Locan anesthesia principles and facial blocks

1. CME Phase I
Local Anaesthesia and How to
Block Face
Dr Ahmad Rizal Bin Abdul Hamid

2. References
1. Lipschitz A.H , Kenkel J.M . Local Anesthetics . Selected Reading In Plastic Surgery. 10(18) Pt 2,
2007.
2. Regional Nerve Blocks and Infiltration Therapy : textbook and color atlas 3rd Edition by Danilo
Jankovic . 2004.
3. Hadzics Peripheral Nerve Blocks and Anatomy for Ultrasound 2nd Ed by Admir Hadzic . 2012
4. Niamtu J, Smith K, Carruthers J. Pain Control in Cosmetic Facial Surgery. Procedures in Cosmetic
Dermatology. Elsevier Saunders 2nd Ed.2005
5. Zide B.M, Swift. R. How To Block and Tackle The Face. Plastic and Reconstructive Surgery .Vol.
101, No.3. March 1998.
6. http://www.frca.co.uk/

3. Presentation outline
1. Historical Perspective
2. Anatomy and Physiology of nerve conduction
3. Local Anesthetics
• Mechanism of action
• Physiochemical Properties
• Systemic Toxicity
• Types of LA and additives
4. Relevant Anatomy for Nerve Blocks
5. Nerve Blocks in Clinical Practice

4. Introduction
Definition:
Anesthesia : Absence of loss of sensation
Local anesthetics : Drugs which reversibly prevent transmission of the nerve
impulse in the region to which it is applied, without affecting consciousness.
The basis of local anaesthesia is to prevent perception of a noxious stimulus in the
periphery by blocking impulse conduction along sensory nerves.
Local anesthetic techniques were popularized early in the history of surgery with
the advent of injectable nerve blocking agents.

5. Historical Perspective
Cocaine
• Dates back at least 2500 BC
• Active ingredient of Erythroxylon coca – grows in the Andes, 2000- 1000 feet
above sea level.
• Incas – as a stimulant and imaginary stimulant – enabled to endure fatigue
and exertion for many hours and days.
• Also used as stimulant drink , medicine and for mystical ceremonies.
• Brought to Europe by the Spanish Conquistadores
• 1708 – Herman Boerhaave ( Founder of organic chemistry) included coca in
his text Institutiones Medicae
• “ the plant contained chemical properties that could increase stamina,
alleviate hunger and thirst’

6. Historical Perspective
Albert Niemann
• First person to isolate cocaine – the active coca alkaloid from erythroxylin extract.
• He tasted the newly isolated compound and caused numbing of the tongue.
Tomas Moreno y Maiz ( 1868)
• Described experiments with cocaine
• Probably first publication suggesting potential as a local anesthetic
• Sigmund Freud – studied cocaine’s physiological properties further
• Carl Koller ( 1884) – utilized cocaine anesthetic effect to perform ophthalmic
surgery.
• Willstatter ( 1895) – defined chemical structure of cocaine

7. Historical Perspective
Late 19th century
• Used by physicians to remedy phychiatric disorders, depression and morphine
addiction.
• Multiple reports of systemic cocaine intoxication and death.
• Created dependence and psychosis.
1924
• Safety guidelines issued by American Medical Association
• Condemned as toxic the use of cocaine “ mud” – a paste made from cocaine
crystals dissolved in epinephrine.

8. Local Anesthetics
• Carl Koller ( 1858-1944) - Search for better methods of pain relief in
Opthalmology.
• Achieved success in use of topical cocaine.
• William Steward Halsted ( 1852 – 1922) – Performed the first successful nerve
block – mandibular block with cocaine.
• August Bier ( 1861-1949) – Gave first spinal anesthetic in 1898. Developed IV use
of procaine to induce anesthesia.

