LOCAL LOCAL ANAESTHESIAANAESTHESIA

INDIAN DENTAL ACADEMY

Leader in continuing dental education www.indiandentalacademy.com

www.indiandentalacademy.com

Contents Contents

HistoryArmamentariumDefinition &ClassificationComposition Different Agents , Vasoconstrictors Mechanism of ActionBio Transformation Systemic Action

INTRODUCTIONINTRODUCTION

‘No pain no gain’Ancient time – dental treatment associated with painEarliest pain relief – Coca shrub mood elevator Incas

Cocoa shrub – foot hills of AndesIntroduced by Europeans to South AmericaCocaine

1855 – Gaedicke extracted alkaloid Erythroxylin

1860 – Dr. Scherzer cocaine from this alkaloid

1844 – Francis Rynd (Dublin) Acetate of morphine + Creosote Skin incision TGN treatment First time liquid used - intradermally

1884 – marks birth of LA

Sigmund Freud Carl Koller Cocaine for eye operation

William Steward Halsted Cocaine for inferior dental nerve

1886 – BDJ William Alfred Hunt et al Cocaine - dental anesthetic documented

1901 – E Mayers Vasoconstrictor + cocaine

1905 13 lives claimed – addiction A Einhorn & E Uhlfelder(Sweden)

Synthesized Procaine hydrochloride Procaine sterilizable, non-additive, non-toxic

1943 N Lofgren(Sweden)

Synthesized Anilide called Lignocaine Lignocaine – amide linked synthetic derivative

1946 – Lignocaine introduced Dental practice

1948 – Lignocaine ; published in BDJ – Lofgren

Sweden – Birth place of newer LA agents

Bupivacaine

Ropivacaine

Pain and pain controlPain and pain control

DEFINITION -- It is defined as an unpleasant emotional

experience usually initiated by a noxious stimulus and transmitted over a specific neural pathway to the central nervous system where it is interpreted as such.

Methods of pain control.Methods of pain control.

Accupuncture Analgesia -- Originated-CHINA,between600BC to 200AD

Hypnotism – Still employed—susceptible patients, Time consuming, lasts for less time

Audio Analgesia – 1959 Gardner and licklider Loud noise used to produce analgesia

Electric analgesia -- Peripheral nerve- Direct electric current Elos-1,powered by 18v battery- Siemens Never more than 30 ma

Analgesia by Cold air– Inability to conduct AP at low tempr Nondolar-French-60 lts/min-Cold air Dis adv-Mucosa dry, Cotton stick to mucosa,ulcers-if not

moistened.

ArmamentariumArmamentarium

Syringe- Breech loading, metallic cartridge-aspirating

AdvantageVisible cartridge

Aspiration- 1 hand

Autoclavable

Rust resistance, Long lasting

DisadvantageWeight

Size-Too big

Possibility of infection

PISTON WITH HARPOON

FINGER GRIP

THUMB RING

SYRINGE BARRELNEEDLE ADAPTOR

Breech loading plastic cartridge-aspirating

AdvantageLight weight

Cartridge visible

Rust resistance, Long lasting

Low cost

DisadvantageSize – Too big / small

Possibility of infection

Repeated autoclaving – Plastic looses its properties

PLASTIC REUSABLE SYRINGE

Breech loading metallic cartridge-Self aspirating

AdvantageCartridge visible

Autoclavable

Easier to aspirate

Piston is scored – Qty Known

DisadvantageWeight

Possibility of infection

Finger has to be moved from thumb ring to disc-Aspiration

Takes time to accustom

SELF ASPIRATING SYRINGE

Pressure syringe --

AdvantageMeasured dose

Overcomes tissue resistance

Non threatening – Cartridge protected

DisadvantageCost

Inject too rapidly -Possibility

PRESSURE SYRINGE

WILCOX- JEWETT OBTUNDER

Jet injectors

AdvantageDoes not require – needle

Very small volume – Delivered

Topical anesthesia-effective

DisadvantageInadequate – Pulpal / Regional block

Patient disturbed by jolt of jet.

Cost

PDL damage – common

JET INJECTOR

Disposable syringe

AdvantageSingle use

Sterile-Till opened

Light weight

DisadvantageDoes not accept – Dental cartridge

Aspiration – Difficult – 2 hands

Needle Type – Stainless steel – Disposable

Platinum

Iridium platinum

Ruthenium platinum Parts – Bevel

Shank

Hub-Leur lock, Friction grip.

