Regional Anesthesia Nerve Blocks

2011
Dr Azam's Notes in Anesthesiology

– Second Edition
Regional Anesthesia & Nerve

Blocks
Dr. Mohammed Azam Danish

Consultant Anesthesiologist & Critical Care Specialist
www.DrAzam.com
Dr Azam's Notes In Anesthesiology 2010
-Second Edition
Dr Azam’s Notes in Anesthesiology

2nd Edition
Regional Anesthesia& Nerve Blocks

By
Dr. Azam
Consultant Anesthesiologist & Critical Care
www.DrAzam.com
-Second Edition
PREFACE
This book grew from notes first written in 2003 - 2004 for the students at the J J M
Medical College in Davangere.
There are many textbooks to choose from when preparing for the “Anesthesiology
examination”. The candidate suffers not from the lack of information but rather from
being inundated with it. The candidate then has the task of information sorting and
data compression to memorize and utilize all this information.
Graphic representation of data is an excellent form of data compression; figures or

drawings are frequently asked about at the viva examination, particularly since the
candidate’s understanding of a problem comes across most clearly when drawing a
figure or a using a picture. Figures are also a good way of approaching a topic.
I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate

students when preparing for the Anesthesiology examination and later when
preparing for tutorials.
Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more

experienced practitioners may find it useful as a refresher in recent concepts and
advances
Dr Azam’s Notes is not a substitute for the major anesthesiology text books but
concentrates on principles of management of the most challenging anesthetic cases.
The format is designed to provide easy access to information presented in a concise

manner. I have tried to eliminate all superfluous material. Selected important or
controversial references are presented as well as suggestions for further reading.
Some relate more to basic principles, physiology, pharmacology, etc. – bookwork.
Others are more practical in nature, discussing the principles of anesthetic techniques
for certain high-risk situations.
Dr Azam’s Notes have been created keeping the Postgraduate needs while preparing
for the exams, and also help in his day to day practice. I am sure that Dr Azam’s Notes
will not only help him to secure highest marks but also help him to gain knowledge to
its full.
www.DrAzam.com
-Second Edition
A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be

followed, but as new research and clinical experience broaden our knowledge, changes
in treatment and drug therapy may become necessary or appropriate. Readers are
advised to check the most current product information provided by the manufacturer
of each drug to be administered to verify the recommended dose, the method and
duration of administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences,

neither the author nor the publisher nor any other party who has been involved in the
preparation or publication of this work warrants that the information contained
herein is in every respect accurate or complete, and they disclaim all responsibility for
any errors or omissions or for the results obtained from use of the information
contained in this work. Readers are encouraged to confirm the information contained
herein with other sources. It is the responsibility of the licensed prescriber, relying on
experience and knowledge of the patient, to determine dosages and the best treatment
for each individual patient. Neither the publisher nor the editor assumes any liability
for any injury and/or damage to persons or property arising from this publication.
www.DrAzam.com
-Second Edition
DEDICATION
To Mohammed Shafiulla, my father, my oxygen,

companion, and best friend; for being my major pillar of
support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless
gratitude, for the sake of your children. I owe you a debt I
can never repay.
I also would like to thank my mom (Naaz Shafi), my wife

(Roohi Azam), my two lovely kids (Falaq Zohaa &
Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
I also thank my Colleagues Dr Rajshekar Reddy & Dr Sachin for

their support.
Finally, I would like to thank my teachers. The dream begins

with a teacher who believes in you, who tugs and pushes and
leads you to the next plateau, sometimes poking you with a
sharp stick called "truth."
www.DrAzam.com
-Second Edition
Contribution
01. Dr. Rajshekar Reddy – UAE
02. Dr. Surendra – UAE
03. Dr. Nagaraj Chandy – Hubli
04. Dr.Kusuma – Bangalore
05. Dr Sachin Doijode – London
06. Dr Chandrashekar – Bangalore
07. Dr Sidhu – Bangalore
08. Dr Ravindra B K – Bangalore
09. Dr Harshavardhan – Mangalore
10. Dr Anil Kumar – Tamil Nadu
11. Dr Mashooda – Kerla
12. Dr Anusuya – Bangalore
13. Dr Sudhir – Bangalore
14. Dr Uma – Davangere
15. Dr Rajeev – UAE
16. Dr Surendra – UAE
17. Dr Shivananda – Shimoga
18. Dr Soujanya – Bangalore
19. Dr Aslam Faris – Kerla
20. Dr Nandakumar – Tamil Nadu
21. Dr Anuradha – Bangalore
22. Dr Arun G Pai – Kerla
23. Dr Geetha – Bangalore
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Table of Contents
PREFACE .......................................................................................................................................................... 3
DEDICATION .................................................................................................................................................... 5
CHAPTER 1 PRINCIPLES OF REGIONAL ANAESTHESIA ..................................................................................... 12
DEFINITION:......................................................................................................................................................... 12
TYPES OF RA:....................................................................................................................................................... 12
PRE-BLOCK EVALUATION: ....................................................................................................................................... 12
Premedications:........................................................................................................................................... 12
ANATOMIC CONSIDERATION: ................................................................................................................................... 13
NERVE FIBRES ................................................................................................................................................... 13
PHARMACOLOGIC CONSIDERATIONS: ........................................................................................................................ 14
MECHANISM OF ACTION:........................................................................................................................................ 14
ORDER OF BLOCK: ................................................................................................................................................. 15
PHARMACODYNAMICS ........................................................................................................................................... 16
CHAPTER 2 - LOCAL ANESTHETICS .................................................................................................................. 19
DESIRABLE PROPERTIES: ......................................................................................................................................... 19

POTENCY AND TOXICITY:......................................................................................................................................... 19
CHEMICAL CLASSIFICATION OF L.A.:.......................................................................................................................... 20
PHARMACODYNAMIC CLASSIFICATION OF L.A: ( ....................................................................................................... 20
LIDOCAINE ........................................................................................................................................................... 21
BUPIVACAINE: .................................................................................................................................................. 21
ROPIVACAINE: .................................................................................................................................................. 23
DETERMINATES OF TOXICITY .................................................................................................................................... 25
Factors affecting disposition of L.A.: ........................................................................................................... 26
TOXIC REACTIONS TO L.A ....................................................................................................................................... 26
CLINICAL CAUSES OF TOXIC LEVELS: ........................................................................................................................... 27
CNS stimulation: .......................................................................................................................................... 27
FACTORS INFLUENCING ARE:.................................................................................................................................... 27
Summary of prophylaxis of CNS toxicity:..................................................................................................... 28
Treatment: .................................................................................................................................................. 28
CVS TOXICITY:...................................................................................................................................................... 28
LIPID EMULSION: ......................................................................................................................................... 30
A NOTE ON NERVE FIBERS:...................................................................................................................................... 30
PERIPHERAL NERVE FIBER TYPES .................................................................................................................. 30
COMPONENTS OF PERIPHERAL NERVE FIBER ................................................................................................................ 30
CLASSIFICATION OF PERIPHERAL NERVE FIBERS ............................................................................................................ 31
A group ........................................................................................................................................................ 31
B group ........................................................................................................................................................ 31
C group ........................................................................................................................................................ 31
CHAPTER 3 BLOCK OF CRANIAL NERVES ......................................................................................................... 33
GASSERAIN GANGLION BLOCK: (MECKEL’S CAVE) ............................................................................................... 33

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OPHTHALMIC NERVE BLOCK ............................................................................................................................ 33
MAXILLARY BLOCK ........................................................................................................................................... 34
MANDIBULAR BLOCK ....................................................................................................................................... 35
LINGUAL NERVE BLOCK .................................................................................................................................... 35
GLOSSOPHARYNGEAL NERVE BLOCK ............................................................................................................... 36
SUPERIOR LARYNGEAL NERVE BLOCK .............................................................................................................. 36
CERVICAL PLEXUS BLOCK ................................................................................................................................. 37
PHRENIC NERVE BLOCK .................................................................................................................................... 39
INTER COSTAL NERVE BLOCK............................................................................................................................ 39
INTERPLEURAL BLOCK:............................................................................................................................................ 41
CHAPTER 4 BLOCKS OF UPPER EXTREMITY..................................................................................................... 44
BRACHIAL PLEXUS BLOCK ................................................................................................................................. 44

INTERSCALENE BLOCK. ..................................................................................................................................... 44
SUPRACLAVICULAR BLOCK ............................................................................................................................... 46
SUBCLAVIAN PERIVASCULAR BLOCK ................................................................................................................ 48
AXILLARY BLOCK ............................................................................................................................................... 48
WRIST BLOCK ................................................................................................................................................... 50
AUTONOMIC BLOCKADE .................................................................................................................................. 51
SYMPATHETIC BLOCKS ..................................................................................................................................... 52
CELIAC PLEXUS BLOCK ...................................................................................................................................... 54
PHYSIOLOGY OF CELIAC PLEXUS BLOCK: ...................................................................................................................... 55
CELIAE PLEXUS: ................................................................................................................................................ 58
LUMBAR SYMPATHETIC BLOCKS ...................................................................................................................... 58
THORACIC SYMPATHETIC BLOCKS: T4-T9.......................................................................................................... 59
STELLATE GANGLION OR CERVICO THORACIC SYMPATHETIC BLOCK ............................................................... 60
CHAPTER 5 FIELD BLOCKS .............................................................................................................................. 64
FIELD BLOCK FOR TONSILLECTOMY .................................................................................................................. 64

HERNIA BLOCK ................................................................................................................................................. 65
CHAPTER 6 - PERINEAL ANAESTHESIA ............................................................................................................ 69
PUDENDAL NERVE BLOCK ................................................................................................................................ 69

PARACERVICAL N BLOCK: ........................................................................................................................................ 71
PENILE BLOCK ................................................................................................................................................... 71
CHAPTER 7 - NERVE BLOCKS OF THE LOWER EXTREMITY ............................................................................... 72
ADVANTAGES OF NERVE BLOCKADE OF THE EXTREMITY: ............................................................................................... 72

PSOAS COMPARTMENT BLOCK ........................................................................................................................ 74
FEMORAL NERVE BLOCK .................................................................................................................................. 76
OBTURATOR NERVE BLOCK .............................................................................................................................. 77
INGUINAL PARAVASCULAR TECHNIQUE OF LUMBAR PLEXUS ANAESTHESIA (WINNE’S 3 – IN – 1 BLOCK)....... 78
SCIATIC NERVE BLOCK (L4,5 S1,2,3) ...................................................................................................................... 79
BLOCKS AROUND THE KNEE JOINT ................................................................................................................... 84
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-Second Edition
SAPHENOUS NERVE BLOCK (L3 – L4) .................................................................................................................. 85
TIBIAL NERVE BLOCK (L4 - S2) ........................................................................................................................... 87
ANKLE BLOCK ................................................................................................................................................... 88
CHAPTER 8 - ANATOMY & PHYSIOLOGY OF SPINAL / EPIDURAL AND CAUDAL SPACE (IN SHORT) ................. 92
TOPOGRAPHIC LINE OF TUFFIER:............................................................................................................................... 94

SPINAL CORD .................................................................................................................................................... 95
COMPARTMENT RELATED TO SPINAL MENINGES ............................................................................................ 99
THE EXTRA DURAL (PERIDURAL OR EPIDURAL) SPACE: .................................................................................. 101
CAUDAL SPACE: .............................................................................................................................................. 102
PHYSIOLOGY OF SPINAL ANAESTHESIA .......................................................................................................... 102
Effect o gastric emptying: ......................................................................................................................... 105
DIFFERENCE BETWEEN SPINAL AND EPIDURAL ........................................................................................ 108
Testing for levels of block for different nerve modalities: ......................................................................... 108
BROMAGE SCORE: ..................................................................................................................................... 109
Test for sympathetic block: ....................................................................................................................... 109
CHAPTER 9 SPINAL NEEDLES ........................................................................................................................ 112
TYPES ............................................................................................................................................................... 113
CHAPTER 10 COMPLICATIONS OF SPINAL ANAESTHESIA& EPIDURAL ANESTHESIA ...................................... 115
COMPLICATIONS OF EPIDURAL ANAESTHESIA ............................................................................................... 115

Differential block: ...................................................................................................................................... 116
CHAPTER 11 POST DURAL PUNCTURE HEADACHE (PDPH) ............................................................................ 118
AETIOLOGY: .................................................................................................................................................... 118

LOW CSF PRESSURE THEORY: ................................................................................................................................ 118
Differential diagnosis: ............................................................................................................................... 118
Factors affecting PDPH: ............................................................................................................................ 119
CHAPTER 12 TOTAL SPINAL ANAESTHESIA ................................................................................................... 123
CHAPTER 13 CAUDA EQUINA SYNDROME .................................................................................................... 126
CAUDA EQUINA: ................................................................................................................................................. 126

CAUDA EQUINE SYNDROME: .................................................................................................................................. 126
CHAPTER 14 DETECTION OF EPIDURAL SPACE .............................................................................................. 128
NEGATIVE PRESSURE TECHNIQUES: ......................................................................................................................... 128

DISAPPEARANCE OF RESISTANCE TECHNIQUE: ........................................................................................................... 128
CHAPTER 15 IVRA (IN SHORT) ...................................................................................................................... 130
MECHANISM:..................................................................................................................................................... 130
CHAPTER 16 EPIDURAL ANAESTHESIA (IN SHORT) ....................................................................................... 135
FATE OF EPIDURAL AGENTS. .......................................................................................................................... 137

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CHAPTER 17 - CAUDAL EPIDURAL ................................................................................................................ 143
HISTORY..................................................................................................................................................... 144
ANATOMY ...................................................................................................................................................... 144
THE SACRAL FORAMINA’S: .................................................................................................................................... 145
Sacral hiatus: ............................................................................................................................................. 146
PHYSIOLOGY ...................................................................................................................................................... 147
INDICATIONS .................................................................................................................................................. 148
CONTRAINDICATIONS................................................................................................................................ 151
Techniques ................................................................................................................................................ 151
Three main techniques are available ........................................................................................................ 152
Confirmation of Landmarks:...................................................................................................................... 152
The continuous techniques: ....................................................................................................................... 155
Drugs and Dosage: .................................................................................................................................... 158
Complications: ........................................................................................................................................... 161
CHAPTER 18 - ANATOMY AND PHYSIOLOGY OF SPINAL ANAESTHESIA ........................................................ 165
SPINAL ANAESTHESIA ..................................................................................................................................... 165

DEFINITION:....................................................................................................................................................... 165
HISTORY OF SPINAL ANESTHESIA: .................................................................................................................. 165
ANATOMY OF VERTEBRAL COLUMN ......................................................................................................... 165
MEANINGS OF SPINAL CORD .......................................................................................................................... 167
Compartments related spinal meanings ................................................................................................... 168
Curves of the SPINE ................................................................................................................................... 168
PHYSIOLOGY OF CEREBROSPINAL FLUID ........................................................................................................ 169
COMPOSITIONS AND CHARACTERISTICS OF CSF ....................................................................................... 169
CIRCULATIONS OF CSF .................................................................................................................................... 170
PHYSIOLOGY OF SPINAL ANAESTHESIA: ......................................................................................................... 170
DIFFERENTIAL NEURAL BLOCKADE: DNB ....................................................................................................... 173
PROBABLE MECHANISMS OF DIFFERENTIAL BLOCK: ...................................................................................... 173
CARDIAC REFLEXES: ............................................................................................................................................. 176
BARORECEPTOR REFLEX (CAROTID SINUS REFLEX): ..................................................................................................... 176
MAP / HYPOTENSION ..................................................................................................................................... 177
TECHNIQUE OF LUMBAR PUNCTURE: ............................................................................................................ 182
LEVEL OF SPINAL ANAESTHESIA FOR COMMON SURGICAL PROCEDURES ..................................................... 184
INDICATIONS / ADVANTAGES......................................................................................................................... 184
COMPLICATIONS: ........................................................................................................................................... 185
HYPOTENSION ................................................................................................................................................ 186
PONV .............................................................................................................................................................. 187
POSTDURAL PUNCTURE HEADACHE .............................................................................................................. 188
RISK FACTORS FOR PDPH ..................................................................................................................................... 188
TREATMENT OPTIONS FOR PDPH:.......................................................................................................................... 189
MANAGEMENT OF HYPOTENSION ................................................................................................................. 190
VASO PRESSORS ............................................................................................................................................. 191
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SPINAL ANAESTHESIA IN CHILDREN ............................................................................................................... 191
SPINAL ANAESTHESIA FOR SPECIAL CATEGORIES OF PATIENTS SPINAL ANAESTHESIA IN GERIATRIC AGE
GROUP ........................................................................................................................................................... 193
Problems faced with geriatric age group: ................................................................................................. 193
SPINAL ANESTHESIA IN OBESE PATIENTS ....................................................................................................... 194
CHAPTER 19 - ANATOMY AND PHYSIOLOGY OF EPIDURAL ANAESTHESIA.................................................... 196
DEFINITION........................................................................................................................................................ 196
ANATOMIC CONSIDERATIONS: ...................................................................................................................... 196
BOUNDARIES .................................................................................................................................................. 196
CONTENTS ...................................................................................................................................................... 197
Clinical correlation: ................................................................................................................................... 197
EPIDURAL FAT .................................................................................................................................................... 198
SIZE OF PERIDURAL SPACE ............................................................................................................................. 199
Distance to epidural space: ....................................................................................................................... 199
PHYSIOLOGIC CONSIDERATIONS ............................................................................................................... 200
SITE OF ACTION ......................................................................................................................................... 200
FATE OF EPIDURAL AGENTS ...................................................................................................................... 201
POSITION OF PATIENT .................................................................................................................................... 205
DETECTION OF EPIDURAL SPACE: ................................................................................................................... 205
NEGATIVE PRESSURE TECHNIQUES ........................................................................................................... 205
DISPPEARANCE OF RESISTANCE TECHNIQUES: ......................................................................................... 206
Criteria for Correct Position of Needle and Successful Block: .................................................................... 213
COMPLICATIONS – TECHNICAL.................................................................................................................. 213
COMPLICATIONS RELATED TO EPIDURAL CANNULATION: ........................................................................ 214
COMPLICATIONS – CATHETERS: ................................................................................................................ 214
CHAPTER 20 - INTRAVENOUS REGIONAL ANESTHESIA (IVRA) ...................................................................... 216
HISTORY..................................................................................................................................................... 216
INDICATIONS IN SURGERY: ............................................................................................................................. 217
CONTRAINDICATIONS: ................................................................................................................................... 217
CHOICE OF LOCAL ANESTHETIC AGENTS ................................................................................................... 218
DOSAGE: .................................................................................................................................................... 218
BLOOD VOLUME IN THE EXTREMITIES: ..................................................................................................... 219
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Chapter 1 PRINCIPLES OF REGIONAL ANAESTHESIA
Definition:
Is defined as reversible blockade of nerve conduction by L.A. in the part where it is
applied.
Types of RA:
4 types:
1. Topical anaesthesia: Surface application to skin or mucous.
2. Infiltration anesthesia: Injecting LA into the tissue to be cut
3. Field block: Injecting LA into the area to be operated.
i. Ex: Inguinal field block.
4. Conduction block: (Referred to RA): Accomplished by depositing a solution
along the course of nerve supplying a region of the body where elimination of
sensory and / or motor innervation is required.
i. Ex: Spinal / Epidural analgesia.
Psychological management done.
Pre-block evaluation:
1. Aspirin ingestion (consider RA with BT < 10 minutes)
2. Congulopathies
Premedications:
Benzodiazepines, narcotics, antihistamines, anticholinergics, diversion and
distraction.
These provide: comfort, protection from CNS toxicity, protection from allergy,
from reflex bradycardia.
Facilities: proper room, ventilation, light, equipments for CPR etc.
Asepsis:
Hexachlorophene or tincture of zephiran used over face, scrotum, perineum.
Betadine, 70% ethyl or isopropyl alcohol used.
Skin preparation:
Soap water scrub or 70% ethyl alcohol for 5 min.
Normally skin contains 200-600 bacteria / inch2 of surface area.
Above measure decrease it by 20-40 bacteria / inch2.
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Iodine Tincture of iodine (1%) provides 300 ppm free

