breakage has become
an extremely rare complication.

76. • In all situations, needle fracture occurs at the hub (not along the
shaft)
Additional factors include:
• Intentional bending, before injection.
• Sudden movement by the patient while the needle is still.
• Forceful contact with bone.

77. • Ready access to a haemostat, enables to grasp the proximal end and
remove it.
• When the soft tissue has dimpled under pressure from the syringe, the
fragment will not be visible.

78. PREVENTION
• Don’t use short needle for inf. alveolar nerve block.
• Don’t use 30-gauge needle for I.A.N. block.
• Don’t use bent needles.
• Don’t insert a needle into tissue to its hub.
• Caution while inserting in young adults / phobic adult / child.
• Don’t use reusable needles (to ensure sharpness).
• Don’t surprise with a sudden unexpected needle insertion.

79. PROLONGED ANAESTHESIA
• Numbness (frozen)
• Paraesthesia / persistent anaesthesia
• Most frequent cause of dental MALPRACTICE
litigation.
• Associated oral dysfunction – tongue biting, loss of
taste, and speech impediment.
• PARESTHESIA – persistent anesthesia or altered
sensation, beyond the expected duration of anesthesia.

80. CAUSES OF PARAESTHESIA
• L.A contaminated with alcohol / sterilizing solution  irritation,
edema, pressure over the nerve. Alcohols are neurolytic (long term
trauma to the nerve).
• Trauma to the nerve sheath can be produced by the needle. C/O
“electric shock” throughout the distribution of nerve.
• Trauma and swelling in proximity to a nerve  transient decrease
sensation.

81. • Hemorrhage into or around the neural sheath
Bleeding increases pressure on the nerve  paraesthesia (hemorrhage is
resorbed VERY SLOWLY because of poor circulation)  degeneration of
nerve fibres.
• Infections – common cause pain after L.A.

82. PROBLEMS OF PARAESTHESIA
• Mostly it is partial, can lead to self-inflicted soft tissue injury.
• Biting / thermal / chemical insult can occur without awareness.
• HYPERESTHESIA - increased sensitivity to noxious stimuli.
• DYSESTHESIA – a painful sensation occurring to usually non
noxious stimuli.

83. PREVENTION OF HYPERESTHESIA
• STRICT adherence to injection PROTOCOL and PROPER
CARE and HANDLING of cartridges help minimize the risk.
• The insertion of needle should be slow / atraumatic.
• Multiple insertion – avoided.
• Sterile solution.
• Should be forced into the tissue – VERY SLOWLY.

84. • Excessive volumes in the constricted areas should be avoided.
• Injected solution should be as close to body temperature.

85. MANAGEMENT OF HYPERESTHESIA
• Most paraesthesia resolve within = 8 weeks without treatment.
Only when damage to the nerve is severe will the paraesthesia
be permanent.
• Assurance (speak personally, it is NOT UNCOMMON, re
examine, record in dental chart)
• Excessive volumes in the constricted areas should be avoided.
• Injected solution should be as close to body temperature.
• Mechanisms for permanent nerve involvement is UNKNOWN
and there is no known prevention / treatment

86. HEMATOMA
• Effusion of blood into the surrounding tissues as a
result of a torn blood vessel, during administration of
L.A.
• COMMON COMPLICATION of intraoral regional
analgesia.
• Most commonly associated with
posterior superior alveolar and infraorbital block /
IANB.

87. • Mainly because of improper technique.
• They all absorb in due time, with little residual effect other than
discolouration.
• No attempt should be made to aspirate.
• COMPLICATIONS: trismus, pain, swelling, discolouration.

88. PREVENTION
• Knowledge of anatomy – important.
• Penetration for a PSA nerve block may be decreased in a patient
with smaller facial characteristics.
• Use of short needle.
• Minimize the number of needle penetration.
• DON’T use needle as a probe in tissues.

89. MANAGEMENT
• IMMEDIATE – direct pressure – 2 minutes.
• IANB – pressure – medial aspect of mandibular ramus.
• INFRAORBITAL – pressure – skin directly over the infraorbital
foramen. Clinically – discolouration of skin below lower eyelid.
• MENTAL NERVE – pressure over mental foramen, externally on the
skin or intra orally. Clinically – discolouration of chin / swelling in
mucobuccal fold in the region of mental foramen.

90. EDEMA
• Usually a symptom and rarely an entity.
• Trauma, infection, allergy, hemorrhage,
other factors can produce edema.
• PREVENTION: proper care / handle, use atraumatic, medical
evaluation.

91. TREATMENT
• After hemorrhage, edema resolves slowly, as extravasated blood
elements are resorbed.
• Angioedema – histamine blocker, supine position, A-B-C-Definitive
treatment-Epinephrine 0.3 ml IM or 3 ml I.V.
• Steroid.
• Prepare for cricothyrotomy.