Gauge –23 (IM) – Length 23 mm 25 (D) – Length 36/26 mm - +ve asprn

Blood – 100% 27 (D) – Length 27 mm - +ve asprn Blood – 87% 30 (D) – Length 22 mm - +ve asprn Blood – 2-5%

Cartridge—

Consists of -- Cylindrical glass tube

Stopper

Aluminum cap

Diaphram

Rubber diaphragm

Aluminum capNECK

GLASS TUBE

RUBBER PLUNGER

Additional Armamentarium – Topical antiseptic

Topical anesthetic

Cotton Gauge

Hemostat

Applicator Stick.

Definition of L.A --Definition of L.A --

It is defined as a transient loss of sensation to

a painful or potentially painful stimulus, resulting

from a reversible interruption of peripheral

conduction along a specific neural pathway to its

central integration and perception in the brain.

Classification--Classification--

Based on composition – A) Natural – eg – cocaine. B) synthetic nitrogenous compd – para amino benzoic acid-procaine, benzocaine. acetanilide - lignocaine quinoline - cinchocoline C) non Nitrogenous compounds -

benzyl alcohol D) miscellaneous – clove oil , phenol .

Based on intermediate group --

Esters –Benzoic acid Para Amino benzoic Acid

Butane Chloroprocaine

Cocaine Procaine

Benzocaine Propoxycaine

Hexylcaine

Tetracaine

Amides – Articaine

Bupivacaine

Dibucaine

Lignocaine

Mepivacaine

Prilocaine

According to biological site and mode of action— Class A Class B

Class C

Class D

Agents acting at receptor site –external surface.

Agents acting at receptor site- internal surface..

Agents acting at receptor independent physico chemical mechanism.

Agents acting in combn of receptor and independent mechanism.

Biotoxin -eg tetrodotoxin

Quaternary amonium-scorpion venom

Benzocaine

Clinically useful agents –Lignocaine etc

Injectables -- Surface -- Ultra short acting *Soluble - eg <80 min eg Lignocaine Cocaine Lignocaine Short acting 45-50 *Insoluble- egMin 2% ligno with Benzocaine1:1 lakh VC Medium acting 90-1502% ligno with Vc or4% prilocaine with 1:2 epin Long acting > 180 5% Bupivacaine with 1:2 epin

Composition--Composition--

Local anesthetic drug –eg lignocaine .

Vasopressor drug - eg adrenaline.

Preservative - eg Sodium meta bi sulfide.

Germicide – eg methyl paraben.

For isotonicity – Normal Saline .

Distilled water to equal the desired amount .

Individual Agents --Individual Agents --

Lignocaine-- Classified under – Amide 2-diethylamino 2,6 acetoxylidide hcl 1943 – Nils Lofgrens- intro 1948(dentistry) Metabolised- Liver by microsomal fixed function

oxidases to monoethyl glycerine and xylidide Excretion -<10% unchanged, >80%-metab Vasodilaton ->Procaine, <Mepivacaine Pka –7.9 , ph(plain)-6.5,ph(with Vc)5 –5.5,Onset of

action 2-3 min,Anesthetic half life 1.6hrs,topical anesthetic -yes

NH.CO.CH2.N

CH3

CH3

C2H5

C2H5

LIGNOCAINE

Recommended dose – 7mg/kg not>500mg with VC 4.4mg/kg not>300mg For children with VC 3.2 mg/kg Council for dental therapeutics- ADA 4.4mg/kg It is non allergic available in three formulations Ligno2% with out Vc Ligno2% with VC 1:80,000 Ligno2% with VC 1:100,000 Adverse reactions- CNS stimulation then Depression,Overdose

causes unconsciousness and respiratory arrest.

Bupivacaine –Classified under amide

1-butyl 2,6 pipecoloxylidide

Toxicity <4 times – Lignocaine, Mepivacaine

Metabolism –Liver by Amidases

Excretion by kidney (16% unchanged)

Vasodilation- relatively significant

Pka-8.1,ph(plain)- 4.5-6, ph(vc)- 3-4.5

Onset of action –6-10 min,Anesthetic half life-2.7hrs,Dose

1.3mg/kg ,Maximum dose-not >40mg,Absolute maximum dose-not> 90mg

N

NH.CO

C4H9

CH3

CH3

BUPIVACAINE

Available as 0.5% soln 1:2,00,000 (vc)

Indicaton- pulpal anesthesia->90- min.

Full mouth recontruction.

Extensive perio surgery.

management of post op pain.

Duration –Pulpal- 90- 180 min

Soft tissue-4-12 hrs

Contra indication- burning sensation at site of injecton, in children-anticipating self

trauma .