9. Local Anesthetics
• 1890 – Ethyl Chloride spray for topical analgesia by Redard of Geneva
• 1891 – Tropococaine isolated by Giesel. First alternative to Cocaine.
• 1892 – Karl Ludwig Schleich introduced infiltration analgesia
• 1904 – Procaine ( Novocain) by Alfred Einhorn.
• 1905 – H.F Braun ( Father of local analgesia) added epinephrine to cocaine to
prolong analgesic action . Pioneered the use of Procaine.
• 1925 – Dibucaine developed
• 1932 – Tetracaine ( Pontocaine) developed
• 1943 – Lidocaine ( Xylocaine) synthesized by Lofgren & Lundquist.
• 1963 - Bupivacaine

10. Anatomy
Peripheral Nerves
• Neuron is basic functional unit responsible
for conduction of nerve impulses.
• Neuron consist of cell body that contains a
large nucleus.
• Cell body is attached to several branching
processes called dendrites and a single
axon.
• Dendrites receive incoming messages
• Axons conduct outgoing messages

11. • Central core of a nerve fiber is a cylinder of
neuroplasm ( axon).
• Axon may be myelinated or unmyelinated.
• Large nerve fibers are usually myelinated and
small ones unmyelinated.
• Myelin sheath is produced by Schwann cells and
acts as an electrical insulator.
• Gaps between myelin are nodes of Ranvier.

12. Myelinated Nerve :
• Gaps between adjacent Schwann cells
known as nodes of Ranvier.
• Nerve membrane exposed to
extracellular fluid at NOR.
• During impulse conduction , impulses
travel by saltatory conduction ( hop or
leap).
Unmyelinated Nerve
• Impulse conduction by depolarization
of axon , allowing the nerve signal to
propagate down the nerve fiber.

13. • Individual nerve fibers that make up a nerve, are
bundled together by connective tissue which is
divided into :
• Epineurium: Surrounds entire nerve and contains
blood vessels and delivers nutrients. Easily
permeable and covers one or more bundles of
perineurium
• Perineurium : Enclose bundles of axon and semi-
permeable barrier to local anesthetics.
• Endoneurium: Surrounds every individual nerve
or axon. Local anesthetics easily diffuse through.

14. Types of Nerve Fibers
1. Type A
• Axons of the somatic sensory neurons and motor neurons serving the skin,
skeletal muscle and joints.
• Large diameter and thick and myelin sheaths.
2. Type B
• Axons are lightly myelinated and of intermediate diameter
3. Type C
• Axons are unmyelinated and have smallest diameter.
• Autonomic nervous system fibers serving visceral organs , visceral sensory
fibers and small sensory fibers.

16. Resting membrane potential
• Expressed as the measured potential difference
across the cell membrane in millivolts (mV) at rest
• Expressed as intracellular potential relative to
extracellular potential.
• Resting membrane potential of peripheral nerves
approximately -90 millivolts
• Influenced by:
1. Active transport of sodium and potassium
ions through potassium pump
2. Passive diffusion of sodium and potassium
through nerve membrane

17. Depolarization and Repolarization
• Nerve signals are conducted by action
potential.
• Action potential : Rapid change in membrane
potential that spreads rapidly along the
nerve.
• Divided into 3 stages :
1. Resting stage :
• membrane potential is polarized -90mv
2. Depolarization :
• membrane becomes permeable to sodium ions
& flow to interior of cell.
• Membrane potential becomes less negative (
the cell interior becomes less negative charge).
3. Repolarization :
• Na channels close, K channels open .
• K+ rapidly diffuse out of cell causing membrane
potential to return to its resting ( polarized
state)

18. Local Anesthetics
1. Mechanism Of Action
• Local anaesthetics prevent the generation and conduction of nerve impulses .
• They act by blocking the voltage –gated sodium ion channels, thus preventing
large increase in permeability to sodium influx and depolarization.
• It can be achieved by two mechanisms:
I. Selective binding of local anesthetic molecule to sodium channel.
II. Incorporation of local anesthetic molecule into cell membrane.

19. Binding of LA to sodium channel
1. Unionised LA enter cell
2. LA becomes ionised
3. Binding of LA molecule to Na+ channel
4. Prevent the influx of Na+ into the cell
5. Halting of transmission of advancing wave
of depolarization down the length of the
nerve

20. Incorporation of local anesthetic
molecule into cell membrane
• Mediated by unionised form acting
from outside the neuron.
• Disruption of ion channel function by
incorporation of LA into cell
membrane.