iodine
Povidone – iodine (betadise) 20-25 ppm free
iodine
Betadine: with proper friction and repeated 3 times decrease count to 5/ inch2 .
Single application of 0.5 % chlrohexidine in 70% ethyl alcohol or 1% tincture of
iodine is effective, but have skin reactions.
Anatomic consideration:
Landmarks:
- Superficial
- Deep
NERVE FIBRES
Diameter Velocity
Type Myelin Location Function
m (m/sex)
A 15-22 + 70-120 to & from Motor, muscle
muscles and proprioceptors
A 8-13 + 40-70 joints Touch.
A 4-8 + 15-40 To muscle Touch, pressure,
spindles tone of muscle
A 1-4 + 5-15 Afferent sensory Pain, temp,
nerves pressure
B 1-3 + 3-14 Preganglionic Preganglionic
sympathetic sympathetic
activity
CS 0.3-1.3 - 0.7-1.3 Postganglionic Postganglionic
sympathetic sympathetic
activity
0.4-1.2 - 0.1-2 Afferent sensory Pain, temp, touch
nerves
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Pharmacologic considerations:
LA blockade depends on 4 factors:
1. Diffusion to nerve and into bundle: Depends on solubility.
2. Penetration into nerve cell: Depends on non-ionized (base) form.
3. Distribution in a nerve fiber cell: Solubility.
4. Fixation: Affinity of cation form to channel receptors.
Recovery from LA block depends on 4 factors:
1. Absorption: Into circulation.
2. Release process: Nerve fibers releases fixed drug as gradient of concentration
reverses with time.
3. Redistribution: to other organs after absorption.
4. Metabolism and elimination.
1
Dissociation constants (pKa): ( pKa ionized )
It is defined as a pH at which equal concentration of acid and basic forms of a
substances exist.
The base or nonionized form is responsible for penetration of nerve and the
ionized or cation form is responsible for the action of LA on nerve.
Amount of base form present is inversely proportional to pKa of that agent at pH
7.4. Ex: Lidocaine pKa is 7.74 has 65% ionized and 35% in Non-ionized form at
pH 7.4.
Tetracaine and procaine have high pKa, hence slow onset bupivacaine: 8.1 pKa.
Benzocaine: with pKa 3.5 has rapid onset of action.
Outside nerve PH 7.4  once the base form gets into the axon where PH is 7.2 
the base form converts into ionized form which is now required for its action on
nerve.
Mechanism of action:
1. Block of ionic channels: It prevents Na to enter into cells following stimulation
hence blocks action potential.
2. Receptor expansion.
3. Prior depolarization: also blocks K channels, but its affinity towards Na channels
is great.
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Summary of chemical factors:
1. Degree of hydrolysis determines penetrability.
2. Effectiveness is a linear function of pH of tissues.
3. Alkaline pH of solutions increases activity.
4. Buffering to an alkaline pH has a greater effectiveness.
5. Acid media neutralize anesthetic action.
Minimum anesthetic condition (Cm): Lowest concentration of drug that blocks
conduction is called Cm.
Differential block (Cm):

Small fibres blocked by low concentration whereas myelinated ones need high
concentration of L.A. This is due to differing Cm values of L.A. for different nerve fibres.
Transitional block (Wedensky block ):

A latent period required for a L.A. to change the function of a nerve from an unblocked
state to the blocked state. During this time, one conceives of either a partial or threshold
block and repetitive stimuli may be conducted. During this time patients feels skin
incision but with less intense.
Order of block:
Vasomotor (Sympathetic
Cold block)
Warmth
Slow pain
Fast pain * Pressure produces the reverse effect
Motor
Joint sense
Pressure
Glucose in L.A impair its action due to hypo-osmotic effect.

Contact of L.A on nerve surface: Atleast 3-4 mm of nerve surface has to come in
contact with L.A or atleast 3 node of Ranvier blocked. 8 to 10 mm surface contact
is more practical.
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Pharmacodynamics
1. L.A activity is related to its chemical properties.
2. Diffusibility is related to water solubility.
3. Onset: Related to pKa of L.A and pH of tissues.
4. Duration: Related to protein binding and lipid solubility.
Protein Duration
pH L.A Chemical pKa Onset
binding (min)
6.5 Lidocaine Amide 7.7 2-4 min 64% 100
5.5 Bupivacaine Amide 8.1 5-10 min 95% 175
If pKa – pH of medium is > 1, percentage of ionized will be almost complete 

penetration of cell membrane is delayed.
Ex: Bupivacaine, tetracaine.
If pKa – pH < 1, increased unionized penetration of cell membrane fast 
rapid onset. Ex: Lidocaine, mepivacaine.
Potency: depends on lipid solubility. Bupivacaine, tetracaine, etidocaine are
examples, hence require only low concentration.
Enhancement of action:
1. Alkalinization: by increasing nonionized forms
2. Carbonated L.A.
pharmacokinetics:
Absorption:
Gets absorbed into blood stream after injection into tissue and depends on:
Site of application: Mucous, SC , IM
Blood supply to the site
Presence & abscence epirephrine etc.
a) Disposition: When interstial level decreases, L.A from neural tissue enters interstial
and finally into blood.
b) Protein binding: Determines duration of action and protection against high free
drug in plasma thus decreasing toxicity. Bupivacaine > Etidocaine > Mepivicaine >
lidocaine > prilocaine.
c) Redistribution: Occurs to all other organs depending on blood supply.
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Metabolism:
- Esters: In plasma.
- Amides: In liver.
- Esters: By cleavage of ester linkage and enzymatic hydrolysis.
o Chlorprocaine> procaine > tetracaine.
- Metabolite-- PABA (Paraamines benzoic acid)
o Amides: Oxidative dealkylation and later hydrolysis in liver. Prilocaine >
etidocaine > lidocaine > mepivacaine > bupivacaine.
Elimination: conjugated and excreted in urine.
Technical consideration:
1. Instruments: Tray, sterilization (avoid chemicals) by autoclaving, boiling or
pasteurization.
2. Tests of instruments.
3. Holding the needle: held like a dart.
4. Insertion of needle.
5. Identification of nerve:
6. Proper landmarks.
7. Paresthesia.
8. Nerve stimulator
9. X-ray guidance.
Nerve stimulator: 1913 by Perthes.

1. Use minimal intensity stimulus, output current between 0 and 6 MA and a twitch
stimulus rate from 1/10th sec to 1sec.
2. Goal is to achieve maximum response to very low current ie 0.5 MA.
3. The standard blockade monitor or hand unit can be used.
4. Failure rates: 4 – 6%.
5. Small dose of L.A is given and loss of motor power gradually to current is
established before injecting full dose.
6. Complications
Transient Mechanical
Nerve damage Permanent Ischemic
Chemical or toxic
Endoneural injection: Nerve damage
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Nerve damage can be decreased by using:

1. Small bore needles.
2. Short beveled (450)
3. Parallel to fibres.
Procedure:
- Amides are stable, without preservatives.
- Metabisulfates Na 0.1% (antioxidant) prevents breakdown of epinephrine.
- Methyl – paraben (antimicrobial)
- Do not inject L.A into tumor sites.
- Aspiration test.
- Radiographic aid
o Stereoscopic films
o 2 view studies.
o Use of constrast media.
- Use radioopaque drugs: Diadrast.
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Chapter 2 - LOCAL ANESTHETICS
Desirable properties:
1. Potent and effective in low concentration (increased lipid solubility).
2. Good penetrability.
3. Rapid action.
4. Long duration
5. Low toxicity.
6. Non-irritating.
7. Reversible action.
8. Easily sterilized and stable.
9. Cost effective.
hydrophilic
Molecular configuration:
lipophilic
Potency and toxicity: Relative to procaine

Toxicity Potency
Lidocaine 1-5 3
Bupivacaine 3 4-8
- Chemical nature: All L.A are salts of basic substances.

- Buffers: Sodium hydroxide addition gives more stable solution.
- Glucose: Diminish potency of L.A.
- K: Increase potency of L.A.
Other actions of L.A Antihistamines
o Anticholinergics
o Narcotics
o Antithrombotic action
o Antimicrobial action with tetracaine, lidocaine.
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Chemical classification of L.A.:
Esters Amides Alcohols Miscellaneous
Cocaine Xylocaine Ethyl alcohol Holocaine
Piperocaine Bupivacaine Eucupin
Procaine Mepivacaine THE
Chlorprocaine Dibucaine
Tetracaine Prilocaine
Benzocaine Levobupivacaine
Intracaine Ropivacaine
Esters Amides
Aromatic acid + alcohol Organic acid + amine
Hydrolysed by esterases Metabolized by liver
in plasma Long acting
Short acting More stable
Unstable More potent
Less potent Less toxic metabolites.
More toxic PABA metabolites
(* Amount of nonionized form inversely related to pKa at a given PH).
Pharmacodynamic classification of L.A: ( pKa slow onset) agent

1) Low potency – 2) Intermediate 3) High potency and duration
short duration potency and duration
Procaine (CP) Mepivacaine Tetracaine
Chlorprocaine Prilocaine Bupivacaine
Lidocaine Etidocaine
Dibucaine (180-600 min)
Alpha phase: Rapid

Depending on blood
Distribution: Beta phase: intermediate
Gamma phase: slow supply
Toxic plasma levels of

Lidocaine: > 4 g/ml.
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Bupivacaine: > 3 g/ml.
Lidocaine
Synthetic, in 1943 by Lofgren.
Diethyl amino – 2, 6 acetoxylidide.
MW: 234
Solubility: freely soluble.
pH: 6.5 – 7.0, pKa  7.8, toxic dose: 4-6 mg/kg.
Stability: boiled for 8 hrs.
Sterilization: boiling or autoclaving.
Non-irritant to nerve.
3 time more potent than procaine and 1.5 times toxic.
Metabolism – in liver (MEGX and GX)
Initially oxidative dealkylation to monoethylglycine xylidide (MEGX) and 2, 6 xylidide
later conjugation and exertion in urine – in the form of 4-hydroxy 2-6 xylidide.
MEGX: has antiarrhythamic properties, CNS effects, local anesthetic also.
Total dose: 4.5 mg/kg (200-400 mg for adults).
Infiltration: 0.5% concentration
Small nerve: 1% concentration
Large nerve: 1.5% concentration.
Epidural: 1.5 – 2% concentration.
Cardiac action: antiarrhythmic at 1.2 mg/l
Plasma levels calculated by 0.3 x dose gives (mg/kg) = plasma levels in mg/l.
At 3-4 mg/ml it increases medullary response to CO2.
At 8-10 mg/ml it depresses ventilation (subconvulsant levels).
At 20-25 mg/ml cardiac arrest.
Causes Ca+ extrusion from sarcoplasmic reticulum.
Decrease defense mechanism of body.
BUPIVACAINE:
- long acting amide L.A.
- pH 3-3.5.
- 1-n-butyl-PL-piperidine-2-carboxylicacid-2,6dimethylamilide hydrochloride.
- Solubility: base is sparingly soluble, but hydrochloride is readily soluble in
water.
- Stability and sterilization: stable and can withstand repeated autoclaving.
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Potency: 3 times than lidocaine,
8 times than procaine.
- Duration: 180 – 600 minutes.
- Anesthetic index: potency / toxicity ratio: 3-4.
- Infiltration: 0.25%
Small nerve: 0.25%
Nerve block:
Large nerve: 0.5%
- Caudal: 0.25 – 0.5%

- Epidural: 0.5% - 0.75% for abdominal surgery.
- Subarachnoid 0.5 – 0.75% + 8.25% dextrose (hyperbaric).
- 2ml ampule of 0.75% with pH of 4-6.5 (NaOH/HCl buffer) specific gravity: 1.035.
- 200 mg without epinephrine

Total 400 mg/day
- 250 mg with epinephrine
- Onset: 5-10 minutes, peak at 15-25 minutes.
- Toxicology: plasma toxic levels: 3 g/ml.
- Alpha half life: 2-5hrs.
- Beta half life: 4-5 hrs.
- Plasma binding: 95% to globulin
- Metabolism: in liver by N – dealkylation. Placental transfer not significant due to
high protein binding.
- Systemic effects: At low levels 1-2 g/ml) causes increase MAP by
vasoconstriction. At high levels  vasodilation.
It has direct depressant effect on CVS.
Sympathetic effect:
1. 2 receptor blockade.
2. No effect on receptors.
3. No effect on pressor effects of noradrenaline.
Shivering more common after epidural.

- Lack of tachyphylaxis.
- Toxicity : because of fast in slow out property.
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ROPIVACAINE:
- Levoisomer of bupivacaine
- Synthetic LA with low cardiotoxicity than bupivacaine is levo-isomer (no
asymmetric carbon) of bupivacaine.
- A propyl group replace butyl group of bupivacaine.
- pKa: 8.1
- Protein binding: 90-95%.
- Lipid solubility: half of bupivacaine.
- Potency: 30% more potent than bupivacaine and potency ratio is: Ropivacaine /
bupivacaine: 1.3/1
- Dosage: 0.5, 0.75 and 1%.
- Sensory block greater than bupivacain and last for 5-7 hrs.
- Onset shorter than bupivacaine, i.e 3-6 minutes with 0.5% concentration.
- Motor blocks: profound with 1 %, less with 0.5 and 0.75%.
Initial rapid
- Systemic absorption has biphasic
- t½  5 hrs for 0.75%. Later slow
- CVS: Prolongation of QRS time as an indicator showed
2 mg bupivacaine
Were needed for CVS effects
mg ropivacaine
30 mg lidocaine
No change in contractility, HR, BP. It produce vasoconstriction.
Dose of 2-5 g/kg produce no CNS/CVS effects.
Duration: 10-14 hrs.
Potentiation of L.A can be achieved and by adding:

Epinephrine
1 ml to 10cc of lidocaine
1. NaHCO3
0.1 ml to 20cc of
bupivacaine
1. K+ by decreasing resting potential.
2. Carbonated L.A.
3. Hyaluronidase – by increasing diffusibility.
4. Dextran prolongation – by increasing pH.
5. Increase pH of solution.
Toxicology of L.A:
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Absorption factos
- Blood levels = K x
Dispositio n factors
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Determinates of toxicity
Absorption Disposition
Vascularity Distribution into tisseus
Total dosage Protein binding and inactivation
Properties of L.A Metabolism
Rate of absorption Pulmonary disposition
Peak critical plasma levels Excretion
Epinephrine ±
Toxic levels:
- Lidocaine: 5 g/ml.
- Bupivacaine: > 3 g/ml
- Peak blood levels in decreasing order at various sites.
- Intercostals (interpleural) > Paracervical > caudal > epidural > brachial >
subarachnoid > subcutaneous.
Clinical factors influencing toxicity:

a. Physical status: poor general condition increase toxicity.
b. Type of procedure.
c. Detoxification potential: liver and renal dysfunction.
d. Nutrition: decrease albumin, decrease vitamin C increase toxicity.
e. Period of latency: time taken after injection to complete establishment of its
effect.
f. Drug interaction:
g. Barbiturates induce enzymes and the metabolism of L.A.
h. Chloramphenical, ATT prolong toxic effect of L.A.
i. Phenoborbitone decrease toxic effects of L.A.
j. Promethazine, meperidine increase convulsion due to L.A.
k. Diazepam shortens half life of L.A.
l. Protein binding decreased by meperidine, quinidine.
Testing for hypersensitivity of L.A: skin test
1mm intradermal wheal with 1: 1000 L.A – no response
1mm intradermal wheal with undiluted L.A. – no response
3-4 mm L.A. undiluted S/c.
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Factors affecting disposition of L.A.:
1. Age: prolong half-life in neonates due to protein binding immature liver and
renal function.
2. In older patients half-life is prolonged due to increased VD and greater uptake by
adipose tissue.
3. Acid-base status: PaCO2 and pH: toxicity ion trapping occurs due to
decreased protein binding.
4. Altered HBF: HBF decrease clearance of drugs
5. Hepatic disease:
Impaired uptake
Impaired metabolism Prolonged half life
Impaired secretion
6. Renal disease: metabolites of L.A accumulate, but do not have significant effect.
7. Pregnancy: volume by 25%
protein by 18% Limit transfer of drug into fetus
Toxic Reactions to L.A