92. FACIAL NERVE WEAKNESS
• 7th cranial nerve carries motor impulse to facial
expression.
• Paralysis – terminal branches, occurs when an
infraorbital nerve block is administrated /
maxillary canines are infiltrated.
• Muscle droop (L.A into the deep lobe of parotid,
through which terminal portions of nerve extends)

93. CAUSES
• Transient paralysis is common (L.A into capsule of
parotid, located at posterior border of mandibular
ramus, covered by medial pterygoid and masseter.
• Directing the needle posteriorly / inadverently
deflecting, during an IANB, or overinserting during
Vazirani-Akinosi nerve block, may place the tip
within the body of parotid.

94. PROBLEMS ASSOCIATED
• Loss of motor function is transient (last for several hours) – depend
upon formulation / volume / proximity of nerve. NO sensory loss.
• Unilateral paralysis.
• Persons face appear lopsided.
• No treatment.
• Patient is unable to voluntarily close one eye.
• Protective lid reflex – abolished.
• Winking and blinking – impossible.
• Cornea retains its innervation  irritated  tears lubricate the eye.

95. PREVENTION
• A needle tip that comes in contact with bone (medial
aspect of ramus) before depositing L.A essentially
precludes the possibility that anaesthetic will be
deposited into parotid gland during IANB.

96. MANAGEMENT
• C/O weakness of the muscle on the affected side of
the face.
• Reassure the patient – transient, resolve without
residual effect.
• Remove contact lens.
• Eye patch, manually close the affected eyelid
periodically.
• Record the incident.

97. TRISMUS
• Prolonged tetanic spasm of the jaw muscles
(LOCKED JAW)
• CAUSES – trauma to muscle / blood vessel in
infratemporal fossa – most common.
• L.A with alcohol / cold sterilizing solutions – diffused
 irritation of muscle.
• Injection of L.A – intramuscularly or supramuscular
 progressive necrosis of muscle.

98. • Hemorrhage – another cause. Large volumes of extravascular blood
 irritation  muscle dysfunction as the blood is slowly resorbed.
• Low-grade infection – also cause trismus.
• Multiple needle penetration  greater incidence of trismus.
• Excessive volumes of L.A deposited into a restricted area produce
distension of tissues  post-injection trismus.

99. PROBLEM - TRISMUS
• The average inter incisal opening – male – 44.8 mm
• The average inter incisal – female – 39.2 mm
• The average inter incisal opening in case of trismus – 13.7 mm
• In acute – pain produced by hemorrhage  spasm  limitation of
movement.
• Chronic phase develops if treatment is not begun, due to organization
of hematoma  fibrosis  contracture

100. PREVENTION
• Use a sharp, sterile, disposable needle.
• Proper care and cartridges.
• Aseptic technique.
• Atraumatic insertion and injection technique.
• Avoid repeat injections / multiple insertions
into same area, by gaining knowledge of anatomy.
• Use minimum effective volume of L.A.

101. MANAGEMENT - TRISMUS
• Heat therapy – apply hot, moist towel, for 20 mins
• Warm saline rinses
• Analgesics
• If necessary – muscle relaxants
• Physiotherapy – opening / closing, lateral excursions, chewing gum.
• Record the incident, findings, treatment. Avoid further dental treatment in the
involved region.

102. • The Vazirani-Akinosi mandibular nerve block usually provides relief of
motor dysfunction  permitting to open his mouth  allowing
administration of injection for clinical pain control.
• If pain / dysfunction continue beyond 48 hours, consider the
possibility of infection  add antibiotic.
• Complete recovery takes about 6 weeks.

103. SOFT TISSUE INJURY
• Self-inflicted trauma to the lips and tongue – caused
by the patient inadvertently biting / chewing these
tissues while still anesthetized.
• CAUSES: mostly occur in children, mentally /
physically disabled, old age.

104. PREVENTION: L.A of appropriate duration should be selected.
• A cotton roll is placed between teeth and lip, and secured with dental
floss.
• A self-adherent warning sticker may be used on children.

105. MANAGEMENT
• Analgesic.
• Antibiotics
• Lukewarm saline.
• Petroleum jelly to cover the lip.
• Discolouration is due to extravascular blood elements
(resorbed 1-2 weeks).
• Ice is applied immediately (acts as analgesic /
vasoconstrictor).
• DON’T apply heat for 4 to 6 hours (heat produces
vasodilatation  increase hematoma). Next day,
apply warm moist heat.