21. Local Anesthetics
2. Physiochemical Properties
i) Ester and Amide Linkages
• All local anesthetics have three
characteristic molecular sections in
their chemical structure.
1. Aromatic end( lipophilic)
2. Intermediate chain ( contains
either amide or ester bonds)
3. Amine end ( hydrophilic)

22. Ester and Amide Linkages
• An ester or amide linkage is present
between lipophilic end and
hydrophilic end.
• The linkage determines the site of
metabolic degradation of the drug.

23. Comparison
Amino Ester Amino Amide
Rapidly hydrolyzed by plasma
pseudocholinesterase that creates short half
life except cocaine ( metabolized in liver)
Excretion is renal.
Metabolized by liver cells intracellularly.
Due to longer process, accumulation of repeated doses can cause
systemic doses can cause systemic toxicity.
Patients with poor liver function and congestive heart failure will
have prolonged amide half-life.
Normal half life is 2-3 hours
Products of metabolism include para-
aminobenzoic acid ( PABA)
Associated with hypersensitivity reactions in
certain patients.
True allergies are rare
Eg. Cocaine, procaine, benzocaine, tetracaine Eg. Lignocaine, prilocaine, bupivcaine

24. • Three important properties of local anesthetics :
1. Potency
2. Duration of action
3. Speed of onset
• Determined by three physiochemical properties of local anesthetics:
1. Lipid solubility
2. Protein Binding
3. pKa

25. Lipid Solubility
• Neural membrane rich in lipid -> The more lipid soluble LA -> the higher affinity
for axon- > relates directly to potency of LA
• More lipid soluble local anesthetics penetrates cell membrane more easily to
exert its effect.
• The more potent the drug – the smaller amount of local anesthetic required to
produce effect.
• Example:
• Bupivacaine is 4 times more potent than lidocaine.
• 0.25% bupivacaine is equipotent with 1% lidocaine.

26. Protein Binding
• Protein binding is an important determinant of duration of action/ blockade.
• Local anesthetics are largely bound to plasma and plasma protein.
• Fraction of drug bound to protein in plasma correlates with LA duration of action.
• Example:
• Lignocaine – 65% protein bound
• Bupivacaine – 95% protein bound
• Procaine( ester) – 6% protein bound -> very short duration of action
• In general, local anesthetic can be divided into 3 categories:
• Short acting ( 45 -90 minutes) – 2- Chloroprocaine
• Intermediate ( 90-180 minutes) – Lidocaine, Mepivacaine
• Long action ( 4-18 hours) – Bupivacaine, Levobupivacaine, Ropivacaine

27. pKa
• All local anesthetics are weak bases and exist in two forms:
• Non- ionized
• Ionized
• pKa : pH at which the ionized and non-ionized forms of the compound are in
equilibrium ( 50 % each)
• pKa value is constant for any single compound.
• The closer the pKa to the physiological extracellular pH( 7.4)-> faster onset of
anesthesia.

28. pKa
• Only the unionized base form can cross the epineurium , perineurium and cell
membrane.
• The greater % LA in unionized base form -> more rapid diffusion across cell
membrane -> more rapidly produce local anesthetic effect.

29. pKa
• Proportion of unionized to ionized molecule depends on pH of solution and pKa
of compound.
• Decrease pH: shift equilibrium towards ionized form
• Increase pH: shift equilibrium towards un-ionized form

30. Intrinsic Vasodilator Activity
• All local anesthetics except cocaine exhibit a vasoactive effect on vascular smooth
muscle.
• At very low concentrations they cause vasoconstriction
• Tend to be vasodilatory at clinically relevant concentrations.
• Vasodilation promote removal of LA molecules from site of action thus decreasing
intensity of block and duration.
• Epinephrine added to local anesthetic counter these effects and prolongs duration of
action.