Classification of toxic reaction:
I) CNS:
Stimulation:
I. Cortex: convulsions
II. Medullary vagal centers activity is increased causing increase in RR or CVS
activity or vomiting.
Depression
I. Cortex: unconscious and anaesthesia.
II. Medullary: 1) Vasomotor
2) Respiratory
II) CVS:
a. Cardiac: Bradycardia
b. Vascular: vasodilation
III) Allergic response:

a. Cutaneous
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b. Respiratory
IV) Miscellaneous reactions:
a. Psychogenic
b. Other drugs: vasopressors and additives.
Clinical causes of toxic levels:

I. IV administration accidentally.
During IVRA: i) high dose / 1oose tourniquet
ii) Release of tourniquet within 20 minutes.
CNS stimulation:
- Incidence: 1 in 300 to 4 in 1000.
- Early convulsions within 2 minutes due to accidental IV.
- Late convulsions after 4-6 minutes due to rapid absorption.
Site of CNS action:

Hippocampus and limbic system (in particular is amgdala) are stimulated
causing convulsions.
Mechanism:
Blockade of amygdaloid complex, followed by inhibitory pathway in cerebral cortex
leads to excitation by unopposed excitatory pathways.
Later on even these pathways are blocked leading on to unconsciousness and death
(depression).
Factors influencing are:

I) Drug:
a. Intrinsic potency of L.A used.
b. Dose
c. Rate of absorption: IV, infiltration etc.
Lidocaine toxic effects in humans at 6.4 mg/kg.
Bupivacaine toxic effects in human at 1.6 mg/kg.
II) Hypoxia: Increase convulsions.
III) Acidosis: Convulsive threshold is reduced by pH or PaCO2 PaCO2 CBF 
more drug reaches CNS. It also causes intracellular ion trapping.
IV) K+: K increase toxicity.
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Summary of prophylaxis of CNS toxicity:
1. Use least amount and concentration necessary.
2. Use epinephrine to decrease rate of absorption.
3. Pretreatment with diazepalm.
4. Test dose
5. Inject at 10ml/minute i.e, slow.
6. IVRA – avoid bupivacaine. Release cuff only after 20 minutes.
Treatment:
PaO2 with 100% O2
PaCO2 by hyperventilation
If conclusions is present
a. Patent airway
b. 100% O2
c. Diazepam
d. Thiopentone 50-100 mg IV
e. Paralyse if needed and give PPV.
CNS depression: Exeitation may be bypassed sometimes due to blocked of both
pathways at same time.
- Psychomotor impairment: like attention, coordination, response time.
Treatment: 1) O2 100%
2) Fluids
3) Vasopressors (ephedrine & Co2 it crosses BBB).
CVS toxicity:
- Mechanism due to direct effect on heart and vessels. Dose required is 3 times more
than required for CNS toxicity. In direct effect by ANS blockade: causing
dysarrhythmias. It acts on fast Na channel of cardiac membrane (especially when they
are open) to block them.
It also
1. Decrease automaticity
2. Decrease conduction through AV node & purkinje fibres.
3. Decrease rate of depolarization.
4. Decrease AP rise.
5. Decrease contractility by interferance with Ca+ channel leading to decrease
output.
Bupivacaine 6 times more toxic than lidocaine
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6. Both negative chronotropic and inotropic effects.
On vascular system:
- Low dose: vasoconstriction.
- High dose: vasodilatation.
- Cocaine cause: V.T and V.F.
Treatment:
1. O2 100%.
2. Fluids
3. Vasopressors: phenylephrine, methoxanine, norepinephrine.
4. Arrhythmias: by massage, defibrillation.
5. CPR: if needed
Cutaneous: rashes etc
Allergic reactions to L.A:
Respiratory: spasm etc
Tests:
1. Scratch test: not reliable.
2. Intradermal test: 0.02-0.04 ml.
Wheal reaction
4 mm or less : negative
5–8 : ++
8-12mm : +++
> 12 : ++++
If above test is negative, then perform subcutaneous challenge testing by increasing
dose 0.1- 1 ml.
- Reactions common with ester L.A. Ex: procaine.
Additive and preservative in L.A.: 3 types
1. Antioxidants: Bisulfites sulfur dioxides, Na or K sulfite, Na or K metabisulfite.
2. Buffers: Acidification to lower pH to prevent oxidation of epinephrine. Ex: Na
carbonate.
3. Bacteriostatics:
I. Methyl paraben
II. Benzethonium
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LIPID EMULSION:
Infuse 20% Lipid Emulsion (values in parenthesis are for a 70 kg patient)
Bolus 1.5 mL/kg (lean body mass) intravenously over 1 min (~100 mL)
Continuous infusion at 0.25 mL/kg/min (~18 mL/min; adjust by roller
Clamp)
Repeat bolus once or twice for persistent cardiovascular collapse
Double the infusion rate to 0.5 mL/kg per minute if blood pressure remains low
Continue infusion for at least 10 mins after attaining circulatory stability
Recommended upper limit: approximately 10 mL/kg lipid emulsion over the
first 30 mins
A note on Nerve fibers:
In the central nervous system, nerve fibers differ in terms of size, conduction velocity,
and presence or lack of myelin. For example, the olfactory nerve fibers are short and
without myelin, but the optic nerve fibers are myelinated (the olfactory and optic
nerves are considered as a parts of the CNS, while other cranial nerves are a component
of the PNS). A bundle of nerve fibers constitutes a tract in the central nervous system.
The pyramidal tract and extrapyramidal tracts have long nerve fibers that descend from
the brain to the spinal cord. These fibers have an important role in motor control, and
are known as descending tracts. There are other bundles of nerve fibers in the CNS that
are called ascending tracts.These carry sensory information from the periphery to the
different areas of the brain (such as the cerebral cortex, cerebellum, and brain stem).
Peripheral nerve fiber types

A peripheral nerve may be sensory, motor or sensory-motor (mixed). There are three types of
nerve fibers in a mixed nerve that include:
Sensory nerve fibers (afferent fibers)

Motor nerve fibers (efferent fibers)
Autonomic nerve fibers (autonomic fibers)
Components of peripheral nerve fiber

Each peripheral nerve fiber contains:
An axon (or a long dendrite of sensory fiber that also is known as an axon)
Axolemma
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Myelin sheath (if existence)
Schwann's sheath (neurolemma)
Endoneurium
Classification of peripheral nerve fibers

There are three types of peripheral nerve fibers based on their diameter:
A group
B group
C group
A group
Fibers of the A group have a large diameter and high conduction velocity, and are myelinated
fibers.
The A group consists of four types of nerve fibers:
A alpha fibers (afferent or efferent fibers)

A beta fibers (afferent or efferent fibers)
A gamma fibers (efferent fibers)
A delta fibers (afferent fibers)
B group
Nerve fibers in these group, are myelinated with a small diameter. they are the preganglionic
fibers of the autonomic nervous system. Preganglionic fibers have a low conduction velocity.
C group
The C group fibers are unmyelinated and as the B group fibers have a small diameter and low
conduction velocity. These fibers include:
Postganglionic fibers in the ANS

Nerve fibers at the dorsal roots (IV fiber). These fibers carry the following
sensory information:
o Pain
o Temperature
o Touch
o Pressure
o Itch
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Chapter 3 BLOCK OF CRANIAL NERVES
GASSERAIN GANGLION BLOCK: (Meckel’s cave)
- Used for trigeminal neuralgia (Tic douloureux)
- Anatomy: exit through foramen ovale present in the base of lateral pterygoid
plate just in front of TMJ.
Landmarks:
1. Skin over lying upper 2nd molar tooth a wheal is raised.
2. Midpoint of zygomatic arch
3. Pupil
Agents used
1. LA
2. 50% glycerol 0.3 ml
3. Themogengliolysis
4. Fogatry saloon inflation.
Technique:
1. Sitting / supine
2. Insert 3-inch 21G, needle at skin wheal of directed towards midpoint of zygoma
 for nearly 5 cm depth.
Contact with infra temporal plane obtained.
- Now withdraw and slightly elevate to reach foramen ovale.
- Inject 1cc procaine or of alcohol
- Can be done propofol anesthesia to pain.
Complications:
1. Pain
2. Dry eye due to peralysis of optithalmic division.
3. SAS injection.
4. Blockade of other C.N.
OPHTHALMIC NERVE BLOCK

Supratrochlear
Supraorbital
Infratrochlear
External nasal
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lacrimal
Main branch is supraorbital nerve
Landmarks
- Supranbital notch: 2-3 cc
- Intraorbital foramen: 1.5 cm below eye in the line of pupil.
MAXILLARY BLOCK
Indication:
To evaluate facial neuralgia.
To facilitate surgical procedures in its cutaneous distribution.
Anatomy:
The nerve exits through the foramen rotundum and passes through the pterygopalatine
fossa medial to the lateral pterygoid plate on its way to-enter the infra orbital fissure.
Techniques:
The patient is positioned supine, with the head and neck rotated to the opposite
direction. The mandibular notch is palpated by asking him to open and close his mouth.
A 22G, 8 cm needle is inserted through the notch in a slightly cephalomedial direction.
The needle will contact the lateral pterygoid plate at a depth of approximately 5 cm. The
needle is withdrawn and in a stepwise manner walked off the plate into the fossa. 3-5
ml. of the solution can be injected.
Complications:
Haematoma formation
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Due to close association of the maxillary nerve with the infra orbital fissure, the
local anaesthetic can spread into the orbit and cause temporary blindness.
MANDIBULAR BLOCK
Anatomy:
It exits from the cranium via the foramen ovale and is parallel to the posterior margin of
the lateral pterygoid plate and descends inferiorly and laterally towards the mandible.
The nerve innervates the skin overlying the lower jaw and antero superior to the ear.
The branches are
Buccal nerve
Auriculotemporal nerve
Lingual nerve
Technique:
Patient in supine, head and neck turned to the opposite direction, mandibular
notch is identified. Needle is inserted in the mid point of the notch and directed
cephalomedial to reach the lateral pterygoid plate. The needle is withdrawn and
redirected stepwise to walk off the posterior border of the lateral pterygoid plate 5 ml
of solution is injected.
Complications:
Haematoma formation
Subarachnoid spread
LINGUAL NERVE BLOCK

Indications:
1. Surgery on tongue.
2. Ca of tongue to relieve pain.
- Combined with glossopharyngeal nerve block.
Anatomy:
- Branch of mandibular nerve other branch is inferior alveolar nerve.
- It is located at the medial aspect of ascending ramus of mandible.
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Technique:
- Oral approach
- Extra oral
- Oral route: just about 2 cm behind lower 3rd molar tooth inject 5 cc L.A. into the
buccal mucosa.
- Extraoral route:
- Locate angle of mandible.
- Measure distance between angle and zygomatic arch.’
- Introduce needle upward along ascending ramus. One-half distance to arch.
Inject 5-10cc L.A.
GLOSSOPHARYNGEAL NERVE BLOCK

- Leaves skull through Jugular foramen along with X and XI CN.
- Supplies: pharynx, tonsils, soft palate, posterior 1/3 of tongue.
Technique:
a. Mark point midway between mastoid and angle of mandible.
b. Insert needle 2-4 cm depth to reach styloid process.
c. With draw and slip backward about 0.5 cm to block the N.
Indications:
1. Surgery on tongue.
2. Neuralgia
3. Awake intubation
4. Ca tongue to relieve pain.
Gag reflex: elicited by touching root of tongue and posterior wall of pharynx.
Afferent: glossopharyngeal nerve.
Indication: direct laryngoscope and awake intubation.
Inject: 2 cc 2% lidocaine at the base of anterior tonsillar pillar (palatoglossal
arch).
SUPERIOR LARYNGEAL NERVE BLOCK

Supplies sensory to supra glottic region.
Anatomy
- branch of vagus.
- It can be blocked before it enters larynx through thyrohyoid M.
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Technique:
Locate greater cornu of hyoid with index fingure. Insert needle to touch the bone
and then slip back and inject 2 ml 2% idocaine.
Indication:
1. Awake intubation.
2. Laryngectomy.
3. T.B.
4. Laryngitis
5. Ca larynx.
Complications:
1) Injury to surrounding structures.
2) Difficult in phonation, cough, deglutition.
CERVICAL PLEXUS BLOCK

- Classic technique
- Rovenstine --
- High interscalene -- at C4 vestebral level.
Anatomy:
1st cervical nerve is called suboccipital nerve, is mainly motor.
- Emerge from inter vertebral foramina, cross vertebral artery vein and fit into
concave surface of transverse processes. They are held in fibrous tunnels and lie
between muscles.
- Muscles attached to anterior tubercle are:
1. Longus colli
2. Longus capitis.
3. Scalenes anticus
- Muscle attached to posterior tubercle are:
1. Scalenes medius
2. Splenius cervices
3. Longissimus cervices.
2 , 3 and 4th nerve divide into ascending, descending branches on reaching tip of
nd rd
transverse process. These two branches are connected by series of lops lying close to
transverse processor under cover of SMM. This constitutes cervical plexus.
Superficial branches: supply back of head and neck and part of thorax and shoulders.
Deep branches: supply deep structures on the lateral and anterior regions of neck and
gives branches to phrenic nerve and hypoglossal loop.
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Indications:
1. Surgery on neck (Ex: thyroidectomy etc.).
2. For hiccough, (phrenic paralysis one side)
3. Pain relief in cancer patients.
4. Neuralgias
5. Carotid endartercectomy.
Landmark:
1. 1 cm below tip of mastoid process.
2. Transverse process of 5th C.V it is located on a horizontal plane through the
superior corner of thyroid cartilage.
3. Anterior tubercle transverse process of 6th C.V, the most prominent C.V.
(chassaignacs or carotid tubercle)
Technique:
1. Supine, head towards opposite but chin in midline.
2. Draw line between (1) and (3) landmark.
3. One fingure breadth below mostoil tip on this lime is 2nd C.V. measure 2, 3 and 4
can down from 2 and C.V. on this line to lacate 3rd 4th and 5th transverse
processes.
4. Insert needle at each point perpendicular to skin with stight anterior deviation to
contact tips of transverse processes. Infect 5 cc at each point.
5. 15 cc L.A injected subcutaneous at midpoint of posterior margin of SCM muscle
to block all superficial branches.
Rovenstine technique: Of landmarks are observed; this technique is used with
patient in supine position.
Palpate zygomatic arch and draw a vertical line from its midpoint along the neck.
Draw a horizontal line from thyroid notch to intersect first line.
Intersection locates C4 transverse process. Inject 5 cc L.A here then redirect
needle upword towards C3 give 5cc L.A and also downward at C5 – 5cm.
Inter scalene technique for cervical plexus:

If done at higher level i.e. at C3 or C4 same as that of branchial block, it can block roots of
C23 and 4.
Technique:
1. Supine, head tumed to opposite side.
2. Elevate head to make land marks prominent.
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3. Palpate posterior margin of SCM muscle at upper border of thyroid cartilage
level C4 to lie on anterior scalene muscle.
Roll back finger to palpate groove. Insert needle perpendicular to all surrounding
structure.
Direct needle medial and caudad to avoid vertebral artery, SAS, epidural space.
Elicit paresthesia and inject 30 cc L.A with distal pressure to avoid branchial
block.
PHRENIC NERVE BLOCK

Inject 5cc L.A at C4 cervical vertebrae and redirect needle towards C3 and C5 later.
INTER COSTAL NERVE BLOCK

Anatomy:
Primary rani of T1 to T11

1) Paired grey and white
Branches communicants
2) Posterior cutaneous
branch branch
3) Lateral cutaneous
4) Anterior cutaneous branch
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- They lie between internal and external intercostals M.
- Paraverterial block: if blocked at the origin.
- Intercostals block if blocked beyond the angle of rib.
Technique:
Posterior approach: done at midaxillary about 8-10 cms from midline prior to lateral
cutaneous branch is given off.
Bilateral block is called Bartlett’s block.
Indications:
Surgical Nonsurgical
Breast surgery Pain relief from fracture rib.
Lithotripsy Pleuritic pain
Pacemaker insertion Pain from flail chest
Umbilical/incisional hernia repair Thorocostomy / gastrostomy tube (ICD)
Intra abdominal along with Celiac block Hespes zoster pain
Intra thoracic along with stellate block Differential diagnosis
Post operative relief 
Ex: T10 11 12 appendicectomy.
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Complications:
1. Hypotension
2. Epidural / spinal
3. Pneuemothorax
4. Toxic effects
Catheter can be placed for continuous block.
Technique:
- Lateral or semi prone.
- 18G Touhy needle with leur lock syringe used.
Interpleural block:
- 8-10 cms from spinous process.
Pleural space: 20-30 ml 0.25% bupivacaine with

epinephrins
- Detected by loss of resistance to air technique.