106. PAIN ON INJECTION
• CAUSES: careless injection technique,
• Palatal injection always hurt
• Needle can become dull from multiple injections,
rapid deposition of L.A may cause tissue damage,
• Needles with barb may produce pain as they are
withdrawn.

107. PREVENTION
• Proper techniques,
• Use sharp needles,
• Use topical anesthesia before injection,
• Sterile techniques / solution,
• Inject slowly,
• Correct temperature.
• pH – 7.4, are more comfortable.

108. BURNING ON INJECTION
• CAUSES: depends upon pH of the solution.
• The pH of plain L.A is 6.5, with vasopressor is 3.5
(acidic).
• Rapid injection in the more adherent tissue of palate ,
produces a burning sensation.
• Contamination of cartridges with alcohol / sterilizing
solution.

109. • Transient, due to tissue irritation.
• When a burning sensation occurs as a result of rapid injection, a
contaminated solution, or an overly warm solution, and subsequent
complications such as post-anaesthetic trismus, edema, or possible
paraesthesia are reported.

110. PREVENTION
• By buffering the pH up to 7.4
• Slowing the speed of injection (1 ml/min)
• TREATMENT: it is transient and doesn’t lead to
prolonged tissue involvement

111. INFECTION
• CAUSES: contamination of needle.
• Injecting L.A into infected area.
• L.A are less effective when injected into
infected tissues. If deposited under pressure
(periodontal ligament), it transport the
bacteria into adjacent healthy tissues 
spreading infection.
• It may lead to trismus.

112. PREVENTION
• Sterile needle.
• Avoid contamination.
• Avoid multiple injections with same needle.
• Prepare the tissue before penetration.

113. TREATMENT
• Mange trismus: heat, analgesic, muscle relaxant,
physiotherapy
• If signs and symptoms of trismus do not begin to
respond (in 3 days), the possibility of a low-grade
infection  start antibiotics.

114. SLOUGHING OF TISSUES
• Prolonged irritation / ischemia of gingival soft tissue  epithelial
desquamation
• EPITHELIAL DESQUAMATION: application of topical L.A to
gingiva for long time, sensitivity of tissue, reaction in an area.
• PREVENTION: don’t use overtly concentrated
vasoconstrictor solutions
• TREATMENT: symptomatic, analgesic

115. POST ANESTHETIC INTRAORAL LESION
• C/O ulcerations in the mouth (after 2 days).
• Recurrent aphthous stomatitis
/ herpes simplex
can occur intraorally after a L.A injection
or after any trauma.
• Trauma by a needle, L.A, swab, other instrument  activate the latent
form of disease.
• PREVENTION: herpes may be prevented, if treated in its prodromal phase.
• Prodromal – mild burning / itching sensation at the site.
• Acyclovir is applied locally, to minimize the acute phase.

116. TREATMENT
• Symptomatic.
• A mixture of equal amounts of diphenhydramine and milk of magnesia
rinsed in the mouth effectively coats the ulcerations and provide relief.
• Tannic acid preparation.
• Steroid is contraindicated.
• Ulcerations lasts for 7 to 10 days with or without treatment.

117. DIPLOPIA
• Diplopia is one of the very rare complications that follow a posterior
superior alveolar (PSA) nerve block.
• PSA nerve block used for the extraction of
the upper right third molar tooth.
• After the extraction, of double vision and
not being able to gaze laterally with the right eye.

118. • The origins of middle meningeal artery and inferior alveolar artery are closely
situated
The solution may gain access to the middle meningeal artery which may enter the
cranial cavity through the foramen spinosum and gives off many branches.
The ophthalmic branch of the middle meningeal artery may anastomose with the
lacrimal artery.
The blood supply of the lateral rectus muscle derives from the lacrimal artery and
from the lateral muscular trunk of the ophthalmic artery.
Therefore, the intra-arterial injection of the local anaesthetics may reach and
paralyse the lateral rectus muscle and cause diplopia.

119. PRECAUTIONS
• Although it is rare to have ocular complications after local anesthetic
injection, the occurrence is alarming to both the dentist and the
patient.
• For the proper administration of the PSA nerve block, the patient is
positioned such that the maxillary occlusal plane is at a 45-degree
angle to the floor.
• After palpating all the anatomical landmarks, a 1⅝ inch, 25 gauze
needle is inserted to the depth of 14 – 16 mm and the LA is injected.

120. • The following guidelines are to be followed for better management
of the complications.
• a. Reassure the patient regarding the usually transient nature of the
complications.
• b. Cover the affected eye with a gauze dressing to protect the cornea
for the duration of anaesthesia.
• c. The patient should be escorted home by a responsible adult.
• d. If ocular complications last longer than six hours, refer the
patient to an ophthalmologist for evaluation

121. THANK YOU