31. Types of Local Anesthetics
• Amides
• Lidocaine
• Bupivacaine
• Mepivacaine
• Prilocaine
• Levobuvipacaine
• Ropivacaine
• Esters
• Cocaine
• Chloroprocaine
• Tetracaine
• Benzocaine

32. Lidocaine ( Lignocaine, xylocaine)
• Onset : 5-10 minutes
• Duration of action :
• Without epinephrine : 1-2 hours
• With epinephrine : 2-4 hours
• Recommended maximum safe dose :
• Without epinephrine : 3 mg/kg
• With epinephrine : 7 mg/kg
• Clinical Usage :
• Skin infiltration : 0.2 -1.0 % lidocaine. Use with epinephrine 1: 200.000 or
1: 400,000
• Peripheral nerve block : 1-2% lidocaine
• Dental blocks : 2% lidocaine ( with epinephrine 1: 80 000)

33. Lidocaine expressed as g % .
1% Lignocaine
= 1gr of lidocaine in 100 mls of solution or
= 10 mg/ml
• 1%= 1gr/100ml=1000mg/100 ml= 10mg/ml
• 0.1% = 0.1 g/100 ml = 100 mg/100 ml = 1mg/ml
• 2% = 2 gr/100 ml = 2000 mg/100 ml = 20 mg/ml

34. 1st step
1. Adrenaline 0.5 cc
(they use 1: 1000 adrenaline = 1 mg/ml)
Adrenaline 0.5 cc = 0.5 mg/ml
9.5 ml of distil water added -> volume becomes
10 ml so
0.5 mg : 10 cc ( current concentration)
= 500 mcg : 10cc
-> 1cc = 50 mcg
2nd step
2. Plain Marcaine 0.5 % 5 cc + distil water 5 cc
= 5 mg/ml ( Marcaine ) -> 25 mg Marcaine
Concentration 10 ml
-> 1ml = 2.5 mg
Final:
1cc adrenaline + 9cc diluted Marcaine
-> 1: 200 000 adrenaline
2.5 mg in 1cc marcaine

35. • Max. dose of lidocaine in liposuction by tumescent .
• Safe max dose : 35 mg/kg – in view of 12-14 hr delay in peak plasma levels
following infiltration into subcutaneous fat.
• Large dose can be administered safely due to :
• Dilution by wetting solution
• Slow infiltration into poorly vascularized space
• Vasoconstrictive effect of adrenaline
• Bupivacaine should not be used – severe toxic reactions reported with small
doses ( < 0.5 mg/kg)

36. EMLA cream
• Eutectic Mixture of Local Anaesthetics
• Mixture of 2.5% lidocaine and 2.5% prilocaine
• Topical local anesthetic that penetrates intact skin
• Onset of effect :1 hour.
• 1g of EMLA Cream = circular area with a diameter of about 18
mm (a 1 pence coin) and depth of about 5 mm
• Contains polyoxyethylene hydrogenated castor oil. This may
cause skin reactions

37. Dosage
*Maximum of 2 doses at least 12 hours apart may be given to children over 3 months in
any 24 hours
Adults
• Minor dermal procedure : 2.5 gr over 20-25 cm² of at least 1 hour
• Major dermal procedure : 2.0 gr per 10 cm² of skin and remain in contact at least 2 hours
Age Dose Maximum area of application Maximum application time
< 3months 1 gr 10 cm² 1 hr
3-12 months 2gr 20 cm² 4 hr
1-6 year 10 gr 100 cm² 5 hr
7-11 year 20 gr 200 cm² 5 hr

38. Mepivacaine
• Onset : 5-10 minutes
• Duration of effect : 1-3 hr
• Dose :
• Without adrenaline : 4.5 mg /kg
• With adrenaline : 7 mg/kg
Available preparations:
• Scandonest 2% ( Mepivacaine + Adrenaline 1: 100
000)
• 1 cartridge ( 2.2 ml)
• Mepivacaine hydrochloride : 44 mg
• Adrenaline: 22 mcg
• Potassium metabisulfite ( reduce oxidation of
vasoconstrictor)
• Hydrochloric acid ( lower pH of solution)

39. Bupivacaine ( Marcaine)
• Slower onset : 10 -15 min
• Duration of action : 3 -12 hrs
• 4 times more potent than lidocaine.
• Therefore 0.25% bupivacaine is equipotent with 1% lidocaine.
• Available in 0.25 % and 0.5% solution.
• Cardiotoxic – adding epinephrine decrease toxicity by delaying absorption.
• Recommended maximum safe dose :
• Bupivacaine without adrenaline -> 2.0 mg/kg
• Bupivacaine with adrenaline -> 2.5 mg/kg