- Avoid during Ippv, since it can mislead U and cause tension pneumothorax.
- Maintain position for 20-30 minutes to settle the drug.
- Analgesia for 5-8 hrs, hence repeat every 8 hrs.
-
Surgical
Same as intercostals block
Indications
Nonsurgical
Ex: Renal surgery

- Thoraco abdominal (along with celiac block)
- ICD
- Fracture rib etc.
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Cathetor inserted for about 5-8 cms.
Complications:
1. Toxic reaction
2. Pneumothorax (2%)
3. Lung injury
4. Phrenic nerve palsy
5. Horner’s syndrome
6. Bronchospasm
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Chapter 4 BLOCKS OF UPPER EXTREMITY
BRACHIAL PLEXUS BLOCK

Relevant anatomy:
The brachial plexus provides both motor and sensory nerve supply to the upper
extremity. It is formed by the fusion of the anterior rami (ventral rami) of C5, C6, C7, C8
and T1, in addition toasmaller contribution from C4 and T2. The plexus stretches from
the lateral aspect of the cervical vertebral column downwards and laterally between the
scalenus anterior and the scalenus, medius muscles along with the subclavian artery. It
then passes above the first rib behind the mid point of the clavicle to reach the axillary
fossa.
Sites at which the plexus can be blocked:

The brachial plexus can be blocked by injection of the local anaesthetic solution into the
fascial compartment surrounding the brachial plexus at several levels like: -1
lnterscalene 2. Supraclavicular 3 Infraclavicular 4.Axillary
The sensory and motor blocks are significantly different among these various levels of
brachial plexus blocks.
INTERSCALENE BLOCK.
Indications:
Shoulder joint surgeries, reduction of shoulder dislocation
Surgery on the clavicle
Surgery on the humerus
Contraindications:
Severe lung disease with decrease in vital capacity
Coagulopathies
Infection at the site of injection
Uncooperative patients
Technique:
Patient position:
Supine, head turned to the opposite side, arm by the side of the patient, sniffing or lifting
the head by the patient to identify the interscalene groove.
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Anatomical Landmarks:
Cricoid cartilage
Level of C6
Lateral border of sternomastoid
Interscalene groove
Needle:
25 G insulated needle if nerve locator is used or a 22 G 1 ½ inch needle.
Puncture site:
In the interscalene groove at the level of cricoid.
Direction of needle:
Medial, caudal (at an angle of 30 degree to the sagittal plane) and slightly dorsal,
directed to the transverse process of C6.
End point:
Eliciting twitches (at a current of 0.4mA or less) or paraesthesia or click.
Drug:
20-30 ml of (mixture of 1 – 1.5% lignocaine with adrenaline 1 in 2 lakhs with
0.5% bupivacaine. Soda bicarbonate can be added to the solution to hasten the onset of
block.
Complications:
Phrenic nerve injury (30% decrease in vital capacity)
Recurrent laryngeal nerve damage
Horner’s syndrome
Inadvertent extradural/spinal injection
Inadvertent vertebral artery injection (Avoid bilateral blocks)
Local anaesthetic toxicity
Haematoma, Ecchymosis
Total spinal
Missed nerves:
The ulnar nerve may be missed
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SUPRACLAVICULAR BLOCK
Mainly two types, classical Kulenkampeff and plumbob approach.
Indication:
Operations of the upper arm lower arm and hand.
Contraindications:
Haemorrhagic diathesis
Contralateral phrenic nerve paralysis
Contralateral recurrent laryngeal nerve paralysis
Contralateral pneumothorax
Children (relative contraindication)
Narrow-chested patients
Bilateral supraclavicular brachial plexus block
Technique:
Patient position:
Supine with the head turned to the opposite side, arm as down as possible, that is hand
touching the knee.
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Landmarks:
Midpoint of the clavicle
Subclavian pulsation
External jugular vein
Needle:
25 G insulated needle or a 22G, 2 inch needle.
Puncture site:
Immediately dorsolateral from the palpated pulsation of the subclavian artery 5H cm
posterior to the midpoint of the clavicle.
Direction of needle:
Caudal direction and slightly lateral, parellel to the scalene muscles to contact the first
rib.
Endpoint:
Eliciting twitches or paraesthesia or click
Drug:
8-10 ml of local anaesthetic per division
Complications:
Phrenic nerve damage
Recurrent laryngeal nerve damage
Homer's syndrome
Subclavian artery puncture
Pneumothorax
Missed nerve:
Median nerve may be missed.
Practical Tips:
Coughing by the patient while paraesthesia is being sought may indicate pleural
puncture, and the procedure must be discontinued. A chest X-ray will reveal any
possible pneumothorax. The patient should be observed for24 hours.
Puncture of the subclavian artery indicates that the needle has been inserted too far
medially. The plexus should be sought more laterally.
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SUBCLAVIAN PERIVASCULAR BLOCK
Technique:
Landmarks:
Interscalene groove, caudal to the cricoid cartilage, subclavian pulsation.
Site of needle insertion:

Interscalene groove just behind the subclavian pulsation.
Direction of needle insertion:

Only caudally {unlike supraclavicular block)
End point:
Paraesthesia in the arm or hand (not in the shoulder).
Complications:
Similar to supraclavicular block. The incidence of pneumothorax is less and the risk of
subclavian artery puncture is more as compared to supraclavicular block.
AXILLARY BLOCK
Major nerves are blocked at thejevel of the third part of the axillary artery.
Subclavian artery, at the lateral border of the 1st rib continues as the axillary artery .
Pectoralis minor divides the axillary artery into 3 parts at the lateral border of the
muscle.The median nerve lies anterosuperior to the artery, the ulnar nerve lies
anteroinferiror and the radial nerve lies posterior . The musculocutaneous nerve has
already left the sheath and lies in the substance of the coracobrachialis.
Technique:
Position the patient supine with the arm at right angle to the body and the elbow flexed
at 90 degrees, The dorsum of the hand rests on a pillow to prevent forward
displacement of the humerus. The artery is palpated as proximally in the axilla as
possible.
Transarterial technique:
A 22/25G needle is introduced till bright red blood is aspirated and is then advanced
posterior to the artery. Drug is injected posterior to the artery or half the solution is
injected posterior and half anterior, the total volume being 40 ml.
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Elicitation of paraesthesia: This can be done by inserting the needle near the location
of the nerve and 10 ml is injected at each nerve.
Perivascular injection:
A needle is advanced superior to the artery, till a fascial click is felt. The proximity of the
artery within the sheath can be observed by seeing the transmitted pulsation. 30-40 ml
of solution is injected after negative aspiration. Alternatively, 15-20 ml solution can be
injected above and below the artery, after placing the needle in the sheath.
Disadvantage:
Musculocutaneous nerve is missed, which can be blocked by injecting 5 ml of local
anaesthetic into the substance of the coracobrachialis.
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WRIST BLOCK
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Median nerve:
It lies deep between the flexor carp iradialis and the palmaris longus tendon,
which is identified by asking the patient to flex his wrist after making a fist. A small
gauge needle is inserted between the tendons at a point 2-3 cm proximal to the wrist
crease; loss resistance will be felt as the needle passes through the retinaculum. 2-4 ml
of solution injected.
Ulnar nerve:
It lies immediately lateral to the tendon of flexor carpi ulnaris and medial to the ulnar
artery. The tendon and artery are palpated immediately proximal to the styloid. A small
gauge, needle is inserted perpendicular to the wrist at this point and 3-5 ml of solution
is injected after elicting paraesthesia or in a fan like manner.
Radial Nerve:
Field block is perrforrned at the subcutaneous level in and around the anatomical snuff
box. The extensor pollicis longus tendon is identified and the needle is inserted above
the tendon at the base of the first metacarpal. 2-3 ml is injected proximally along the
tendon, which crosses the anatomical snuff box.
AUTONOMIC BLOCKADE
Sympathetic outflow – thoraco lumbar
Parasympathetic outflow - cranio-sacral.
Sympathetic preganglionic fibers exit spinal cord from T1 to L2 level.
Neuraxial block does not block vagal nerve.
Neuraxial block primarily results in varying degrees of sympathetic block and
physiological responses, resulting from sympathetic tone and / or unopposed
parasympathetic toe.
CVS manifestations:
Neuraxial blocks typically produce variable in BP that may be accompanied by
a in the HR and cardiac contractility.
o Vasomotor tone is primarily determined by sympathetic fibers arising
from T5 to L1, innervating arterial venous smooth muscle.
Blocking these nerves causes
Vasodilatation of venous capacitance vessel.
Pooling of blood.
venous return to heart
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Arterial vasodilatation may SVR  the effects of which may be minimized by
compensatory vasoconstriction above the level of block.
A high spinal block

Prevents compensatory vaso constriction.
Blocks sympathetic cardiac accelerator fibers that arise at T1- T4.
Profound hypotension may result form
Vasodilation
Bradycardia
contractility.
Treatment:
Preloading 10-20 ml/kg of IV fluids.
Excessive / symptomatic bradycardia should be treated with Atropine.
Hypotension with vasopressors. Direct α adregnergic agonist (phenylephrine
venous tone, arteriolar constriction. Ephedrine (direct adrenergic effects) HR
and contractility indirect effects – vasoconstriction.
SYMPATHETIC BLOCKS
General description.
Benefits of sympathetic blockade

a. To produce pain relief.
b. To improve blood flow in vasospastic disorders
c. To improve drainage of local edema.
Indications for sympathetic blockade:

Obliterative arterial disease.
Renal colic
Acute pancreatitis
Pancreatic cancer pain
Cardiac pain
Pagets disease of bone
Reflex sympathetic dystrophy
Phantom limb pain
Central pain
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Raynand’s disease
Accidental intra arterial injection of thiopeatone
Early frostbite
Testing the completeness of sympathetic blockade.
Sympathetic function:
Skin conductance response (SCR)
Or
Sympathogalvanic response (SGR)
Skin potential response
Sweat test
a. Ninhydrin
b. Cobalt blue
c. Starch iodine
Skin plethysmography and ice response
Blood flow
Plethysmography (Muscle and skin)
Xenon – 133 clearance
Sodium – 24 clearance
Doppler technique
Electromagnetic flow meter
Laser Doppler flowmetry
Pulse wave
Temperature
Distal perfusion pressure
Capillary O2 tension
Metabolism.
Pain: Pain score, analgesic requirements, activity.
Contraindications of sympathetic block:

I. Patient on heparin.
II. Bilateral blocks avoided.
III. Bilateral injection in the lumbar region for permanent blockade cause loss of
ejaculation.
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Agents used for sympathetic blockade:
For short term: local anaesthetics used. For permanent block (chemical
sympathectomy).
a. 6 – 7% phenol in water.
b. 7 – 10% phenol in water soluble constrast medium.
Ex: Angiographin, omnipaque.
c. 50 – 100% alcohol.
d. Aluminium salt
e. Sulpate.
f. Glycerol 50%
CELIAC PLEXUS BLOCK

Anatomy:
Celiac plexus lies anterior to aorta at the level of 1st lumbar vertebra.Nerve
fibers reach the plexus from:
1. Preganglionic sympathetic fibres from splanchnic nerves.
2. Pre ganglionic parasympathetic from vagus.
3. Some sensory fibres from phrenic and vagus.
4. Afferent fibres concerned with nociception.
There are 3 pairs of splanchnic nerves which descend to the celiacplexus. They are 1)
Greater splanchnic nerves arises from T5-T9 (sometime T4 and T10 also) spinal
segments. 2) Lesser splanchnic nerves arises from T10 and T11 spinal segments and 3)
Least splanchnic nerve arises from T12 spinal segment. These nerve fibre synapse in the
ganglia of celiac plexus. There are 3 pairs of ganglia exist within the plexus. They are:
1. Celiac ganglia
2. Superior mesenteric ganglia
3. Aortico-renal ganglia
The Nociceptive afferent fibres travel from viscera along the sympathetic fibres, through
the ganglia, splanchnic nerve, sympathetic chain, white rami communicants and then
synapse in the dorsal root ganglia. The proximal axon of these cell bodies synapse in the
dorsal horn of spinal cord.
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Physiology of celiac plexus block:
Blockade of afferent nociceptive fibres:
Any pain originating from visceral structures innervated by celiac plexus can be
effectively alleviated by this blockade. This include pancreas, liver, Gall bladder,
omentum, mesentry, alimentary tract (from the stomach to transverse colon).
Blockade of sympathetic fibres to GIT:
The complete sympathetic denervation of GIT allows unopposed
parasympathetic activity and increased peristalsis, increase in gastric motility and
relaxed spincters lead to increased gastric emptying. Diarrhea may develop. Nausea and
vomiting seen in GIT malignancy may be abolished after celiac plexus block.
Blockade of sympathetic fibres to splanchnic vessels:
Secondary to vasodilatation of large splanchnic bed, hypotension may develop
after well placed celiac plexus block.
Drugs used for celiac plexus blockade:

1)Local anaesthetic alone
- 0.5% sensorcaine with 1: 200,000 dilution of adrenalin.
- 15ml on each side (Total 30 ml).
- Used in non malignant conditions.
2) Local anaesthetic + steroid
- Commonly used steroid is Beta methazone
- In chronic abdominal pain following multiple surgeries it will give good results.
3) Neurolytic blockade:
- Most commonly used compounds are alcohol or phenol.
Alcohol:
- 50-100% used.
- Disadvantage – immediate severe pain.
- This can be abolished by using 0.5% bupivacaine and absolute alcohol at a ratio
of 1: 1 (Total amount of 50 ml) to be used 25 ml on each side).
Phenol: used as 6% aquous solution or 12% phenol prepared in renografin.
Indications:
1. Pain relief in upper abdominal malignancies originating from stomach, pancreas,
gall bladder and liver. Neurolytic block is indicated.
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2. Pain after multiple abdominal surgeries.
3. Local anaesthetic and steroid is usually indicated.
4. For evaluation of upper abdominal pain local anaesthetic alone is indicated.
5. Non-malignant pain of upper abdomen eg. chronic pancreatitis.
Here also neurolytic block is indicated. But its long term effect is variable. Regeneration
of new pathways result in development of different pain syndromes in these patients
after 6-12 months.
Technique:
1) Preparation:
- Informed consent to be obtained.
- I/V cannula to be introduced and start an I/V infusion.
- Resuscitative equipments and drugs must be readily available.
2) Position:
Prone position with a pillow under the lower abdomen to remove lumbar lordosis.
Block can be performed in lateral position also, but needle placement is difficult.
3) Premedication:
I/V premedication for patients who are anxious and patients with severe pain.
Avoid premedication if the block is performed for diagnostic purposes.
Procedure:
Sterility has vital importance.
Land marks to be marked are:
a. Spinous process of T12 and 11 vertebrae.
b. Inferior border of 12th rib
c. Site of needle entery is 7-8 cms lateral to the spinus processes in the inferior
border of 12th rib.
Needle used: 12-18 cm long 20-22 G needle with an attached skin marker.
Infiltrate the skin and muscle with local anaesthetic solution.
Introduce the needle at the point of needle entry and advance. The direction is
towards the L1 spine and proceeds to hit on the 11 vertebral body. After the vertebral
body has reached, a skin marker is placed on the needle, 2-3 cm from the skin.
The needle is then withdrawn to the subcutaneous plane and make minor
adjustments and reintroduce laterally until it just slip from the lateral surface of the
vertebral body. After the lateral aspect of vertebral body has passed a “POP” is often felt
when the needle passes through the psoas fascia. At this point needle approaches the
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great vessels and should advance slowly. The needle should pass 2-3 cm beyond the
lateral part of vertebral body.
After proper placement of the needle a careful aspiration is performed. If blood is
encountered, the needle is slowly withdrawn until negative aspiration is achieved.
Alternatively, on the aortic side the needle can be advanced through the aorta until no
blood is returned, and injection is made at this location.
Same procedure can be repeated on the other side also. After proper needle
placement, 2-3 ml of local anaesthetic containing epinephrine is injected for further test
of either I/V or intrathecal placement. If this is negative full dose of local anaesthetic or
neurolytic drug can be injected.
Image intensification techniques like radiography, fluoroscopy and CT scan
increase the accuracy of celiac plexus block.
Catheter placement can be done in non malignant conditions and can give local
anaesthetic infusion for prolonged blockade.
Single needle approach using left side needle and injecting the drug posterior
and anterior to aorta is also described.
Complications:
1. Due to blockade of sympathetic fibers.
2. Hypotension: Can be avoided or minimized by giving I/V infusion of 500-1000
ml of R.L before the block. Orthostatic hypotension may persist after a neurolytic
block. But in most cases, it is self limiting with in a week.
Complications due to the technique

Backache
IVC damage
Injury to blood vessels  retroperitoneal haematoma
Injury to spinal nerves
Injury to kidney
- Renal haemorrhage.
- Nephro cutaneous fistula
Complications due to local anaesthetic/neurolytic agent
a. I/V injection can lead to toxicity.
b. Intrathecal injection can produce total spinal block.
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CELIAE PLEXUS:
LUMBAR SYMPATHETIC BLOCKS
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Anatomy –
Gangilion lie on anterolateral surface of the body of lumber vertebra.
Inject at L2 or L3 level.
Injection 25 ml 0.25% bupivacaine.
22G, 15cms needle used.
Technique.
Mandl or two needle.
Single injection technique
Bryce smith technique
Neurolytic agents should be given under x-ray control using radiopaque
constrast medium
- Angiographin
- Omnipaque
THORACIC SYMPATHETIC BLOCKS: T4-T9

Technique:
In thoracic region somatic block

Locate spine in midline
Measure 5cm lateral from midline
Insert 10cm needle perpendicular to skin to hit rib.
Withdraw and incline 450 so that needle is advanced medially, farward and upward.
Needle will be at intervertebral foramina, inject 5 – 8 cc.
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Indications:
Arteriosclerotic disease: Ex: Gangrene pain. Claudication, diabetic gangrene,
buerger’s disease.
After reconstructive vascular surgery.
Arterial embolus
Renal colic
Complex regional pain syndrome (CRPS)
Herpes zoster
Phantom limb
Urogential pain
Hyperhidrosis
Trench foot, acrocyanosis
STELLATE GANGLION OR CERVICO THORACIC SYMPATHETIC

BLOCK
Anatomy:
Fusion lowest 3 cervical C6,7,8 T1 ganglion + 1st thoracic ganglion.
1-3 cm long.
Differs in same person on 2 sides
Leriche and pontaine – 1934 – for CVA.
Usually cervical – stellate – T2, T3, T4 are also block interruption of sympth fibers
of head and neck, arm and thorax.
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Landmark:
C7, 1st rib, T1 transever process.
Behind subclavian artery and origin of vertebral artery.
Posterior to carotid sheath.
Anterior to C8, T1 nerves.
Right side – anterior relation – apex of lung and dome of pleura
Left side these are 2.5cm lower.
Technique
Anterolateral:
- Locate midpoint of clavicle, raise skin wheal 1 cm above.
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- Palpate transverse process of C6 (anterior tubercle or chassaighads tubercle or
carotid tubercle)
- Insert needle here and direct it medially, backward and downward to contact 1st
rib neck or C7, transverse vertebra.
- Now redirect more medially to contact body of C7 vertebrae and inject 10ml.
Anterior approach:
- Locate a point 2cm above medial end of clavicle.
- At cricoid level is upper border of C6 vertebrae and palpate chassaignois tubercle
just lateral here.
- 2 cm below is C7 vertebrae.
- Palpate trachea and carotid vessels here.
- Insert needle lateral to trachea until it impinges on body of C7 vertebrae about 2-
3 cm deep. Inject 10cc.
Supplies:
- Gray rami to C7, C8
- Inferior cervical / cardiac nerves
- May communicate with vagus.
Indications:
a) Vascular Pain relief
Accidental injection of thiopentone in artery 1) Phanthom limb pain
Raynauds disease 2) Herpes zoster
Vascular anastomosis 3) Causalgia
Thromboembolism 4) Paget’s disease
Occulusive vascular disease 5) Neoeplasms
6) Pain due to CNS lesion
MI
Amblyopia due to rentinal vessel occlusion
Menieres disease
Signs of stellate block: (Horner-Bernasds sign/syndrome)