Procaine- Classified under –Esters

2Diethylamino ethyl 4aminobenzoate hcl

Metabolised-in Plasma by plasma pseudocholine esterases

Excretion >2%unchanged, 90% -PABA,8% diethyl aminoethanol

in urine.

Pka-9.1,High degree of vasodilation, 2% procaine 15-30min soft

tissue LA

no pulpal anesthesia , > incidence allergy, drug of choice for intra

arterial injection and accidents.

Mepivacine- classified -amide type

1 Methyl 2,6 pipecoloxylidide hcl

Metabolism-microsomal fixed funcn oxidasea in liver.

Maximum dose 4.4 mg/kg , absolute max dose-300mg.

Excretion-1-10% unchanged urine.

Pka-7.6,Anesthetic half life-90min,

Mild vasodilator, 3% mepivacaine used in patients with vc

contraindicaton. Low reported cases-allergy.over dose CNS

stimulation followed by depression.

Articaine- classified- Amide 2 Carboxymethoxy 4 methylthiophene hcl Metabolised- Liver Excretion – Kidney 10% - unchanged. Pka 7.8, Anesthetic half life-1.2-2 hrs, Maximum dose – 1mg/kg , Absolute maximum dose –

500mg first LA Agent with thiophene ring,little potential to

diffuse through soft tissue. Adverse reaction-methymoglobinemia-Rx by using

methylene blue 1mg/kg.

Etidocaine- classified –Amide

Metabolism –Liver

Excretion –urine- Kidney

Pka 7.7 ,Anesthetic half life-56 min.

Maximum dose 8mg /kg, Absolute max dose 400 mg

Employed mainly in epidural or caudal regional block.

VASOCONSTRICTORSVASOCONSTRICTORS

Added – to counteract vasodilation effect of injectable L.A Decreases rate of absorption Reduces the risk of overdose reaction Increases duration of action Reduces bleeding at the site

CLASSIFICATION OF V.CCLASSIFICATION OF V.C

Catecholamines EpinephrineNor epinephrineDopamine

Non catecholaminesAmphetamineMeta amphetamine

Based on chemical stc (Catechol nucleus)

Based on mode of actionDirect acting Epinephrine Nor epinephrine

Indirect acting Amphetamine Tyramine

Mixed acting Ephedrine

Proprietary name

Mode of action

Systemic 1) CVS

EPINEPHRINEAdrenaline

α1& β receptors

Systolic & Diastolic pressure Heart rate Oxygen consumption Stroke volume

FELYPRESSINOctopressin

Direct stimulation of vasculatureNo direct effect onMyocardium Non-arrythmagenicHigh doses – impaired coronary flow

2) CNS

3) RS4) Vasculature

5)Metabolism

CNS stimulation

Bronchodilator α1 – vasoconstrictionβ 2 – vasodilation oxygen consumption blood sugar level

Adrenergic nerve – no effect

Vasoconstriction – coronary blood vessels

Anti-diuretic action Oxytocin like action – uterus

6) Clinical

application

7) Max

dose

8) Side

effect

Allergy, hemostasis

0.2 mg – healthy

0.04mg – CVS impaired

CVS & CNS symptoms

Cerebral hemorrhage

As vaso-constrictor in

L.A

0.04mg

MECHANISM OF ACTIONMECHANISM OF ACTION

Resting membrane potential Excitation of nerve

Stimulus – slow depolarization – electric potential less negative increase in permeability to Na

Electric potential – critical level – firing / threshold potential Rapid depolarization – reversal of electric potential Reaches peak +35 mv - +40 mv rapid depolarization

(0.3msec) Repolarize to RMP -60 to –70mv (0.7msec)

Conduction / propagation Depolarization – 1segment – local current affects

RMP next segment Current flow +ve –ve; never backwards – prevented by

previous unexcitable refractory segm.

Spread Sequential depolarization - non myelinated Saltatory conduction – myelinated – faster & energy

efficient

Rate Non-myelinated 1.2m/s Myelinated 14.8 – 120m/s

Site of action Outer bimolecular lipoprotein layer in nerve membrane

MODE OF ACTIONMODE OF ACTION

Altering the basic RMP of nerve

Altering the threshold potential

Decreasing the rate of depolarization

Prolonging rate of repolarization

THEORIES OF ACTION OF THEORIES OF ACTION OF L.AL.A

ACTEYLCHOLINE THEORY: Involved in nerve conduction in addition to its role as a

neurotransmitter at nerve synapses No such evidence

CALCIUM DISPLACEMENT THEORY: L.A causes nerve block by displacement of Ca from some

membrane site that controls entry of Na Varying conc. Of Ca in nerve – not seen

SURFACE CHARGE THEORY: Action by binding to nerve membrane and changing its

electric potential. Cationic molecules aligned at membrane water interface –

surface elec potn more positively charged - electric potn , threshold potn.