40. Available Preparations:
• Marcaine 0.5% ( 100 mg/20 ml) with adrenaline
• 1 bottle contains:
• Bupivacaine hydrochloride 100 mg in 20 mls
solution
• Adrenaline 0.10 mg
• pH of solution : 3.5 -5.5
• 1ml of Bupivacaine = 5 mg

41. Levobupivacaine
• Relatively new agent, similar to bupivacaine ( long acting)
• Greater vasoconstrictive action and less motor block compare to bupivacaine.
• Less cardiotoxic.
• Dose : 3-4 mg/kg
Ropivacaine
• Developed due concerns of bupivacaine toxicity
• Less cardiotoxic
• Dose : 3-4 mg/kg

42. DRUG LIDOCAINE PRILOCAINE BUPIVACAINE LEVOBUPIVACAINE ROPIVACAINE
Description Amide Amide Amide Amide Amide
Relative potency 2 2 8 8 6
Onset 5-10 min 5-10 min 10-15 min 10-15 min 10-15 mins
Duration
without epinephrine
1-2 hours 1-2 hours 3-12 hours 3-12 hours 3-12 hours
Duration
with epinephrine
2-4 hours 2-4 hours 4-12 hours 4-12 hours 4-12 hours
Max dose
without epinephrine
3 mg/kg 6 mg/kg 2 mg/kg 2.5 mg/kg * 3 mg / kg *
Max dose
with epinephrine
7 mg/kg 9 mg/kg 2.5 mg/kg 3 mg/kg * 4 mg / kg *

43. Local Anesthetic Additive
Adrenaline
• Added to local anesthetics to cause vasoconstriction.
• This reduces LA absorption , reduces toxicity and prolongs block duration.
• Does not significantly prolong bupivacaine duration but slows its absorption.
• Should not be used area supplied by end arteries ( finger, toe, penis ,nose, ears)
• Adrenaline commercially available in two ampoule sizes:
• 1 ml ampoule containing 1 mg ( 1: 1000)
• 10 ml ampoule containing 1 mg ( 1: 10000)

44. • Adrenaline 1: 1000 contains 1 mg of
adrenaline per ml
How ?
• 1:1000 means that in every 1000 ml of
solution, you will find 1 gr of adrenaline.
Calculation:
• 1gr = 1 000 ml
• 1000 mg = 1 000 ml
• Divide both sides by 1000
• 1mg = 1 ml

45. • 1: 200 000?
• 1 gr = 200 000 mls
• 1000 mg = 200 000mls
• 1mg = 200 mls
• -> 1ml = 5 mcg
• 1:200 000 concentration commonly
used for peripheral nerve blocks.
• Maximum safe dose of epinephrine : 4
micrograms per kg
• 1mg = 1000 mcg
• Example: What is the maximum dose in a 80 kg
man to be used for peripheral nerve block ?
• 4 mcg x 80 kg = 320 mcg
• 1: 10 000( most diluted vial available) -> we have
to dilute it to 1: 200 000. ( by adding 190 mls
solution + 10 ml adrenaline)
• 1 mg or 1000 mcg in 200 mls
• 320 mcg in 64 mls -> max dose.

46. Adrenaline Concentration
• 1: 1000 : 1000 mcg per ml
• 1 : 10 000 : 100 mcg per ml
• 1 : 100 000 : 10 mcg per ml
• 1 : 200 000 : 5 mcg /ml
• 1: 400 000 : 2.5 mcg /ml

47. Systemic Toxicity of Local Anesthetics
• Adverse systemic effects can occur due to:
• Intravascular injection
• Overdosing
• Failure to adjust dosing ( hepatic /renal disease)
• Clinical toxicity is related to effect of drug on
excitable membranes in CNS and cardiovascular
system.
• Cardiac effect : effects of ion channels may cause
conduction disturbances, depressed cardiac function
and peripheral vasodilation.