A) Principal signs: Miosis, Enophthalmus (Bernards sign), Ptosis (Horner’s law),
Narrowing of palpebral fissure.
B) Supplementary signs:
1) Conjuctival injection
2) Congested nostril
3) Flushed face
4) Anhidrosis
5) Improved blood flow to arm: warmth
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Chapter 5 FIELD BLOCKS
FIELD BLOCK FOR TONSILLECTOMY
Nerve:
Lesser palatine
Lingual nerve Plexus called circulus tonsillaris
Glossopharyngeal
Pharyngeal plexus
Technique:
- Amethocaine lozenges 60mg. ½ hr before
- Mouth and pharynx sprayed with 4% xylocaine (cough reflex abolished) some
prefer active cough reflex.
- 3 to 5 ml xylocaine with adrenaline 1.5%
1. Upper part of posterior pillar Both pillar made edematous
2. Upper part of anterior pillar
whole extent
3. le fold of lower pole.
4. Supra tonsillar fossa after drawing tonsil medial
Position: Sitting and well supported in chair.
Disadvantages: Depression of tongue cause discomfort.
- Fainting
Paratracheal approach:
o 2 finger breath lateral to supra sternal notch.
o 2 finger breath above clavicle.
- This is at medial border of sternocliedomastoid at level of C7 transverse process.
- Position checked by palpating cricoid cartilage and chassaaignac tuberale (C6 –
Tr)
- 22G needle 5-8 cm length  push sternocledomastoid carotid art downward and
backward.
- Advance needle directly backwards.
- Make contact with bone C7 transverse process – needle withdrawn 0.5 to 1cm.
- Aspiration for blood and CSF.
- 15 to 20 ml of 0.5% lignocaine injected.
- Block ganglia and Rami for C2 to T4
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- 30 min later Horner’s syndrome (Miosis, Enopthdmos and Ptosis) and
vasodilation of arm.
Other approach:
Anterior approach
Lateral approach
Posterior approach
Tissue displacement approach
Complications:
- Pleural shock
- Perforation of esophagus
- Intrathecal injection – Total spinal
- Intravascular injection
- Pneumothorax
- Cardiac arrest
- Hoarsness of vice RLN block
- Pnernic nerve block
- Branchial plexus block.
- Mediastinitis
Signs of successful block

- Horners syndrome.
- Flushing of cheek face neck arm and increased skin temp.
- Flushing of conjunctiva and sclera.
- Anhidrosis of face and neck.
- Lacrimation.
- Stiffness of nostril.
- Mueller’s syndrome - injection of tympanic membrane and warmth of face.
HERNIA BLOCK
Indications:
1. Inguinal or genital operations – inguinal herniorrhaphy, orchipexy.
2. Post operative pain relief.
Anatomy:
The inguinal region is supplied by
a. Iliohypogastric nerve
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b. Ilio inguinal nerve
c. Gentiofemoral nerve
a) Iliohypogastric nerve: L1–T12 – emerge posteriorly to the psoas major muscle, lie
on the anterior surface of quadratus lumborum – do not enter the pelvis-penetrates
the transersus abdominis at the level of iliac crest then lies beneath internal oblique
– penetrates aponeurosis.
- Splits in 2 branches before becoming cutaneous
- Lateral branch  sensory to lateral part of buttock and Hip.
- Anterior branch  becomes superficial just medial to anterior superior iliac
spine.
- Innervates the lower abdomen.
b) Ilioinguinal nerve: Follows same course – exits peritoneum to enter inguinal canal
 sensation to scrotum, penis and medial thigh in male or equivalent area of Labia
and mons pubis in female.
c) Genitofemoral nerve: L1 – L2: Femoral branch travels with the femoral artery 
cutaneous sensation just below inguinal ligament.
Genital branch travels in inguinal canal  scrotum (men) labium majus (women)
Land marks:
a. Pubic tubercle
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Anterior superior Iliac spine.
Technique:
1. Raise skin wheal 2-3 cm medial to the upper aspect of anterior superior iliac
spine.
2. (22 G / 3.5 inch spinal needle) insert needle perpendicular to the skin through
wheal to bone and inject 5 ml LA sol.
3. Redirect the needle along the incision but downward and medially and inject 15
ml of LA solution.
4. Palpate public tubercle and raise skin wheal 2 cm lateral to this point.
5. Insert needle perpendicular to skin until bone is hit inject 5 ml of LA solution.
6. Redirect the needle laterally and superirorly along the line of incision for 2
inches and inject 15 ml of LA sol.
LA agent – 1.2% of lignocaine (Maxdose 5 mg/kg)
0.25-0.5% of Bupivacaine (max dose 3 mg/kg)
Complications:
1. Pain when cord is pulled – prevented by infiltrating the superior portion of the
cord.
2. Patient discomfort
3. Persistant paresthesia from intraneural injection.
Contraindications:
(1) Patient refusal

(2) Uncooperative patient
(3) Mentally unstable patients
(4) Obesity
(5) Anxiety
(6) Irreduable hernia
(7) Coagulopathy.
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Chapter 6 - PERINEAL ANAESTHESIA
Pudendal nerve
Should block 3 nerves Posterior femoral cutaneous never
Ilio inguinal nerve

Pudendal nerve  S2 3 4 anterior primry divisions.
It passes through  greater sciatic foramen  lesser sciatic foramen  ischial
spine  enters perineum.
It is blocked just medial and posterior to ischial tuberosity.
Indication:
Delivery (labour pain, episiotomy pain)
Surgery on perineum.
Forceps delivery
PUDENDAL NERVE BLOCK
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Drugs:
Lidocaine 1%
Mepivacaine
Chlorprocaine 1%
Anatomy: formed by anterior divisions of S2 3 4
Indications:
Rectal and perineal surgery.
Vaginal delivery with episiotomy and outlet forceps
Differential diagnosis of pain.
Relief of pain form Ca cervix.
Hemorrpidectomy
Anal dialatation.
Trans perineal
Technique
Trans vaginal
Transperineal: by Muller in Germeny in 1908.

Lithotomy position, palpate posterior medial margin of tubersity of ischium. Fusest 8cm
needle medially and posteriorly to ischium for about 1 inch, inject 5cc L.A., then advance
it linch into ischio-rectal fossa & inject 10cc L.A. Bilateral block is necessary.
Transvaginal: by wilds in 1954.
Ischial spine located by index finger vaginally. Sacrospinous ligament palpated
(attached to spine) needle inserted at these point lateral to finger to avoid fetal parts.
Contact spine and go medial and posterior to it and inject 2-3 cc L.A.
Later advance it further through ligament and inject 8cc L.A. Rt finger to block Rt
pudendal and viceversa.
Complications:
1) Rectum punctures.
2) Hematoma of thigh
3) Intra vascular injection
4) Fetal damage
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Paracervical N block:
Indication: 1) labor analgesia.
2) Delivery
3) Surgery over perineum.
Technique: 15cc into lateral fornix of vagina.
Complications: 1) Fetal bradycardia and acidosis.
2) Toxic reactions and maternal death hence monitor fetal H.R, scalpvein analysis etc.
PENILE BLOCK
Dorsal nerve of penis, branch of pudendal nerve.
Indication – circumcision in childrens.
Technique – sedate with halathone / ketamine / midzolam etc. palpate arch of pubic
symphysis, inject 2-3 ml L.A after hitting symphysis and slipping below it.
- 0.25% bupivacaine 3ml for 1-5 yrs.
- 0.25% bupivacaine 4ml for 6-7 yrs.
1. Ring block where L.A injected superficial to fascia of penile shaft at base.
2. 1-2cc injected deep to Buck’s fascia on either side of dorsal midline at base of
penis. Superficial infiltration done to block branches from genitofermoral nerve
and ilioinguinal nerve which supply skin over base of penis.
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Chapter 7 - NERVE BLOCKS OF THE LOWER
EXTREMITY
Advantages of Nerve blockade of the Extremity:
1. Avoids sympathectomy associated with spinal and epidural blockade.
2. Can be given even in patients with conditions that contraindicate general
anaesthesia, since it avoids pulmonary complications.
3. Provides prolonged postoperative pain relief. In this way, it helps timely
discharge.
4. Not contraindicated in patients taking anticoagulants or those with lumbosacal
disease.
Disadvantages:
The lower extremity blocks are not popular since the nerves are not anatomically
clustered. Therefore they are:
a. Technically more difficult
b. Require more training and expertise.
c. Further, in the case of a persistent block the patient cannot ambulate, so, it
cannot be used in outpatient surgery.
Lower extremity is supplied by the lumbar and sacral plexus.
Guiding principles for plexus blocks:
Local anaesthetic drugs:

Local anaesthetic drugs (LA) that are commonly used for plexus blocks include those
shown in table below
Local anaesthetic drugs and dosages

Drug Duration-hours Concentration % Dose mg.kg-1
Bupivacaine 8 – 12 0.25 - 0.4 2–3
Ropivacaine 8 – 10 0.25 - 0.5 2–5
Lignocaine 4–7 0.5 - 1.0 7
It is inappropriate to use high concentrations of local anaesthetic drugs for peripheral

nerve blocks. The mixing of two local anaesthetic drugs is rarely necessary. Any single
long-acting LA will have a rapid enough onset time. Mixing various concentrations and
types of local anaesthetic drugs usually results in a waste of time, the potential of
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diminished effective concentration of the LA and no significant reduction in onset time.
Additives like sodium bicarbonate may affect neurotoxicity.
Vasoconstrictors:
Adrenaline is the primary drug used. For most nerve blocks, a dilution of 1: 200,000
adrenaline is appropriate although solutions as dilute as 1: 400,000 have been used.
Mixing the adrenaline solution fresh at the time of a nerve block results in a higher pH of
the local anaesthetic solutions. The addition of adrenaline may also affect neurotoxicity.
Equipment:
In general, nondisposable needles provide the best equipment for performance of
regional anaesthesia. However, sterility of these needs to be maintained.
Paraesthesia:
Paraesthesia occurs with all techniques including those using a nerve stimulator use.
Paraesthesia elicited when performing a nerve block serves two purposes; i) it indicates
that the point of needle is in contact with the nerve to be blocked, ii) it serves as a
warning indicating a risk for nerve injury unless the trauma to the nerve is avoided.
Repeated or exaggerated paraesthesia would possibly be undesirable.
Catheter technique:
It is anatomically impossible in most instances to produce surgical anaesthesia in plexus
blocks with catheter techniques. But good postoperative analgesia and continuous
sympathetic nerve block is achievable. The placement of peripheral nerve catheters may
be the next new wave in regional anaesthesia.
Nerve stimulators:
Many authors propose that using a nerve stimulator guarantees correct needle
placement for plexus blocks. However, there are some drawbacks. Fascial layers may
allow passage of electric current but may be impermeable to injection of local
anaesthetics. An “appropriate” muscle response may occur T even when the stimulator
needle is intravascular or intraneural .Slight movement of the patient or the
anaesthesiolgist’s hand may lead to off-target injections.
Nerve Supply Of Lower Extremity:

The lower limb is supplied by anterior rami of 5 lumbar nerves and the first 2 or 3
sacral nerves. These form the lumbar and sacral plexus. The lumbar plexus is formed by
lumbarroots L1 – L4, with a contribution from T12 50% of the time. The upper part of the
lumbar plexus primarily provides innervation to the anterior abdominal wall. Five
major nerves and their branches supply the lower extremity.
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The iliohypogastric nerve (L1) provides innervation to the skin of the buttock and the
abdominal muscles. The ilioinguinal nerve (L1) provides cutaneous innervation to the
perineum and the adjoining portion of the medial thigh. The genitofemoral nerve (L 1,
L2) supplies a portion of the genital area and lumboinguinal branch that supplies the
skin over the femoral triangle.
Nerves arising from lumbar plexus are:

1. Lateral femoral cutaneous nerve (L2, L3)
2. Femoral nerve (posterior rami of L2-L4)
3. Obturator nerve (anterior rami of L2-L4)
Nerves arising from (Lumbosacral plexus) include:

1. Posterior cutaneous nerve of the thigh (S1-S3)
2. Sciatic nerve (L4-L3)
PSOAS COMPARTMENT BLOCK

Anatomy:
The psoas compartment block utilises a technique in which a needle is placed between
the psoas major and quadratus lumborum muscles. It blocks the lumbar plexus at the
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level of L4-L3 and anaesthetises the hip and anteromedial thigh. Cadaveric dissections
have revealed that the lumbar plexus is within the substance of psoas muscle at the
level of L5.
Indications:
Used in combination with other nerve blocks for surgery of the thigh
Used for neuralgia of the thigh and fascia lata pain syndrome.
Postoperative pain relief
Technique:
With the patient lying in the lateral position and the operative side up, hips and knees
are maximally flexed. A line is drawn joining the upper border of the iliac crests
(intercristal line). A mark is made where the intercristal line crosses the spine or the
spinous interspace of L4. From this, a mark is made 3 cm caudad and 4 cm lateral. After
skin preparation, a wheal is raised and a 22G spinal needle is advanced perpendicular to
the skin entry site until it contacts the L5 transverse process. The needle is then
redirected cephalad until it slides off the transverse process. At this point, a needle with
a 20 ml syringe attached is slowly advanced until loss of resistance to injection of air is
detected. The depth of the psoas compartment is about 12 cm. 30 ml of local
anaestheticsblution can be injected. A nerve stimulator may be used to verify correct
needle placement.
While using a nerve stimulator, optimal needle position is confirmed by contraction of
the quadriceps muscle. If contraction of hamstring muscle is elicited, the needle is
directed too far medially. If local anaesthetic is injected at this location the risk of
epidural spread is real and should therefore be avoided.
Complications:
1. Epidural/subarachnoid/intravascular injection
2. Peripheral nerve damage
3. Development of sympathetic block secondary to extravasation of the local
anaesthetic.
Choice of local anaesthetic, dosage and volume:

Volumes of less than 20 ml have been associated with increased failure rates and
volumes greater than 40 ml may introduce the risk of local anaesthetic toxicity and
central neuraxial spread. The current recommended volume is 30 ml. For the
continuous technique, ropivacaine 0.2% with basal infusion rates of 6-10 ml h'1 are
used.
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FEMORAL NERVE BLOCK
Anatomy:
Figure 2: Femoral nerve and its branches

The femoralnerve is the largest branch of the lumbar plexus. It arises from the dorsal
branches of the anterior primary divisions of L2, L3, L4 and descends through the psoas
major to emerge at the lower part of its lateral border. It passes along the pelvic wall on
the iliacus muscle to reach the superior pubic ramus and crosses over this befieatb-
tricinfuinal ligament. On parsing into the thigh, it lies lateral to the femoral artery and
divides into anterior and posterior divisions (Figure 2). In tjjethigh, cutaneous branches
, arise that innervate the skin of medial and anterior parts as far as the knee.
Indications:
When combined with the lateral femoral cutaneous nerve block, the femoral nerve block
provides anaesthesia for many orthopaedic and plastic surgical procedures on the
anterior and lateral parts of the thigh and femur. When combined with a sciatic nerve
block, this block provides anaesthesia / analgesia for surgeries on the lower limb.
Landmarks and technique:

With the patient lying supine, the following landmarks are identified; anterior superior
iliac spine, public tubercle, inguinal ligament and femoral artery pulsations. The
inguinal ligament is located between the anterior superior iliac spine and the pubic
tubercle. The femoral artery is palpated and marked below the inguinal ligament. The
needle insertion is 1 cm caudad to the inguinal ligament and 1 cm lateral to the femoral
artery. The contraction of quadriceps muscle is sought with the nerve stimulator 20 to
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30 ml of local anaesthetic solution is injected. Evidence of successful block is achieved
when the patient is unable perform knee extension.
Complications:
The femoral nerve block is notable because it is simple to perform and has a very low
incidence of complications such as peripheral nerve injury, haematoma, infection and
local anaesthetic toxicity.
OBTURATOR NERVE BLOCK

Anatomy:
The obturator nerve is derived from the lumbar plexus and arises from the ventral
divisions of L2, L3 and L4. The chief contribution is from L3. It descends through the
psoas major muscle over the brim of pelvis into the lesser pelvis where it runs along the
lateral wall to the upper part of the obturator foramen. As the nerve enters the thigh, it
divides into two branches, anterior and posterior. The anterior branch supplies the
adductor longus, adductor and gracilis and sends a main branch to the hip joint. The
posterior branch supplies the obturator externus, adductor magnus and adductor brevis
and sends a branch to the knee joint.
Indications:
Useful as a diagnostic, prognostic or therapeutic procedure in patients with
adductor spasm.
For surgeries at the level of or proximal to the knee.
Technique:
The patient is placed supine, the pubic tubercle e is identified and a skin mark is made 2
cm lateral and 2 cm caudad from this point. A skin wheal is raised at this point and a 22
G, 3-inch needle is inserted perpendicular to the skin. It is advanced until contact is
made with the bone at an approximate depth of 1 to 2 inches. This is usually the inferior
or the horizontal ramus of the pubic bone. The needle is withdrawn and redirected
laterally so that the needle slides off the pubis into the lateral portion of the obturator
foramen. If a nerve stimulator is used, adductor muscle contraction should be sought to
correctly locate the obturator nerve 10 ml of local anaesthetic solution is injected and
the adequacy of the block confirmed by demonstration of adductor muscle paresis.
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INGUINAL PARAVASCULAR TECHNIQUE OF LUMBAR PLEXUS
ANAESTHESIA (WINNE’S 3 – IN – 1 BLOCK)
Regional anaesthesia of lower limbs has been simplified by a technique that involves
blocking three or the four nerves. Femoral, obturator and the later femoral cutaneous
nerves can be blocked with one injection of a large volume of local anaesthetic into the
femoral nerve sheath, just below the inguinal ligament (Figure 3). The main advantage
of this block is that three nerves can be blocked using one injection and the success rate
is also high.
Anatomy:
Femoral nerve and its relationship to the femoral vessels