Demerits- RMP not altered by LA. LA act on nerve channel rather than surface –cannot

explain how uncharged LA molecule causes nerve blockage.

Membrane expansion theory- LA lipid soluble – enters nerve membr and changes

configuration of membr. There by reduced space for sodium to enter and thus cause inhibition.

Explains how non ionised drug causes- blockade, nerve membrane do expand and become more fluid when exposed to LA .

No evidence to tell that the whole blockade is due to this phenomenon.

Specific receptor theory— LA act by binding to specific receptors- sodium channel-

on external/ axoplasmic surface. Once it binds there is no permeability of sodium- no

conduction.

LA molecule replace calcium molecule at calcium gate –

thus prevent sodium entry.

This is by far the most accepted theory.

Mechanism of actionMechanism of action..

All LA are available as acid salt of weak bases.

Weak base(BNHOH) combined with acid (HCL) to give

acid salt(BNHCL)& water.

In mucosa BNHCL dissociates into BNH and CL . Normal

tissue PH 7.4 is necessary for conversion of acid salt to free base.

BNH which is hydrophilic further dissociates to BN and

H. BN is now lipophilic.

Lipophilic BN diffuses through nerve membrane (lipid).

Inside the nerve it combines with intrinsic H. (H in nerve

formed by buffering action.)

Newly formed ionised BNH displaces calcium from the

sodium channel receptor site to cause conduction

blockade.

LA Solution .

Biotransformation. Biotransformation.

Esters- eg- Procaine-

hydrolyzed to pseudo cholinesterase's

Para amino benzoic acid Diethyl amino alcohol

Excreted unchanged urine further transformed-urine

Atypical cholinesterase's --- increase toxicity

Amide eg lidocaine --Mono ethyl xylidide

Glycine xylidide xylidide

Xylidide

Hydroxy xylidide. Excreted kidney .Significant renal diseases – contra indication.

Systemic action.Systemic action.

CNS – Low levels – no action Toxic dose – tonic clonic convulsionsBlood- 0.5-4.0 mg/ml-no complication 4.5-7.0 mg/ml-pre seizure sign/ symptom >7.5mg/ml-tonic clonic seizures.Anti convulsive property –As it causes depression of CNS.Seizure threshold- excitability nerve

CVS- Action on Heart

Electrical excitability of myocardium .

conduction rate

Tone of contraction.

clinically effective level-1.8-5mg/ml –anti arrhythmic

used in premature ventricular contractures , arrhythmias.

Action on vasculature- normal value no change. over dose- hypo tension.( myocardial

contractility) Lethal dose- cardio vascular collapse

( myocardial contractility, massive peripheral vaso dilatation )

Action on Respiratory system– Normal levels- no over dose- bronchial muscles

relaxation . Over dose – Respiratory arrest due to CNS depression.

QueryQuery

Least toxic LA- 2 chlorprocaine.Most toxic LA- tetracaine- for topical-dicyclomineIf allergic to LA –diphenhydramine- anti histamine + mild anestheticFor children - 2 chlorprocaineLA is added with bi carbonate in infections Allergy – delt in detail part II

Ideal requirements- its action must be reversible Must be non irritant and not produce any secondary

irritation Low degree of systemic toxicity Must be potent enough Have sufficient penetrating properties

LOCAL LOCAL ANAESTHESIAANAESTHESIA

part IIpart II

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Techniques of InjectionTechniques of Injection

Basic points- Use a Sterile Sharp Needle

Check The flow of Solution

Determine Whether to Warm soln before use or not.

Position the patient

Dry the tissue/ wipe once.