48. Prevention of Systemic Toxicity
• Use the lowest dose necessary to induce anesthesia
• Before reinjecting an area, allow sufficient time for the anesthetic to work, particularly
when using an agent with long onset of action.
• Avoid intravenous infusion by careful technique and by aspirating before injection.
• Employ nerve blocks when possible.
• Use epinephrine unless contraindicated
• When anesthesizing a large area, use the lowest effective concentration of anesthetic.

49. Anatomy
• Main sensory innervation of the face is derived from cranial nerve V (
trigeminal) and upper cervical nerves

50. Anatomy of Trigeminal Nerve
• Trigeminal nerve exits from the pons with a small motor root and large sensory
root.
• Its branches originate at the semilunar ganglion ( gasserian ganglion) located on
the dorsal surface of pertrous temporal bone.
• The motor root runs along medial side of ganglion to the mandibular nerve.
• Three main branches proceed from the ganglion to supply sensory innervation of
face:
• Opthalmic nerve ( V1)
• Maxillary nerve ( V2)
• Mandibular nerve ( V3)

51. Fig : Main branches of the trigeminal nerve supplying sensation to the
respective facial areas.

52. Opthalmic nerve ( V1)
• Purely sensory nerve.
• Passes lateral to the cavernous sinus and
abducent nerve to the superior orbital
fissure.
• Divides into three branches before entering
the superior orbital fissure:
1. Frontal nerve
2. Nasocilliary nerve
3. Lacrimal nerve
• The frontal nerve courses above levator
palpebral superioris and divides into:
• Supraorbital n.
• Suptratrochlear n.

53. Supraorbital Nerve
• Found in vertical line at level of supraorbital
notch
• Ascends through a notch ( or foramen) in the
supra-orbital ridge approximately 27 mm
lateral to the glabellar midline.
• After exiting the notch or foramen, the nerve
transverses the corrugator supercilii muscle
and branches into medial and lateral portion.
• Lateral branch supplies lateral forehead
• Medial branch supplies scalp

54. Supratrochlear nerve
• Exits the orbit 1cm more medially ,
above the pulley of the superior
oblique muscle.
• Supply upper eyelid , root of nose and
adjoining skin of the forehead , skin
and conjunctiva of the medial
canthus.

55. Maxillary Nerve ( V2)
• The second branch of the trigeminal nerve
is also pure sensory.
• Emerges from skull through foramen
rotundum and enters pterygopalatine
fossa.
• From here, it gives off the Zygomatic nerve
and pterygopalatine nerves.
• Infraorbital nerve penetrates inferior
orbital fissure and infraorbital foramen.

56. • Infraorbital nerve exits orbit
through infraorbital foramen 4 to 7
mm below orbital rim in an
imaginary line from pupillary
midline.
• Anterior and superior alveolar
nerve branches from infraorbital
nerve before it exits the infraorbital
foramen.
• Supplies lateral nose , anterior
cheek , lower eyelid and upper lip.

57. Mandibular Nerve
• Contains sensory and motor root.
• Passes through oval foramen
• Divides into anterior trunk ( mainly motor fibers) and posterior trunk.
• Inferior alveolar nerve exits the ramus of mandible at the mandibular foramen.
• It then passes forward in the mandibular canal ,beneath the teeth as far as the
mental foramen.
• Divides into two terminal branches -> Mental nerve and Incisive nerve.
• Mental nerve emerges at mental foramen -> divides into 3 branches
• One descends to skin of chin
• Two ascend to skin and mucous membrane of lower lip.

58. Mandibular Nerve
• Mental nerve is a branch of the inferior alveolar n. which exits via the
mental foramen.
• It then divides into 3 branches below the depressor anguli oris
muscle.
• One branch : skin of chin
• 2 other branches : skin and mucous membrane of lower lip

59. Nerve Blocks in Clinical Practice
Rules to observe when administering nerve blocks
Before the block
Patient
1. Preoperative information
• Explain the procedure
• Discuss potential side effects and complications
• Advise the patient about what to do after the procedure
• Document the discussion
2. Determine the patient’s neurological status
• Exclude neurological abnormalities
3. Exclude contraindications