Apply topical anesthetic

Topical antiseptic /optional Communicate with patient apply firm hand rest Inject few drops of soln, communicate with patient, Advance to the target slowly ,aspirate , inject Withdraw the needle slowly Observe the patient & check for anesthetic symptoms

Technique for Maxillary Technique for Maxillary BlockBlock

Supra periosteal injection:

Anaesthetize buccal soft tissue & hard tissue

Nerves anaesthetized – large terminal branches

Indication :

1 or 2 teeth need to be anaesthetized / small area

Contra-indication : Infection

Dense bone covering

Target area : Behind apices of tooth

Landmarks : Muco-buccal fold

Crown & root length

Posterior Superior Alveolar Nerve Block Area anaesthetized:

Maxillary 3rd, 2nd & 1st molar (except mesio-buccal root of 1st molar

Bone & periodontium over these Indication:

Treatment of 2 or more molars required Supra-periosteal injection – ineffective Acute inflammation

Contra-indication: Pt with bleeding disorders

Disadvantage: More of soft tissue landmarks used 2nd injection for 1st molar

Landmarks: Mucobuccal fold Zygomatic process of maxilla Infratemporal surface of maxilla Anterior border and coronoid process of mandible Tuberosity of maxilla

Complications:

Hematoma –

Non visible - pterygoid plexus posteriorly

Visible – buccal aspect

Accidental mandibular Anaesthesia

Orbital contents – anaesthetized accidentally

Accidental - parotid gland facial nerve affected

Anterior superior alveolar nerve block Areas anaesthetized

Pulp of maxillary C.Is – Canine Buccal periodontium, lower eyelid, lateral aspect of nose Upper lip

Indications More than 2 anterior teeth

Contraindications Discreet treatment areas Hemostasis of localized area – not adequately achieved

Landmarks Mucobuccal fold, infra-orbital notch, infra-orbital foramen

2 methods:

Intra-oral Premolar approach

Incisal approach

Extra-oral

Palatal AnaesthesiaPalatal Anaesthesia

Pressure Anaesthesia Slow deposition Small quantity Effect only a very small area

Greater palatine nerve block Areas anaesthetized

Palatal soft tissue – posterior aspect Palatal hard tissue

Indication Surgical procedures posterior portion of hard palate Palatal Anaesthesia in conjunction with posterior superior

alveolar nerve block. Landmarks

Greater palatine foramen – junction of the maxillary alveolar process & palatine bone

Between the 2nd & 3rd molars – 1-1.5cms away from gingival margin

Nasopalatine nerve block Areas anaesthetized

Anterior portion of Hard palate and over lying structures back to the bicuspid area.

Indications Anterior palatal procedures supplementing infraorbital nerve

blocks Anaesthesia of nasal septum

Landmarks Central incisor & incisive papilla

Complications Hematoma Necrosis

Technique Single needle penetration Multiple needle penetration

Usually most discomforting block for patient – very painful

Maxillary nerve block Areas anaesthetized

Pulpal Anaesthesia Maxillary teeth – 1 side Periodontium / soft tissue – 1 side

Indications Extensive oral / periodontal / endodontal procedures Other regional nerve blocks not possible Therapeutic procedure to diagnose neuralgias

Contra-indications Pediatric patients Infection / inflammation Hemorrhage – anticipated Greater palatine canal approach not possible – bony obstr.

Landmarks Mucobuccal fold distal to maxillary 2nd molar Maxillary tuberosity Zygomatic process Greater palatine foramen

Complications Hematoma Penetration into orbit

Volume – displaces orbital structures, periorbital swelling, proptosis, 6th nr block – diplopia, transient loss of vision, optic nerve blocked, retrobulbar block / hemorrhage, opthalmoplegias (common)

Penetration into nasal cavity Patient complains – LA running down the throat – to prevent

keep mouth wide open Technique

High tuberosity approach Greater palatine canal approach

Maxillary nerve block – Extra Oral Areas anaesthetised

Anterior temporal & zygomatic region Lower eyelid Side of nose Anterior cheek Upper lip Maxillary teeth / alveolar bone & overlying structures – 1side Hard & soft palate Tonsils – parts of pharynx Nasal septum – floor of nose

Indications Extensive surgery – 1 half of maxilla Others blocks not possible Therapeutic purposes

Technique mid point of zygomatic process Needle gently contact lateral pterygoid plate Maximum length of 4.5cms directed slightly upward & forward

Note: In final position – internal maxillary artery – inferior to needle Temporal vessels on either sides Posteriorly foramen ovale with mandibular nerve & foramen

spinosum with middle meningeal artery Anteriorly pterygomaxillary fissure

Mandibular Nerve BlocksMandibular Nerve Blocks

Inferior alveolar nerve block Areas anaesthetised

Mandibular teeth upto midline Body of mandible Inferior portion of ramus Buccal periosteum & mucous membrane Lingual soft tissue Anterior 2/3rd of tongue

Indications Multiple mandibular teeth – procedures Buccal / Lingual soft tissue anaesthesia

Contraindications Infection / acute inflammation Young children / mentally handicapped

Landmarks Coronoid notch Pterygomandibular raphe Occlusal plane of posterior mandibular teeth

Complication Hematoma Trismus Transient facial paralysis (parotid gland)

Anatomical structures - final position Superiorly –

Inferior alveolar nerves & vessels Insertion of medial pterygoid Mylohyoid nerves & vessels

Anteriorly – Deep part of parotid gland

Laterally – Lingual nerve Internal pterygoid Spehnomandibular ligament

Medially- ramus of mandible.

Closed mouth/ Akinosis technq— Area anesthetized

one half of mandible upto mid line including lingual tissue. Land mark-

occluding plane of the teeth. Muco gingival junction maxillary teeth. Antr border of ramus.

More popular now Land marks easy One prick – mandibular, buccal, lingual n anesthetised. Patient more comfortable.

Gow gates technique– 1973. deposit soln at neck of condyle Area –all mandibular hard and soft tissue Upto mid line. Land marks-

antr border of ramus, tendon of temporalis, corner of mouth, inter tragic notch of ear and exter nal ear.

Final position needle is just inferior to condyle.and insertion of lateral pterygoid.

Gained popularity – single needle penetration, relies on soft tissue landmarks – differ from patient to patient

Lingual nerve block – Area anaesthetised –

Anterior 2/3rd tongue, floor of mouth, lingual mucoperiosteum Only used singly to operate on tongue, floor of mouth

Buccinator / long buccal nerve block Area anaesthetised –

Buccal mucosa & mandibular molar – mucoperiosteum Land marks

External oblique ridge, retromolar triangle

Mental nerve block

Areas anaesthetised Lower lip, mucous membrane – anterior to mental foramen

Landmarks Mandibular bicuspids

Indications Surgery of lower lip or mucous membrane

Extra Oral TechniqueExtra Oral Technique

Mandibular nerve Area anaesthetised

Temporal region with auricle of ear & external auditory meatus TMJ, salivary glands Anterior 2/3rd of tongue Mandible – hard & soft tissue – midline

Landmarks mid point of zygomatic arch Zygomatic notch Cornoid process of mandible Lateral pterygoid plate

Indications

When need to anaesthetise entire mandibular nerve

Infection / trauma – makes terminal anaestheisa not possible

Diagnostic / therapeutic

The needle is pointed posteriorly & to a greater depth of

5 cms

Mental & Incisive nerve block Area anaesthetised

Mandibular hard & soft tissue – labial aspect with lower lip Landmarks

Bicuspid teeth, lower ridge of body of mandible Supra & infra orbital notch Pupil of the eye

2 inch 22 gauge needle used & introduced slightly anteriorly & downwards

ComplicationsComplications

Definition An anaesthetic complication may be defined as any

deviation from the normal expected pattern during or after securing regional anaesthesia

2 types Local Systemic

LOCAL COMPLICATIONS Needle breakage Pain on injection Burning on injection Persistent anaesthesia or paresthesia Trismus Hematoma Sloughing of the tissue / soft tissue injury Facial nerve paralysis

SYSTEMIC COMPLICATIONS

Toxicity

Idiosyncracy

Allergy

Anaphylactoid reaction

Syncope

Classification Primary / secondary

Primary – caused & manifested at time of anaesthesia Secondary – manifested later

Mild / severe Mild – exhibit slight change from normal expected pattern

- reverses itself without treatment Severe – manifests itself – pronounced deviation

- requires specific treatment

Transient / permanent Transient – is one that is severe at occurrence – no residual

effects Permanent – residual effect; lasts for a life time even though it

is mild

Complications could be a combination of any of the above mentioned types

Majority are either Primary Mild & Transient or Secondary Mild & Transient

Complications

Attributed to solutions – toxicity, allergy, idiosyncrasy,

anaphylactoid reaction, local irritation

Attributed to technique / needle – syncope, muscle

trismus, pain, edema, hematoma

Needle breakageNeedle breakage

Cause – Unexpected movement – patient (if patient movement is

opposite to path of needle insertion) Usually at Hub – Magill forceps – hemostat used If needle has penetrated soft tissue – not usually more

than few mms deep – encased in scar tissue in few weeks – removed later on if necessary

Multiple used needle

Prevention Correct gauge – 25 gauge Long needles – prevent penetration till hub Not to redirect when in tissue