60. Local Infiltrative Anesthesia Vs Nerve Block
Local infiltrative anesthesia Nerve Block
Injection of LA at distant site of main nerve
No specific skill necessary
LA placed at specific location around
main nerve trunk
Distortion of tissue around site of injection Small amount of LA needed to
anesthesize area of sensory distribution.
Only selected area of innervation involved Sensation of numbness in areas other
than operative site

61. Face Nerve Block Techniques
Indications
• Wound closure
• Pain relief
• Anesthesia for debridement
• Anesthesia for local excision or biopsy
• Contraindication to general anesthesia
Contraindications
• Any allergy or sensitivity to anesthetic
agent
• Evidence of infection at injection site
• Distortion of anatomical landmarks
• Uncooperative patient
• Physician lack of familiarity with nerve
block
• Coagulopathy

62. Supraorbital and Supratrochlear Block

63. Injection Technique
Supraorbital nerve
1. Locate supraorbital foramen by using non
dominant hand to palpate orbital rim to ensure
needle tip is exterior to bony orbital margin.
2. Palpate notch or measure 27 mm from glabella
midline.
3. Needle introduced perpendicular angle
immediately superior to supraorbital notch.
4. Slightly withdraw needle 1-2mm to avoid
intraneural injection.
5. Aspirate and inject slowly 1-2 mL of LA.

64. Injection Technique
Supratrochlear nerve
1. Locate supraorbital foramen
2. Target area of insertion on supraorbital ridge
approximately 1 cm medial to supraorbital notch
3. Needle introduced between the notch and
bridge of nose
4. Withdraw after bone contact and slow injection
of LA.
5. Aspirate and inject 1-2 mL of LA slowly.

65. Infraorbital Nerve Block
Anatomy
• Located on a line dropped from medial
limbus of the iris.
• Infraorbital foramen located 4 to 7mm below
orbital rim on that line.
• Sensory Innervation
• Lower eyelid
• Lateral portion of nose
• Anterior cheek
• Upper lip

66. Injection Technique
Intraoral Injection
1. Center of lower orbital margin palpated and
marked with middle finger
2. Patient asked to open eyes and look straight
ahead.
3. Upper lip is raised with thumb and index
finger of non dominant hand to palpate
inferior orbital rim .
4. 30 G needle introduced at the vestibule
above second premolar tooth toward
infraorbital foramen
5. 2-4 mL of lidocaine 2% injected and finger
can fell LA bolus beneath infraorbital rim.

67. Injection Technique
Extraoral Injection
1. Patient to look straight ahead and imagine a
line drawn vertically from pupil down toward
inferior border of infraorbital rim.
2. Infraorbital foramen roughly 4-7 mm below
infraorbital rim.
3. 32 G needle injected and aimed at foramen
in a perpendicular direction
4. 2-4 mL of LA injected close to the foramen.
5. Aspirate to ensure needle not within vessel.
Be careful or facial a. and vein.

68. Injection Technique
Transcutaneous nasolabial approach
• Point of injection medial to the upper nasolabial
groove , a few mm lateral to the alar groove.
• Patient asked to look straight.
• Needle held like a pen, index finger of opposite
hand placed on infraorbital rim.
• Needle directed upward and laterally to a point
5-7 mm below infraorbital rim.
• 1-2 cc of LA injected.

69. Mental Nerve Block
Anatomy
Mental nerve exit foramen below apex of 2nd
bicuspid.

70. Injection Technique
Intraoral Technique
1. Palpate mental foramen at level of second
premolar.
2. Mental foramen approx. 1cm inferior to
the gum line.
3. After palpation of mental foramen , lower
lip is pressed downward using a spatula.
4. 32 G needle is inserted between the first
and second premolars into the lower
reflection of the oral vestibule.
5. Aspirate and inject 2-3 ml of LA
6. Do not inject into the foramen.

71. Injection Technique
Extraoral Technique
1. Palpate the mental foramen
2. Needle is inserted about 2.5 cm lateral
to the midline until bone contact is
made
3. 32 G needle injected 2-3 mL of LA

72. Dorsal Nasal Nerve Block
Anatomy
• Branch of the anterior ethmoidal
branch nasocilliary nerve.
• Emerges as dorsal nasal nerve 6 to
10mm off the midline of the nose.
• Nerve exits from a small groove in
distal nasal bones.
• Supply skin of ala, vestibule and lip
Fig: The dorsal nasal nerve is blocked subcutaneously at the
osseous cartilaginous junction of the distal nasal bones.