Management Patient – not to move – hand in the mouth – mouth open Fragment visible – remove it Fragment not visible – inform patient – not necessary for

intervention immediately – Radiograph suggested

Precautions

Avoid bony contact

Avoid heavy pressure

Avoid movement of needle and patient

Pain on injectionPain on injection

Causes – Careless injection technique Multiple used needle Rapid deposition

Problems – Pain – patient anxiety – unexpected movements

Prevention – Proper technique – sharp needles Enter topical anaesthetics Inject slowly – solution sterilized Check temperature of solution

Burning on injectionBurning on injection

Causes Due to pH of solution 5 (LA) – 3 (LA+VC) Rapid injection Contamination Warm solution

Problems pH disappears upon LA action – no residual

sensitivity Contaminated solution other complications – trismus,

edema, paraesthesia

Prevention

Slow injection – 1ml / minute

Cartridge stored at room temperature – away from

containers with alcohol / other agents

Persistent anaesthesia / Persistent anaesthesia / paresthesiaparesthesia

Causes Direct trauma to nerve – bevel of needle LA solution containing neurotoxic substance – alcohol Injection of wrong solution Hemorrhage / infection – near to nerve

Problem Persistent anaesthesia – usually rare Biting / thermal / chemical insult – without patient

awareness When lingual nerve is involved – taste impaired

Prevention Proper care & handling of dental cartridge Adherence to injection protocol

Management Usually resolve in 8 weeks Periodic recall & check up of patients Persistence – consult neurosurgeon LA – not to be injected in the same region

Trismus Trismus

Definition “difficulty in opening the jaws due to muscle spasm”

Causes Trauma – muscle / blood vessel Irritating solution – hemorrhage LA have been known to have slight myotoxicity Excessive volume – distension of tissues

Problems Pain / hypomobility

Prevention

Use of sharp, sterile, disposable needle

Aseptic technique

Practice atraumatic methods

Avoid repeated injections

Use minimum volume

Management Heat therapy

Warm saline rinses, moist hot packs Analgesics

Aspirin, Codeine (30-60mg) Initial physiotherapy

Thrice a day Antibiotic regime

Possibility of infection

HematomaHematoma

Causes Arterial & venous puncture – common in PSA & Inf Alv

nerve blocksProblem Bruise – may / may not be visible extraorally Complications – pain & trismus Swelling & discolouration

Prevention Knowledge of normal anatomy – proper technique Shorter needle – PSA, minimise the number of

penetration

Management Immediate – apply firm pressure 5-10minutes

Inf Alv Nr. Block – medial aspect of ramus Infra orbital, Mental, Incisive block – directly over foramen PSA – pressure on soft tissue with finger as posteriorly as

tolerated by patient – medial superior direction

Patient to be reviewed after 24 hours, advice analgesics, cold application upto 4-6 hours, heat application next day

Infection Infection

Comparitively rare complication

Instrument needle solution to be as aseptic as

possible

Area & operative hands – cleaned

Avoid passing needle through infected area

Edema Edema

Causes Trauma during injection Infection, hemorrhage Allergy (Angioedema) Injection of irritating solution

Problems Pain & dysfunction Airway obstruction

Prevention Proper care & handling of armamentarium Atraumatic injection technique Complete medical evaluation prior to injection

Management Trauma – resolve in few days without therapy Hemorrhage – resolve slowly 7-14 days Allergy – life threatening, airway impairment – basic life support,

call medical help, Epinephrine – 0.3mg, Antihistamine, Corticosteroids

Total airway obstruction – Tracheostomy / Cricothyroidectomy

Sloughing of tissueSloughing of tissue

Causes Epithelial desquamation – topical anaesthesia – long

time, heightened sensitivity to LA Sterile abscess – secondary to prolonged ischemia – VC

in LA site – hard palate Problems Pain & infection

Prevention Topical – for not more than 1-2 minutes VC – minimal concentration in solution

Management

Symptomatic – pain – analgesia

Epithelial desquamation – resolve few days

Sterile abscess resolve 7-10 days

Soft tissue injurySoft tissue injury

Causes Trauma occurs – frequently mentally / physically

challenged children Primary cause – significantly longer duration of action

Problem Pain & swelling Infection of soft tissue

Prevention Cotton roll between lip & teeth Patient – guarded against eating / drinking

Facial nerve paralysis Facial nerve paralysis

Cause LA solution into parotid gland – usually while giving Inf

Alv Nr. Block, Akinosis technique

Problem Ipsilateral loss of motor control – Buccinator muscle Inability to raise the corner of Mouth, close Eye lid

Prevention Needle tip to contact bone, redirection of needle to be

done only after complete withdrawl

Management Reassure the patient Eye patches to the affected – eye drops Contact lenses if any – removed