73. Injection Technique
• Palpate nasal midline
• Feel end of nasal bone using thumb
on one side and indec finger on the
other
• The nerve exts about 6 mm to 10 mm
from midline of the nasal bones.
• 1 to 2cc is injected

74. Zygomaticotemporal Block
• Zygomatic nerve is a branch of the
maxillary nerve ( V2) and supplies
skin over zygomatic and temporal
bone.
• Zygomaticotemporal nerve emerge
through a foramen located the
anterior wall of the temporal fossa.
• Foramen is located behind the
lateral orbital rim posterior to the
zygoma at appox. level of the
lateral canthus
S.M. Jeong, K.J.Park.S.H. Kang,et al. Anatomical Consideration of the Anterior and Lateral Cutaneous Nerves in the
Scalp. J Korean Med Sci 2010;25: 517:22

75. Injection Technique
1. Palpate lateral orbital rim at level of frontozygomatic suture.
2. Index finger placed in the depression of the posterolateral aspect of
the lateral orbital rim.
3. Needle placed just behind the palpating finger.
4. Needle is ‘walked’ down the concave posterior wall of the lateral
orbital rim to the approximate level of lateral canthus.

76. Zygomaticotemporal Nerve Block
Zygomaticotemporal nerve blocked by placing needles on concave
surface of posterior lateral orbital rim

77. Zygomaticotemporal Nerve Block
• Anesthetized area formed by
Zygomaticotemporal nerve:
• Lateral orbital rim and skin of
temple from above zygomatic arch
to temporal fusion line.

78. Zygomaticofacial Nerve Block
• Nerve emerges through foramen on anterior
surface of zygoma.
• The foramen is a few milimeters lateral to
inferior orbital rim.
• Palpation of junction of the inferior lateral
portion of the lateral orbital rim, the nerve
emerges several milimeters lateral to this
point.
• Nerve block by injecting just lateral to the
palpating finger.

79. Zygomaticofacial Nerve Block
Zygomaticofacial nerve blocked by injecting the inferior
lateral portion of the orbital rim

80. Zygomaticofacial Nerve Block
• Anesthetized area formed by
Zygomaticofacial nerve:
• Triangular area from lateral
canthus and malar region
• Along zygomatic arch and
some skin inferior to it

81. Great Auricular Block
Anatomy
• Largest ascending branch of cervical plexus
C2 and C3.
• Located 6.5 cm inferior to external auditory
canal.
• Nerve divides into end branch that supply
skin over parotid and and of mandible.

82. Injection Technique
1. Patient asked to flex SCM
2. Mark the skin of upper anterior and
posterior CM borders with 2 parallel
lines.
3. A 3rd line drawn between first 2
lines.
4. Measure down 6.5 cm from EAC to
mid SCM
5. LA injected at this intersection onto
the muscle fascia.

83. Mandibular Nerve Block
• Mandibular nerve exits through oval foramen
and travels behind the pterygoid muscles about 1
cm posterior to the pterygoid plate.
• Branches anesthesized:
• Buccal branch , Lingual , Inferior alveolar
,Mental , Auriculotemporal nerve
• Landmarks :
• Mandibular fossa ( sigmoid notch)
• Zygomatic arch
• Tragus – notch is 2.5 cm anterior to tragus

84. Injection Technique
1. Patient asked to open mouth
2. Localize mandibular fossa between condylar and
coronoid process when patient opens and closes
mouth
3. 22 G Spinal needle directed at angle of 90’ and
advance until lateral pterygoid plate hit/
4. Tip of needle withdrawn 0.5 cm to 1 cm and
redirected posteriorly and inferiorly.
5. Paresthesia in mandibular region elicited at depth
about 1 cm.
6. After aspiration 3-5 ml of LA injected.

86. Complications
• Bleeding
• Haematoma formation
• Allergy or systemic reaction to anesthetic agent
• Infection
• Unintentional injection into artery or vein
• Failure to anesthesize
• Nerve damage