Some post anaesthetic extra oral lesions – recurrent apthous stomatitis, herpes simplex seen in susceptible patient

Mixture of Diphenhydramine, milk of magnesia – relief against ulcers

Systemic complications Systemic complications

Toxicity / toxic overdose Caused by overdose reaction – increased conc. In blood Predisposing factors

Age – any age Weight – greater the body weight greater is the amount of dose

tolerated before overdose reaction Sex – during pregnancy – renal function disturbed – females

more affected at this time Diseases – hepatic & renal dysfunction reduced breakdown Congestive heart failure – less liver perfusion Genetics – pseudocholinesterase deficient – toxicity - Ester LA

Mental attitude and environment – pyschological attitude affects response to various stimuli – larger dose LA needed

Fearful patients – lower seizure threshold for LA Drug factors – Vasoactivity – vasodilation – increase in blood Concentration – greater concentration – greater risk Dose smaller dose should always be preferred Route of Administration – Intravascular – increased toxicity Rate of injection – slower rate preferred Vascularity of injection site – more vascular – greater

absorption Presence of Vasoconstrictor – with VC less absorption

Causes of toxicity – Biotransformation usually slow Drug – slowly eliminated by kidney Too large a total dose Absorption from injection site - rapid Accidental intra-vascular injection

Symptoms – CNS – cerebral cortical stimulation – talkative, restless,

apprehensiveness, convulsions Cerebral cortical depression – lethargy, sleepiness,

unconsciousness Medullary stimulation – increased B.P, Pulse rate, Respiration

Medullary depression – mild fall in B.P– severe cases drops to 0 , Pulse , Respiration – similar effect

Treatment Mild overdose reaction – slow onset reaction – > 5 mins

administer Oxygen (prevent acidosis), monitor vital signs, in case of convulsions – anti-convulsants

Slower onset - >15 mins – same procedure Severe overdose reaction – rapid onset – 1 minute –

unconsciousness with or without convulsion, patient in supine position, convulsions – protect hand, leg, tongue, BLS, administer anti-convulsant ----------- post seizure – CNS depression usually present

Idiosyncrasy Idiosyncrasy

Any reaction neither toxic nor allergic

Common cause – some underlying pathology /

psychological

Pyschotherapy may be helpful

Treatment – symptomatic

Syncope Syncope

Anxiety – increased blood supply to muscles, sitting

position 2mm Hg, less pressure – cerebral arteries

Clinically light headedness, dizziness, tachycardia

& palpitation – may further lead to Unconsciousness

Treatment – discontinue procedure, supine position,

deep breathing, BLS

AllergyAllergy 1 % of all reaction in, LA is allergy

Predisposing factors Hyper sensitivity to ester more common-procaine Most of patients allergic to methyl paraben Recently allergy to sodium meta bi sulfide is also

increasingPrecautions--- Ho of allergy to be recordedHo any asthmatic attack to be noted.Always better to test the patient for allergy before

treatment.

Consultation and allergy testing Refer doubtful cases for allergic skin test – sub cutaneous test

most sensitive. Informed consent that includes cardiac arest end death to be

included. Signs and symptoms of allergy.

Dermatological------ urticaria –wheal and smooth elevated patch seen, ------angio oedema—localised swelling – face hands, common

Respiratory– broncho spasm, respiratory distress, dysnea, wheezing, flushing, tachycardia etc.

Laryngeal edema – type of angio neurotic oedema- life threating.

Edema upper air way – laryngeal edema Lower air way affect broncioles- small.

Management `skin reactions-

Delayed – non life threatening - oral histramine blockers- 50 mg diphenhidramine

Immediate reaction—with conjunctivites rhinitis- vigerous managemennt.

0.3 mg epinephrine. IM 50 mg diphenhydramine Im medical help summoned.

Observe patient for minimum of 60 min Oral histamine blockers for 5 days. Respiratory reaction –

patient in comfortable position. administer - oxygen Admn epinephrine- bronchodilator Observe for 60 min , advise anti histamines to prevent relapse.

Laryngeal edema- Patient position ,oxygen, broncho dilator, oral anti histamines. If condition not improving cricothyrotomy - achieve patent

air way if necessary give artificial ventilation.

Patient with confirmed allergy status- if patient allergic to any one type of anesthetic ester /

amide use the other. Use histamine blocker like diphenhydramine as

anesthetic. General anesthesia alternative method of pain control –

electric anesthesia / hypnosis.

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