The anatomical basis for the “3-in-l block” is the concept of a single sheath for a fascial
compartment forming a closed space which encloses all the nerves involved in the
lumbar plexus. Study of the anatomy shows that when these nerves emerge from the
lumbar plexus, they are sandwiched between the fascial covering of the quadratus
lumborum muscle posteriorly and the psoas major muscle anteriorly. The fascial
sheaths of these muscles enclose the three major branches of the lumbar plexus. The
compartment so formed continues with the femoral nerve and extends below the
inguinal ligament.
Drugs injected into the femoral sheath will travel upwards along this sheath provided
enough volume (more that 2o to 25 ml) is injected and sufficient pressure applied below
the site of injection so that cephalad spread is promoted. The femoral, obturator and the
lateral femoral cutaneous nerve will be reached by the solution in this sequence with a
similar onset of the block.
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Indications:
Surgeries on the anterior part of high
Management of fracture shaft of femur
In combination with sciatic nerve block for acute knee injuries.
For knee arthroscopy
Technique:
The technique of a 3-in-1 block is very similar to femoral nerve block. When
paraesthesia is elicited, at least 20 to 25ml of local anaesthetic solution is used to block
the lateral femoral cutaneous nerve which is at the highest level. Digital pressure is
applied below the injection site to promote cephalad spread. The lateral femoral
cutaneous nerve is often only partially blocked. Hence, it is recommended that it be
blocked separately at the anterior superior iliac spine
SCIATIC NERVE BLOCK (L4,5 S1,2,3)

Sciatic nerve block is usually indicated for providing surgical anaesthesia as well as for
postoperative analgesia of the lower extremity. Contrary to common belief, this nerve
block is relatively simple 10 perform. However, the deep location of this nerve
mandates proper training and adequate knowledge of anatomy of the region. When
performed under adequate sedation it has a reported success rate of 95% when
paraesthesia is elicited. The use of a nerve stimulator is associated with an even higher
success rate and is therefore recommended for these blocks.
Anatomy: The nerve originates from both the lumbar and sacral plexuses and consists
of two major nerve trunks enclosed in a common sneath. The tibial nerve trunk consists
of fibres from the ventral divisions and the common peroneal nerve fibres arise from
the dorsal divisions of the anterior rami of L4,5S1,2,3 roots .
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The sciatic nerve and its branches
Course of the nerve:

In the pelvis, the nerve lies in front of the pyriformis muscle. It enters the gluteal region
through the greater sciatic foramen below the pyriformis muscle and runs downwards
passing between the ischial tuberosity and greater trochanter. The nerve enters the
thigh at the lower border of the gluteus maximus and then runs vertically downwards to
the popliteal fossa where it terminates as the tibial and common peroneal nerves.
Motor supply: To the semitendinosus, semimembranosus, long and short head of
biceps femoris and ischial head of adductor magnus muscle.
Sensory supply: Cutaneous innervation of the entire lower limb below the knee (with
the exception of a medial strip of the leg) and the foot.
Articular branches: To the hip joint.
Indications:
1. Surgical procedures on the lower limb in combination with the lumbar plexus or
femoral nerve block.
2. Surgery below the knee combined with a saphenous nerve block
3. Surgery on the ankle and foot as a sole anaesthetic
4. Postoperative pain management following surgery on the lower extremity.
Techniques Of Sciatic Nerve Block:

The sciatic nerve can be blocked using several approaches and can be performed in the
following positions:
1) Supine
o Anterior approach
o Lateral approach
2) Lateral
o Posterior parasacral
o Gluteal and subglutealapproach
3) Prone
o Popliteal approach
4) Lithotomy
o Raj approach
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Anterior approach:
This approach is convenient especially in painful conditions, e.g., following trauma. This
position also allows for the performance of the femoral nerve block without having to
change the position of the patient. Since the nerve lies medial and posterior to the lesser
trochanter of the femur, it can be approached anteriorly near the lesser trochanter.

A line is drawn connecting the lower border of the anterior superior iliac spine and the
superior aspect of the pubic tubercle. This line overlies the inguinal ligament. A
perpendicular is then drawn at the junction of the medial third and lateral two thirds of
this line. The greater trochanter is identified and a third line is drawn parallel to the
first line. The point of intersection of this third line and the perpendicular line is the
point of entry of the needle .
Landmarks for sciatic nerve block by the anterior approach
Following local skin preparation and identification of the entry point, a 15 cm-long
insulated needle (connected to a nerve stimulator) is introduced after infiltration with
local anaesthetic (LA). With an initial current intensity of 1.5 mA, the needle is
introduced to a depth of 8–13 cm. The sciatic nerve lies 4-6 cm beyond the anterior
surface of the femur. If the bone is contacted, the needle is withdrawn up to the skin.
The skin is then moved medially 1.5 to 2 cm and the needle reintrodnced. If bone is
contacted again, this is likely to be the lesser trochanter. Internal rotation of the foot
helps to swing the lesser trochanter posteriorly and allows the passage of the needle.
The needle position is adjusted to elicit a discernible muscle contraction (extension or
plantar flexion of the toes, foot eversion or inversion) with the lowest possible current
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intensity (0.5 mA for 100 sec stimulation). It is hazardous to inject when neural
stimulation is still present at 0.3 mA as the needle tip may lie in the nerve itself. After
confirming twitch response, 20 to 25 ml of local anaesthetic solution is injected.
Lateral approach:
High lateral approach:
The greater trochanter is identified and the needle entry point is 3 cm distal to the
lateral prominence of the greater trochanter. The needle is introduced close to the
posterior margin of the femur until periosteum is contacted. It is then partially
withdrawn and redirected postero-medially to slide posterior to the femoral shaft. The
sciatic nerve is contacted at a depth of 10-13 cm. Nerve location is confirmed by
contractions of the calf muscles or the anterior compartment muscles on nerve
stimulation. 20 ml solution is injected.
Low lateral approach:

The groove between the biceps femoris and lateral border of the vastus lateral is
identified and marked. A vertical line is drawn from the tip of the patella and the point
where this line intersects this groove line is the point of needle entry. A 10 cm-long
needle connected to a nerve stimulator, is introduced at a 30° angle directed
posteriorly, after local infiltration with LA. Initially, contraction of the biceps femoris
and vastus lateralis is elicited due to direct stimulation of the muscles. When the needle
is 4-6 cm deep, these contractions disappear. On further introduction of 1-3 cm, the
sciatic nerve stimulation is observed.
Posterior approach:
This is the most commonly performed approach and it blocks the nerve at the level of
the sciatic notch using the piriformis muscle as the landmark.
Position:
The patient is positioned in the lateral position with the side to be blocked uppermost.
The knee of this limb is flexed with the heel of the foot placed at about the level of the
contralateral knee.
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Positioning for sciatic nerve block by the posterior approach

A line is drawn between the upper aspect of the greater trochanter and the posterior
superior iliac spine. This corresponds approximately to the superior border of the
pyriformis muscle and upper border of the sciatic notch. A perpendicular line is
extended caudo-medially from the midpoint of the first line. A third line is drawn
between the greater trochanter and sacral hiatus. The site of introduction of the needle
is at the intersection of the second and the third lines.
Following skin infiltration with LA, a 22 G 10-15 cm insulated needle (connected to a
nerve stimulator) is introduced perpendicular to the skin and directed towards the
pubic symphysis. Initially, direct contraction of the gluteus maximus is elicited which is
then followed by stimulation of the sciatic nerve at a depth of 6-10 cm. If the needle is
too superficial the pyriformis muscle alone is stimulated. If too deep, the patient feels an
electrical impulse in the perineum; the needle should be withdrawn and redirected
more medially or laterally. 20-30ml local anaesthetic is injected .
Landmarks for sciatic nerve block by the posterior approach

Gluteal and subgluteal approach:
These approaches have been more recently described. They involve the identification of
the greater trochanter of the femur and the ischial tuberosity as landmarks.
Gluteal approach:
A straight ling is drawn between the above mentioned two points. The entry point of the
needle is at the midpoint of this line where it is introduced perpendicular to the skin. At
a depth of 5-7 cm, the sciatic nerve is stimulated. 20-30 ml of LA is injected.
Subgluteal approach:
This approach has been found to be simple and reliable. A line is drawn between the
ischial tuberosity and greater trochanter. From the midpoint of this line, a
perpendicular line is drawn caudallv for 4 cm. At this level, a skin depression can be
palpated representing the groove between the biceps femoris and semitendinosus
muscle. A 10 cm insulated needle connected to a nerve stimulator is introduced at an
800 angle and the sciatic nerve located at a depth of 5-7 cm.(20-30 ml of LA is injected.
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Lithotomy position (Raj approach):

This approach is useful in obese patients, as they can remain supine with the hip flexed
and the leg supported by an assistant. A line joining the greater trochanter of the femur
and the ischial tuberosity is drawn. The needle is inserted at the midpoint of this line
and the sciatic nerve is usually stimulated at a depth of 4-6 cm. A total volume of 18 to
20 ml of local anaesthetic is injected .
Raj approach to the sciatic nerve in the lithotomy position
Complications of the sciatic nerve block are in general similar to complications

following other peripheral nerve blocks.
BLOCKS AROUND THE KNEE JOINT

To achieve anaesthesia for surgeries on the foot, branches of sciatic nerve and the
saphenous nerve can be conveniently blocked around the knee joint. This technique is
particularly useful in situations where oedema or inflammation around the ankle
jeopardises the success of the ankle block.
Indications:
It can be used for all surgeries on the ankle and foot. It can also be used for the diagnosis
of myotonia and as an adjunct to physiotherapy for severe equines deformities.
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Anatomy:
The following nerves are blocked around the knee joint a) tibial nerve and b) common
peroneal nerve (branches of sciatic nerve,) and c) saphenous nerve, the terminal branch
of the femoral nerve.
Nerves in the popliteal fossa
SAPHENOUS NERVE BLOCK (L3 – L4)

Anatomy:
It courses along the medial side of the knee behind the sartorius muscle and becomes
subcutaneous between the tendons of the sartorius and gracilis muscles distal to the
medial condyle of the tibia. It has no motor component (no ‘M’ in saphenous).
Cutoneous supply: Medial, anteromedial and posteromedial aspects of the leg from
above the knee to the level of medial malleolus.
Technique:
Distal approach: A horizontal line is drawn from the tibial tuberosity to a point just
distal to the medial tibial condyle. Along this line, 3-5 ml of local anaesthetic (LA) is
infiltrated subcutaneously. A nerve stimulator cannot be used to identify this nerve as it
has no motor component.
Proximal approach: The nerve can be blocked beneath the sartorius muscle. The
needle is inserted at the superior border of patella and 10 ml LA is injected deep to the
sartorius muscle between vastus medialis and sartorius muscles. Alternately, a trans-
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sartorial approach can also be used. A Tuohy needle attached to the syringe is inserted
one finger-breadth above the patella through the sartorius muscle till a loss of
resistance is encountered and 10 ml of LA is injected.
Saphenous nerve block- distal approach

COMMON PERONEAL NERVE BLOCK (L4-S3)
Anatomy:
It traverses along the lateral part of the popliteal fossa just below the biceps femoris
tendon.
Motor supply: Extensor muscles of the foot
Cutaneous supply: Lateral aspect of the leg, heel and ankle
Articular branches: To the knee joint.
Technique:
Feel for the head of the fibula and palpate for the common peroneal nerve on the neck of
the fibula the nerve can be blocked by subcutaneous infiltration of 3-5 ml of local
anaesthetic. If not palpable, the needle is advanced to reach the periosteum of the fibula.
It is then slightly withdrawn and 5-7 ml of local anaesthetic is injected. A nerve
stimulator can be used to elicit contraction of anterior compartment muscle.
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Common peroneal nerve at the knee joint
TIBIAL NERVE BLOCK (L4 - S2)

Anatomy:
The tibial nerve runs along the middle of the popliteal fossa just lateral to the popliteal
artery.
Motor supply: Flexor muscles on the back of knee joint and calf muscles.
Cutaneous supply: Popliteal fossa and posteriorportion of leg upto the ankle.
Technique:
The nerve lies in the midline of the triangle formed by the tendons and the popliteal
crease.
Surface marking and point of needle entry for tibial nerve block
With the patient lying in prone position, a small pillow is placed under the leg and the
knee is mildly flexed. The medial and lateral borders of the triangle are marked. The
popliteral crease is marked to complete the triangle. A perpendicular is drawn from the
midpoint of the line along the popliteal crease. The point of entry is marked 5 cm
proximal to the popliteal crease on this perpendicular line and 1 cm lateral to this line.
The needle is advanced at a 45-60° angle in an antero-superior direction. At a depth of
1.5-2 cm, the nerve is identified by paraesthesia in the posterior aspect of the leg. A
nerve stimulator can be used to elicit plantar flexion of the foot. 5 to 7 ml of local
anaesthetic solution is injected. A successful nerve block is confirmed by sensory
anaesthesia in the posterior aspect of the leg and weakness in plantar flexion of the foot.
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ANKLE BLOCK
The peripheral nerves to be blocked at the ankle are all derived from the sciatic nerve
with the exception of the saphenous nerve, which is a terminal branch of the femoral
nerve.
Sciatic Nerve
o Common Peroneal Nerve
o Tibial Nerve
- Post Tibial Nerve
- Sural Nerve
Femoral Nerve
o Saphenous Nerve
TIBIAL NERVE
This nerve continues from the leg, runs about the mid point between the medial
malleolus and the calcaneum on the medial side of the ankle under the flexor
retinaculum; it lies posterior to the pulsation of the posterior tibial artery, divides at the
back of the medial malleolus into medial and lateral plantar nerves. The medial branch
supplies the medial 2/3 of the side of the foot and the plantar portion of the medial
three and a half toes up to the nail. The lateral branch supplies the lateral one third of
the sole of the foot and the plantar portion of the lateral one and a half toe.
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DEEP PERONEAL NERVE
It is the continuation of the nerve in the front of the leg. It innervates the short exten-
sions of the toes as well as the skin on the adjacent areas of the first and second toes.
SURAL NERVE
It is formed by the union of a branch from the tibial nerve and the common peroneal
nerve and it runs on the lateral aspect of the ankle midway between the lateral
malleolus and the calcaneum towards the lateral side of the little toe. It supplies the
lower posterolateral surface of the leg, lateral side of the foot and the lateral part of the
5th toe.
SAPHENOUS NERVE
This follows the great saphenous vein, supplies the cutaneous area over the medial side
of the lower leg anterior to the medial part of the foot.
SUPERFICIAL PERONEAL NERVE

It pierces the deep fascia on the anterior aspect of the distal 2/3 of the leg and runs
subcutaneously to supply the dorsum of the foot and the toes.
Position
1. Foot on the bed with knee flexed.
2. Supine position with leg to be anaesthetized crossing the other knee.
Indication
1. All surgical procedures of the foot.
2. Amputation of the mid foot and toes
Drug and Volume

5 ml of local anaesthetic per nerve
Landmarks: Medial Malleolus, Lateral Malleolus, Tendo calcaneus, pulsation of the
tibial artery, external hallucis longus (EHL) tendon, Tibilias anterior tendon.
Technique:
TIBIAL NERVE BLOCK

Skin wheal is raised lateral to the posterior tibial artery; if pulsation is not palpable,
then a wheal is placed to the medial side of the Achilles tendon at the level of the upper
border of the medial malleolus. A 22G, 4 cm needle is advanced through the wheal at
right angles to the posterior aspect of the tibia, lateral to the artery. If paraesthesia is
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elicited , then 3.5 ml. of LA solution should be injected. If paraesthesia is not obtained, 5-
7 ml. of solution is injected against the posterior aspect of the tibia.
SURAL NERVE BLOCK
A skin wheal is raised lateral to the Achilles tendon at the upper border of the lateral
malleolus. A 22G, 4 cm needle is inserted anterolaterally ( towards the fibula ) and if
paraesthesia is not obtained, the needle is allowed to contact the lateral malleous and 5-
7 ml. of LA is injected.
DEEP PERONEAL NERVE SUPERFICIAL PERONEAL NERVE and SAPHENOUS NERVE

BLOCK
Select the midpoint on a line joining the two malleoli. The midpoint will be
lateral to the tibilias anterior tendon and in between that and the EHL tendon.
Raise a skin wheal.
Introduce a 22G, 5cm. needle at this point, perpendicular to the skin until contact
with the anterior surface of tibia is made. Withdraw 1 cm and inject 5ml. of LA
solution to block the deep peroneal nerve.
From the midline skin wheal used to block the deep peroneal nerve, use a 22G,
8cm needle and advance it subcutaneously, medially towards the medial
malleolus and laterally towards the lateral malleolus to block the saphenous and
superficial peroneal nerves and inject 3-5 ml. of LA solution
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Chapter 8 - ANATOMY & PHYSIOLOGY OF SPINAL / EPIDURAL
AND CAUDAL SPACE (in short)
INTRODUCTION:
It is important that the anaesthetist should posses a good knowledge of the
anatomy of vertebral column and a lumbar vertebrae in particular, since it is in this
region that a needle can be introduced into spinal canal most safely and easily. He must
be familiar with the disposition of the 3 membranes which envelop the CNS. In the
vertebral canal these 3 tubular membranes enclose the cord in an elongated
compartment, annular in cross section the subarachnoid space, in which the local
anaesthetic solution can be made to spread to any desired height after it has been
introduced low down in the lumbar region.
Vertebral column:
The vertebral column (The spine or back bone) forms the central axis of the
skeleton and forms a canal which functions to protect the spinal cord.
Made up of 34 vertebra: 7 – cervical
12 – thoracic
5 – lumbar
5 – sacral and
4 to 5 – coccygeal vertebrae.
In the adult normal spinal column has 4 curves when patient is supine and
horizontal.
1. Cervical curve – convexity anterior
2. Dorsal curve – convexity posterior
3. Lumbar curve – convexity anterior
4. Sacrococcygeal curve – convexity posterior.
The high point of spinal curve when the patient is supine and horizontal is at L3 vertebra
and low point at T5 vertebra.
Thus solution heavier than spinal fluid deposited at L3 will flow away both cranial and
caudad.
Abnormal curves may be:
1. Kyphosis – an exaggerated A-P dorsal curve.
2. Lordosis – an exaggerated lumber curve.
3. Scoliosis – an exaggerated lateral curve.
A typical lumbar vertebra: composed of two parts.
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Body or base anteriorly which bears weight.
The arch – which surrounds the cord laterally and posteriorly consisting of lamina and
pedicles.
There are 7 processs.
a. 3 muscular processes: 2 transverse, 1 spinous
b. 4 articular processes: 2 upper and 2 lower.
There are certain gaps between any two vertebrae these are:
1. The lateral intervertebral foramen: the spinal nerves emerge through this gap.
2. The posterior inter laminar gap.
In extended position: it is triangular and small.
In flexed position: Diamond shaped.
It is the site where spinal puncture is done for spinal or epidural space.
Articulation of the vertebrae is by ligamentous connections:
There are 5 ligaments.
Supraspinous ligament: Strong thick fibrous band connecting the apices of the
spines.
Interspinous ligament: Thin, fibrous structure connecting adjacent spinces.
Ligamentum flavum: Consists of yellow elastic tissue, extend between lamine.
Posterior longitudinal ligament.
Anterior longitudinal ligament.
Primary curves:
Present from bloth
Thoracic sacrococxgeys
Secondarycurves:
Develop later in life
Cervical lumbar cancave
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Ossification of vertebra: 3 primary centers ( 7-8 wks)- 1 for body and 1

each for vertebral arch.
3 secondary centers: 1 each for transverse process (16 th yr ) and 1 for spinous process
Topographic line of tuffier:

A line across the back between the crests of ilica passes over the spine of the 4th
lumbar vertebra in upright position.
It passes over the interspace between 4th and 5th lumbar vertebrae when patient
is lying in the lateral position.
This line serve as a surface landmark on the back for the identification and
numbering of the interspaces between the spinous process of the vertebrae.
Intervertebral disc:
Present between bodies of the vertebrae.
Each disc consists of a fibrous outer covering “annulus fibrosus”, which encloses
a core of gelatinous material “the nucleus pulposus”.
Acts as a shock absorbed and gives flexibility to the vert-column.
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‘Prolapsed disc’: A protrusion of the nucleus pulposus can occur following
careless technique of lumbar puncture.
Venous plexus of the vertebral column:

These are:
External plexus: Marked in cervical region.
- Lie outside the vertebral canal.
- They communicate freely.
Internal plexus:
Lie inside the canal between duramatter and the vertebra.
Get tributaries from spinal cord and bone.
Freely communicate each other.e
Basivertebral veins:
Present in the substance of the bodies.
Communicate through openings on vertebral surface to external vertebral plexus
and dorsally with internal vertebral plexus.
The intervertebral veins:

Accompancy the spinal nerves through intervertebral foramina.
Tributaries are spinal cord veins, internal and external vertebral plexus.
End is segmental veins – they are: verterbral, intercostals and sacral veins.
These finally drain into Azygous and Hemiazygous veins  Superior venacava.
SPINAL CORD
It is the cylindrical mass of nervous tissue.
Length 42-45 cms. Weight – 30 gm.
Occupy upper 2/3 of the vertebral canal.
Rostral end is continous with the medulla oblongata.
Extends caudally to either lower border of L1 vertebra or upper border of L2
vertebra.
Form the conical lower end – ‘conus medullaries’.
“The filum terminale” – a delicate filament stretches from conus medullaries to
the first segment of the coccyx.
Developmental anatomy:
At birth the tip of the spinal cord lies at the level of lower border of 3rd lumbar
vertebra and dural sac at the 3rd sacral vertebra.
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After birth, the lengthening and growth of the cord as well as meninges lag
behind the growth of the bony vetebra.
This differential growth rate results in the development of the epidural space
and the caudal space.
The spinal cord becomed relatively free of it’s dura, but is surrounded by
arachnoid and is engulfed in the CSF in the SAS.
Results in the downward fanning of the spinal nerves, forming ‘cauda equine’.
Internal structure:
On cross section, spinal cord consists of
A central grey matter (cell bodies)
Outer white matter (fibres)
Spinal nerve roots:

There are 31 pairs of spinal nerves attached to spinal cord.
Each nerve arises form a ventral and dorsal nerve roots – which unite in the
intervertebral foramina to form spinal nerve trunks – which soon divide into
anterior and posterior primary divisions.
It is block of spinal nerve roots which produces typical effect in spinal analgesia.
Formation of spinal nerves

1. The dural sac consisting of the dura mater and the arachnoid mater: the pia
mater coverage the spinal cord and projecting laterally as the denticulate
ligaments seperating the rows of dorsal and ventral rootlets.
2. Cerebrospinal fuid circulates between pia and arachnoid. In the subarachnoid
space:
3. On each side, two rows of rootlets attach to the cord; the dorsal filaments carry
sensory information to the centralnervous system; the ventral filaments convey
motor information from the central nervous system to the periphery:
4. A number of rootlets combine to form at each segment dorsal and ventral roots:
5. The swollen area on the dorsal root the spinal (dorsal root) ganglion contains
cell boodles of sensory neurons:
6. Dorsal and venural roots unite to form a spinal nerve:
7. Dura (and arachnoid) continues as a sheath around nerves leaving the spinal
cord.
Blood supply:
Arterial supply: from one anterior and two pairs of posterior spinal arteries.
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- Anterior spinal artery.
Formed at the foramen magnum.
Branch of terminal portion of each vertebral artery.
Lies in the midline on the anterior median fissure.
Supplies anterior 2/3 of the spinal cord.
- Posterior spinal arteries.

4 longitudinal running vessels – 2 on each side.
One lies in front of the dorsal nerve root and the other behind it.
Derived – either directly from vertebral artery or from primary branch of
posterior inferior cerebellar artery.
Supplies posterior 1/3 of spinal cord.
Reinforcement of arterial supply:

Spinal radicular branches: arises from local segmental arteries like vertebral,
ascending cervical, posterior intercostals, spinal lumbar and lateral spinal
arteries – these enter vertebral canal through intervertebral foramina.
One of the radicular branch is considerably larger termed. ‘Arteria radicularies
Magna’ or ‘Artery of Adamkeiwicz’. It may be responsible for major blood supply
of lower 2/3 of spinal cord in 50% of population.
Venous drainage:
Veins of the spinal cord are situated in the pia matter, and drain parenchyma of
the cord.
They are 6 in number and form longitudinal plexiform channels.
They are 1) Two median longitudinal veins: anterior and posterior.
2) 4 lateral longitudinal veins.
These veins communicate with internal vertebral plexus and drain finally into
external vertebral plexus.
At the base of the skull, some veins drains into internal vertebral plexus and
others drain into cranial venous sinuses – ending in inferior petrosal sinuses.
Blood flow:
Perfusion pressure range  60 – 120 mm Hg.
Average flow  60 ml/gm/min at 60 mm Hg pp.
Gray matter flow  40 ml / 100 gm / min.
White matter flow  8 – 12 / 100 gm min.
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Regulation of spinal cord circulation:
The circulation to spinal cord and cord perfusion dependent on:
MAP
Integrity of circulation
Autoregulation at the micro circulatory level.
If P.P. is reduced to 50 mm Hg Spinal cord blood flow is reduced.
Intrinsic regulation is dependent largely on normal tissue Co2, PaCo2, Po2 and PH
and cord temperature.
Hypoxia and hypercarbia – increases blood flow.
Hypocarbia and hypothermia – decreases blood flow
Meninges of the spinal cord:

Spinal cord has 3 covering membranes or meninges: The Dura matter,
Arachnoid matter and Pia matter.
Dura matter:
Dural covering of the brain is double membrane.
Dural covering of spinal cord is a continuation of the innerlayer (meningeal
layer) of the cerebral dura.
Made up of dense fibrous tissue.
Dural sac extends to the level of 2nd sacral segment.
Occasionally ends as high as L3 or extends to S3 vertebra.
The dural sac then continues as the covering of filum terminale to end by
adhering to the periosteum on the back of the coccyx.
The sac widens out in the cervical and lumbar regions corresponding to the
cervical and lumbar enlargements of the spinal cord.
It lies loosely in the spinal cord, but it attached at the following points to its bony
surroundings.
a. Above to the edges of the foramen magnum and to the posterior aspect of the 2nd
and 3rd cervical vertebra.
b. Anteriorly to posterior longitudinal ligament.
c. Laterally blend with the epineurium of the spinal nerves.
d. Inferiorly by the filum terminals to coceyx.
e. Posteriorly it is completely free.
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Arachnoid matter:
It is membrane of spider web delicacy, which lines the dural sheath and sends
prolongations along each nerve root.
Above it is continuous with cerebral archnoid.
The pia matter:
It is the innermost of 3 membranes.
It is a vascular connective tissue sheath which closely invests the brain and
spinal cord and projects into their sulci and fissures.
Anteriorly it is thickned into ‘linea splendens’ along the length of the anterior
median fissure. On either side it forms ligamentum denticulatum, which is
attached to dural sheath.
Posteriorly it forms posterior subarachnoid septum passing from the posterior
median sulcus of the cord back wards to the dura.
Inferiorly it continues as filum terminale, with a covering sheath of dura attached
to the coccyx.
Nerve supply of meninges:

The posterior (unlike the anterior) aspect of the drua and arachnoid are not
supplied by the afferent nerve fibres, so that pain is not felt when the dura is pierced by
L.P. Needle.
COMPARTMENT RELATED TO SPINAL MENINGES

These are
Sub archnoid space.
Subdural space
Extra dural space
THE SUB ARACHNOID SPACE:

The SAS is lined externally by the arachnoid matter and internally by the pia
matter.
It contains innumerable cob web like trabeculae.
It is traversed by the cranial and spinal nerves.
It contains the main blood vessels of the CNS and extends along the capillaries
and small arteries into the nervous tissues of the spinal cord and brain.
It contains CSF, which functions as the lymph found in other parts of the body.
In cervical and thoracic region, the space is annular and the distance between the
arachnid and pia is only 3 mm, hence the danger of injuries the cord if spinal tap
is done here.
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Below the L1 vertebra (where cord ends) the space is circular ad has diameter of
15 mm. The lumbar puncture below L1 is easyand constituent nerve roots of
caudaequina escape damage on account of their relative mobility and the
absence of cord greatly increases the cross sectional area of the SAS.
In the skull the pia and arachnid membranes are for the most part is in fairly
close apposition.
Cerebrospinal fluid (CSF):

CSF is analogous to the lymph in other parts of the body.
Volume: Total volume is adults  120 – 150 ml.
In spinal SAS  25 – 30 ml.
Formation of CSF:
By process of ultra filtration through choroids plexus.
About 0.4 ml/min (25 ml/hr) or 600 ml/day.
Control of production:
Is under sympathetic control.
Increased sympathetic stimulation, increases production and fluid pressure.
Carbonic anhydrase enzyme is essential for active secretion.
In children:
4 – 12 yr of age, formation of CSF is 0.35 ml/min with standard error of 0.02
ml/min.
Mean CSF volume (5-10 yr age) – 75 ml. (66 – 100 ml)
Absorbtion of CSF:
Through cerebral arachoid villi to venous sinuses.
For absorbtion intraventnicular pressure should be more than sinuses pressure.
SUBDURAL SPACE:
It is potential one only.
The arachnoid is in close contact with the dural sheath.
Contains thin film of serous fluid.
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THE EXTRA DURAL (PERIDURAL OR EPIDURAL) SPACE:
The epidural space is the circular space surrounding the dural sac and all of its
contents.
Extends from the foramen magnum to the sacral hiatus.
The space is more extensive and easily discernible posteriorly, while anteriorly,
the dura adheres closely to the periosteum of the vertebral bodies.
Lateral boundaries and the intervertebral foramina and the peduncles of the
vertebrae.
The space extends laterally accompanying the spinal nerves through the
intervertebral foramina into the paravertebral space up to the angle of the ribs.
This communication between the extracural and paravertebral spaces explains
the – ve pressure in epidural space.
The contents of the epidural space:
Aeriolar tissue, fat and 4 spinal nerve roots with their dural sleeves.
The spinal arteries.
The venous plexus and capillary network
There are strong lateral attachments of the dura at the cervical and lumbar areas
to the spinal canal wall.
Posteriorly, in the midline, a distinct connective tissue, named “Plica mediana
donsalis” connects dura matter to ligamentum – Flavum.
To reach the epidural space in the midline sagital plane, the following structures are
penetrated from outside to inside:
Skin and subcutaneous tissue.
Supraspinous ligament
Inter spinous ligament
Ligamentum flavum
Size of epidural space:

In the anterior region it is almost non existent.
Posteriorly it is measured readily in the midline, as shown in the table
Epidural space (mm) Thickness of dura (mm)
Cervical 1.0 – 1.5 2.0 – 1.5
Upper thoracic 2.5 – 3.00 1.0
Lower thoracic 4.00 – 5.00 1.0
Lumbar 5.00 – 6.00 0.66 – 0.33
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Distance to epidural space:
The over all median distance in normal adult female is 4.7 cm at L3 – L4 level.
The maximum depth occurs at L3 – L4 inter space.
The depth decreases above L3 and below L4 level.
Epidural space in children:

In children under 6 yrs of age, the epidural space has spongy, gelatinous lobules
and distinct space. (This is contrast to densely packed fat globules and fibrous
strands characteristic of the mature epidural space).
Because of this difference there is a more rapid longitudinal spread of drugs
within the juvenile epidural space.
CAUDAL SPACE:
It is the continuation of the epidural or extradural space in the sacral canal.
The volume of extradural space is considerable greater within the sacral canal.
The vertebral canal ends at the sacral hiatus.
The hiatus is V or U shaped notch located between the sacral cornua formed by
failure of fusion of the spine of the fifth sacral vertebra.
The mean distance between the apex of the hiatus and dural sac is 47 mm.
The hiatus is covered by the sacrococcygeal ligament (1 – 3 mm thick),
subcutaneous fat and skin.
The sacral hiatus usually lies 2 inches above the tip of the coccyx and directly
beneath the upper most limit of the natal cleft.
In clinical practice it is located by direct palpation of the depression which is
forms between the sacral cornua.
PHYSIOLOGY OF SPINAL ANAESTHESIA

There are three sites of action of local anaesthetics placed in subarachnoid space.
In order of importance are:
Primary: On nerve roots of spinal cord
o Weaker concentration – cause sensory block
o High concentration cause – motor block
Secondary: On donsal root ganglia and posterior and anterior horn synapses.
Limited and incomplete: In spinal cord parenchyma on ascending and
descending tracts.
Determinants of nerve fibre susceptibility:

1. Fibre size: Small fibres are more sensitive than large fibres.
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2. Degree of myelinisation and distance between the nodes of Ranvier: The greater
the myelinisation and the distance between the nodes, the greater will be the
resistance to drug action.
3. A functional characteristic: The axons with a high frequency of impulse traffic
are more sensitive to local anaesthetic blockade.
Difference of levels of block according to fibre type:

Sympathetic paralysis is more diffuse and will extend 2 – 4 segments above the
sensory block.
Motor blockade, 1 – 4 segments below the sensory level.
Sequence of nerve modality block:

1. Vasomotor block – dilatation of skin vessels and increases cutaneous blood flow.
2. Block of cold temperature fibres
3. Sensation of warmth by the patient due to above
4. Temperature discrimination.
5. Slow pain
6. Fast pain
7. Tactile sense
8. Motor paralysis
9. Pressure sense abolished
10. Proprioception and MTJ sense
INDIRECT EFFECTS
Due to paralysis of nerves.
Sympathetic blockade is major determinant
Hemodynamic changes as shown in the table:

Low High
Mean brachial arterial Decreased 21% Decreased 44%
pressure
Systolic Decreased 50%
Diastolic Decreased 43 %
Right auricular pressure Decreased 36 % Decreased 53 %
Pulmonary artery pressure Decreased 15 % Decreased 35 %
Cardiac rate Decreased 8 beats Decreased 10 beats
Stroke volume Decreased 73 to 68 cc Decreased 57 to 43 m
Minute output Decreased 16 % Decreased 31 %
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Peripheral resistance Decreased 14 % Decreased 18.5 %
Calculated left ventricular Decreased 30% Decreased 62 %
work
Peripheral blood flow Decreased Increased
Fingers
Toes Decreased Increased
Oxygen consumption
A-V O2 difference 2.8 to 4.2 3.9 to 5.0
Art. O2 saturation None None
Oxygen consumption Decreased Decreased
Hematocrit Decreased 1 % Decreased 2 %
Estimated hepatic blood flow Decreased 24 % Decreased 33 %
Brachial Art – Hepatic V O2 Increased 16% Increased 35%
diff.
Splanchnic vascular Slightly increased Increased 7%
resistance
Splanchnic oxygen Decreased 4 – 6% Increased 2-8%
consumption
Venous pressure Decreased 12% Decreased 35%
Circulation time Increased Increased 20%
Theories to explain these circulatory changes are:

1. Hematogenous intoxication: Rapid absorbtion into blood steam of anesthetic
drugs precipitates the lowering of B.P.
2. Direct action on medullary centers.
3. Paralysis of adrenal nerve.
4. Respiratory depression. The hypoxia due to decreased ventilation will cause
these circulatory changes.
5. Loss of skeletal muscle tone: This effect diminishes intraabdominal pressure and
causes splanchnic pooling and diminishes support and milking action on veins,
 impair venous return  decreases cardiae output.
Primary mechanism of hypotension: Paralysis of vaso constrictor nerve fibres 
arteriolar and venous dilatation  peripheral pooling of blood  decreased venous
return  decrease CO  hypotention.
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Paralysis of vasoconstrition nerve Fibres.
Arteriorlar and venous dilation
Peripheral pooling of blood
Venous return
CO
Hypotension
II. Autonomic nervous system:
- Blocks sympathetic out flow.
- Parasympathetic – vagal action becomes more prominent and hece cause the
physiologic disturbances in the heart, bronchi and GIT.
III. Cardiac effect:
- In high spinal block of upper five thoracic spinal roots cause block of
cardioaccelerator fires, with the vagas itact will cause bradycardia.
IV. Bronchial effect:

- Sympathetic fibres to bronchial musculature comes from upper 5 or 6 thoracic
segments.
- High block cause, bronchospasm
Affective dyspnea ; due loss of the MTJ
sense or position sense in the thoracic cage
structures.
V. GIT effect:
- The gut gets contracted after spinal anaesthesia. Intestines are usually active and
show segmental movements as well as slow peristalisis.
- With high spinal antiperistalitic movements seen which can result in
regurgitation.
Effect o gastric emptying:

- S.A promote gastric emptying which was delayed by surgery.
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VI. Ventilatory effects:
- S.A. to sensory level of at least T4 does not affect pulmonary ventilation in
unpremedicated patient.
VII. Enodocrine effects:
Endocrine effects of surgical stress are:

- Increased plasma epinephrine and nonepinephrin.
- Increased production of ADH.
- Increased production of growth hormone.
- Increased production of cortisol.
- Increased cyclic AMP  proportional to severity of stress.
- Increased prostaglandins, Renin
- Endorphin activation
- Increased prolactin  six fold more in females
These neuroendocrnine responses are inhibited by regional anaesthesia i.e., spinal or
epidural.
Mechanism: Regional anaesthesia block afferent impulses to the CNS specifically to
hypothalamic pituitary axis, so that release of endocrine substances are inhibited.
In addition they block peripheral efferent sympathetic out flow.
VIII. Reduction of blood loss:
Is related to the redistribution of blood flow to other parts (mainly splanchnic
bed and pulmonary bed) of the body away from the operative site.
IX. Thromboembolic complication: reduced
X. Effect on Carbohydrate metabolism:
Glucose tolerance is minimally affected compared to surgery done under GA.
XI. Fat metabolism:
Decreases plasma glycerol and free fatty acids.
XII. Effect on pulmonary function and pulmonary complication post operatively.
Regional anaesthesia (particularly post operative epidural analgesia) will
promote breathing more efficiently.
XIII. Effect on mental function:
Particularly in elderly, post operative confusion and disorientation are reduced
following RA compared to GA.
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EFFECT OF AGE ON SPINAL ANAESTHESIA
(Kinetics and Dynamics)

1. Absorbtion from the SAS is slowed  Sclerotic vessels.
 Decreased blood flow
2. Specific gravity of CSF more: Hperbaric solutions may act more like isobaric 
Spread is less.
3. Decreased CSF volume.
1. Changes in curvature of lumber and thoracic spine  greater upward spread and
pooling in the thoracic cavity in the presence of exaggerated lumbar lordosis or
thoracic kyphosis.
2. Slightly higher levels of analgesia.
3. An increased latency time to maximal spread.
4. Faster onset of motor block.
Pharmacokinetics:
Peak plasma concentrations of bupivacaine show an insignificant increase.
Peak plasma times are prolonged and terminal half life is incrased.
Plasma clearance slowed.
INFANTS AND CHILDREN:

Duration of spinal motor block is shortest.
After 2 yrs there is linear increase in duration upto about 15 yrs, when duration
attains adult value.
Dosage of anaesthetic depends on body weight or body surface area (unlike in
adults where dosage depends or body height)
Factors modifying the dose are
o Larger circumference of the spinal cord.
o Greater filling of vert. Canal
o Smaller volume of CSF and low density of CSF.
Effect of epinephrine:
Spinal sub arachnoide bupivacaine 0.5% (15 mg), isobaric anaesthesia is
prolonged by the addition of epinephrine.
Opitimal dose – 100 g / ml or dilution of epinephrine of 1: 10,000.
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DIFFERENCE BETWEEN SPINAL AND EPIDURAL
Spinal Epidural
Speed of onset Very rapid Delayed
Upper limit of block Variable unpredictable Can be controlled
Intensity of block Profound Variable agent depended
Lower limit of block Satisfactory S4 Variable( sacral space )
Motor blockade Complete Incomplete
Systemic absorption Negligible Substantial toxicity
possible.
Hypotension Common, rapid onset Variable, gradual onset
Provision of post operative Nil Ideal roots for continuous
analgesia analgesia
Dose Small Large
Cardiovascular responses:
Spinal E.A. without E.A. with
anaesthesia epinephrine epinephrine
MAP Pressure (torr) - 21.3 - 8.9 - 22.0
H.R. (beats/min) + 3.7 + 6.7 + 15.8
COP (L/min) - 17.7 - 5.4 + 30.2
Stroke volume (ml / beat) - 25.4 - 10.2 + 7.9
Total peripheral vascular - 5.0 - 2.9 - 39.6
resistance
Testing for levels of block for different nerve modalities:

A. Testing for sensory level of anaesthesia:
Using loss of recognition to pinprick using a sterile needle.
It occurs 2-3 dermatomes more cephalad than the sense of touch
Using cold stimulus – such as alcohol sponge
particularly recommended in elderly, debilitated or those with delicate skin.
B. On set and assessment of motor block:
Motor block develops after sensory block.
Sequence and onset of motor block, can be assessed by a modified Bromage scale
as shown in table.
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BROMAGE SCORE:
Scale Criteria Degree of block
0 Free movement of legs and feet with ability to raise None
extended leg
1 Inability to raise extended leg and knee flexion is Partial 33%
decreased but full flexion of feet and ankles is present
2 Inability to raise leg or flex knees ; flexion of ankle and Partial 66%
feet present
3 Inability to raise leg, flex knee or ankle, or move toes Complete paralysis
Recovery from motor block:

Recovery is reverse of onset.
C. Sympathetic block:
2 – 3 segments higher than sensory block.
Due to blockade of preganglianic sympathetic B-fibres.
Test for sympathetic block:

Using sympatho – galvanic reflex (SGR)
Principle: Skin conductance is directly related to the activity of the sympathetic
nervous system.
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Method: Using the electro cardiograph direct writer.
- when sympathetics are intact – A biphasic response seen
1st phase – Direct nerogenic response.
2nd phase – Hormonal response.
when sympathetics blockaded by RA – Graph becomes flat line or amplitude of response
decrease.
Other factors affecting skin conductance are:

Skin moisture
Electrolyte content
Degree of sweating
By testing skin temperature:

It is more refined and sensitive technique of observing level of sympathetic
block.
The temperature in area of sympathetic block may be increased by 0.8 to 1.6 0C,
allowing for core cooling effect.
Level of elevated skin temperature is cephalad to sensory block.
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Chapter 9 SPINAL NEEDLES
1. Vary in regard to the outside diameter (OD), inside diameter (ID) and shape of
their tip.
2. These differences are important because they affect the size and shape of the
puncture hole made in the dura mater and the speed with which CSF appears in
the hub after the SAS is entered.
3. Gauge 22, 25, 26, 29
4. OD (mm) 0.7, 0.5, 0.45, 0.34
1. ID of spinal needles also varies considerably for the same size of OD.
2. ID is important as it affects the rate of flow of CSF down the needle, which is
related to the CSF pressure at the needle tip. With a 26 gauge needle, it can take
10 to 60 seconds for CSF to appear at the needle hub. It is seen sooner if the hub
is translucent rather than opaque. It addition the, flow will be faster if the patient
is sitting up rather than in the lateral decubitus position, as the pressure at the
needle tip is greater.
3. 22 gauge needles can be used without the aid of an introducer, but thinner
needles usually require an introducer which is first inserted into the ligamentum
flavum.
4. The shape and sharpness of the needle tip affects the shape and size of the hole
produced in the dura. This hole is not simply the same size as the OD of the
needle.
5. Often there is a flap similar to that of an opened “tin can” whose lid has not been
completely removed.
6. This flap may move back into the hole, partially or totally preventing CSF escape,
eiven after puncture with large-bore needles.
7. Convenely, it is also possible to tear the dura, producing a large hole even with a
small needle.
8. The dura is made chiefly of collagen fibres and some elastic fibres.
9. The collagen fibers are oriented in diverse directions while the elastic fiber
generally run longitudinally.
10. The dura is also variable in its thickness (0.5 – 2 mm) in the same individual. The
thicker it is, the grater the retraction.
11. Of the hole, the typical “tin-lid” hole is produced by all needle tips with a cutting
edge.
12. When a non-cutting needle is used or when a cutting needle is inserted, With the
point parallel to the longitudinal fibres, an ellipsoidal hole is produced,
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compared to a more round hole when the needle top is at right angles to the
fibers.
13. Because the shape of the needle tip is besseved to be impontant to CSF leak,
several different typer ar available.
Types
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Chapter 10 COMPLICATIONS OF SPINAL
ANAESTHESIA& EPIDURAL ANESTHESIA
1. Hypotension > 25% (on < 90% in normotension).
2. Cardiac arrest
3. Respiratory failure
4. Failed spinal blockade
5. High or total spinal blockade (subdural injection)
6. Post dural puncture headache (PDPH) – nuchal rigidity
7. Backache
8. Neurological complications
a) Trauma to spinal cord
b) Cauda equina syndrome.
c) Spinal cord infarction
d) Space occupying lesion
e) Meningitis
9. Transient neurologic symptoms:
- Urinary retention (S2, S4)
Immediate complications – (1) to (5) + 9
Delayed or late complications (6) to (8)
1. Hypotension: treatment
2. Head down
3. I.V. fluid (preload 10-15 ml/kg)
4. O2 Ephedrine ( ) 10-15
5. Vasopressor therapy mg
Mephentermine
( , )
1. HTN treatment sodium Nitroprusside 30- 60gm NTG > 0.6 g.
2. Respiratory insufficiency; O2 therapy and ventilatory support.
COMPLICATIONS OF EPIDURAL ANAESTHESIA

Above 1 – 9 +
1. Epidural abscess.
2. Spinal or epidural hematoma.
3. Sub dural injection
4. Failed epidural blocks – unilateral block / segmental sparing / sacral sparing /
visceral pain.
Misplaced injections – intrathecal / subdural / intravenous injection.
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LA toxicity.
Differential block:
It is the existence of differential sensitivity of different types of nerves to the
blocking actions of local anesthetics. Etiology is multifactorial.
1. Frequency – dependence on local anaesthetic action means that even under basal
conditions different types of nerves with different frequencies of nerve impulse
transmission have different sensitivities to local anesthetics.
2. Duration of exposure of nerves to local anesthetic solutions alters perceived
sensitivity to local anesthetic action.
3. Most-investigators believe that axonal diameter is by itself, not a determinant of
nerve sensitivity to the blocking action of local anesthetics.
4. Results of in vitro studies of sensitivity to local anesthetics depend in part on
whether nerves normally sheathed remain intact or whether they have been
desheathed.
5. The ability to demonstrate differential sensitivity of nerves to local anesthetics
varies with the type of local anesthetic (amide or ester-linked) as well as within
the same type of anesthetic (eg. amide vs amide).
6. Local anesthetics block myelinated nerves at the nodes of Ranvier. Axonal
conduction block is produced only when several, not just one, nodes are exposed
to pharmacologically active concentrations of local anesthetics. Length of nerve
exposed to local anesthetic also therefore influences sensitivity to local
anesthetics.
Zone of differential T6 sympathetic blockade.
Blockade: T8 sensory blockade.
T10 motor blockade.
Differential blockade: Results in sympathetic blockade (judged by temp sensitivity)

that may be 2 segments higher than the sensory block (pain, light touch) which in turn
is 2 segments higher tha motor blockade.
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Chapter 11 POST DURAL PUNCTURE HEADACHE (PDPH)
Post spinal headache was first documented by August Bier in1899.
Any breach of the dura may result in PDPH – may follow
a) Diagnostic LP b) Myelograma c) Spinal anesthetic
d) epidural ‘wet’ tap e) Epidural catheter may pucture dura.
Incidence: The incidence is about 3-30%. In inadvertent dural puncture, during extra
dural block with Tuohy needle, has its maximum incidence of headache. The incidence
will vary according to size of needle used.
o 16 G needle - 24%
o 20 G needle - 14%
o 24 G needle - 6%
o 25 G needle - 3.5%
o 32 G needle - 1.4%
AETIOLOGY:
Low CSF pressure theory:
The pressure of CSF in sub dura space is 150 mm of H2O. But the pressure in the
lumbar epidural space is sub atmospheric. So some escape of CSF will invariably occur
after L.P. and will continue until the hole become occluded. It is calculated that average,
CSF leakage is about 10 ml/hr. This may lead to decreased CSF pressure as low as 50
mm of H2O. The healing of the dural puncture hole may take up to 3 weeks. So a large
guage needle and any thing which increases CSF pressure like pregnancy increases the
leakage and so incidence of post puncture headache. When the rate of leakage exceed
the rate of formation it results in change in hydrodynamics of the CSF. This lead to loss
of cushioning of the brain and pressure or traction on vessels and pain sensitive
structure like basal dura and tentorium, producing headache.
2) High CSF pressure theory: due to bacterial or chemical arachnoiditis
Differential diagnosis:
Coincidental headache: similar to previous headaches, not influenced by posture.
Spinal headache: postural relationship, occurs within 24-48 hrs of SA.
Equivocal headache: postural relationship, history of migraine type headache
Caffeine withdrawal headache: patients who consume / 200-400 mg/day abstienance
syndrome, develop with in 24 hrs; headache, sleepiness, iractivity and irritability.
Description: Headache is bilateral frontal or retro orbital, occipital extending into neck
– throbbing / coristant – association with photophobia and nausea / associaton with
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body position  aggravated by sitting or standing, relieved or lessened by lying down
flat.
Onset and duration: Soon after assumption of a head up position i.e. 12-72 hrs
following the procedure / duration  range from / day to 1 yr. usual period 4 days by
end of 1 week 75% will have subsided.
Severity classified into 3 categories.
Mild: Incidence 8%, no significant inconvienience, patient mobile, hydration +
analgesics / codeine – sufficient.
Moderately severe: incidence 3% some degree of inconvienience, only partially
mobile, does not like to recline.
Severe headache: incidence 2.3%, interruption of normal activity, prefers to
remain supine, treatment with blood patch.
Factors affecting PDPH:

1. Sex – Frequent in females – young females – nearly twice as in-men obstetric
deliveries SA 20% incidence.
2. Menstruation second part of menstrual cycle  lower freq (higher estrogen and
rising progesterone levels  H2O and salt retention).
Onset of menses and subsequent preovulation period  more frequent.
3. Age: 20-40 yrs  greatest frequency
4. After 50 yrs  sharp in incidence (higher pain threshold, physical sensitivity,
diminished elasticity of cerebral blood vessels).
5. Psyche: spinal taps done with great fan, many precautions and warnings 
headache incidence of 16%.
Spinal taps done with minimum staging – incidence of 4.5%.
Chronic migrane and headache sufferers prone to develop PDPH – SA avoided in these
patients.
1. Type of agent: No difference in incidence with procaine, tetracaine or dibucaine
or lidocaine or bupivacaine.
2. Size of needle: small needle make small holes. Less leakage with 25 guage
Quincke than 22 guage Quincke needle.
3. Type of needle: Whitacare pencil point or Greene conical needles produce less
leakage than needles that have a bevel with a cutting edge, Quincke – Bascock or
Pitkin needle.
4. Orientation of needle: A 22 guage needle parallel to longitudinal dural fibers
produces lesser leakage than when it is perpendicular to the dural axis.
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5. Angle of approach to dural puncture: Less leakage at an angle of 300 than at an
angle of 600 or 900.
6. Altitude: more frequent at high altitude than at sea level.
7. Enforced post-spinal bed rest. incidence, Barly ambulation recommended
practice with incidence. Avoid excessive strain.
8. Procedural factors hyperflexing the patient – streches dura – larger opening
incidence of PDPH.
9. Introducer for advancement of needle incidence of PDPH minimizes the
contamination of deeper structures and SAS.
Mechanism of PDPH: Imbalance in CSF dynamics.
- Continous loss of CSF occurs – rate of loss greater than rate of production. (30-50
ml loss critical point, 10 ml/hr loss).
o Diminished CSF – fall in spinal / CSF pressure – brain loses its “water
cushion” and sags especially in upright position – Traction on pain – sensitive
supporting structures including blood lessels.
- Stimuli from superior surface of tentorium cerebelli transmitted through V. CN.
- Pain in anterior part of head.
- Stimuli arising from below the tentorium and transmitted through IX and X. CN.
And upper 3 cervical nerve  pain in posterior part of head and nuchal region.
- Vascular component – to fill space backing in fluid, vasodilation of the
intracranial vessel occurs and is accompanied by perivascular edema – pain
stimuli arising from dilated vessels.
Prevention: Prophylaxis depends on a) proper care of patient b) minimizing spinal
fluid leakage c) maintaining normal CSF volume.
Recommendations: (1) Allay patients fear (2) Prelimnary hydration oral 2,500 ml/day,
parenteral if needed (3) Use fine guage needles 24 or smaller (4) Use of needle
introducer (5) Spinal needle bevel parallel to longitudinal dural fibers. (6) Expeditious
performance of tap without fan fare. (7) Encourage early ambulation (8) Maintain CSF
volume – equalizing any general loss and maintaining TBW. 9) cough and straining
should be avoided
Treatment: Aimed at restoring normal CSF dynamics. Conservative measures are
Psychological support and positive reassurance.
Confinement to Bed – Head down positin.
Application of Ice bag to head.
General body hydration – oral / I.V.
Sedation and / or analgesia: chloral hydrate, sod amytal asprin codeine.
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Caffeine sodium benzoate 0.5G iv/im (effective in 70-75 % patients, caffeine
causes marked cerebral vasoconstriction).
Cardiovascular stimulants: Ephedrine sulfate 50 mg .iv, Amphetamine sulfate 5-
10 mg TID, Ergotamine tartrate orally 1mg.
I.V. fluids – dext 50% - 5ml every 6-12 hrs, 5% DW infusion
O2 inhalation
Abdominal compression – toraise peridural venousplexus and thus increase CSP
pressure.
Special therapeutic measures:

1. Subarachnoid saline injections: small guage needle inserted 5%glucose, -
physiologic saline solution introduced in 5ml fractions 15-20 ml restores normal
CSF pressure, relief immediate but short with recurrences risk of second dural
puncture.
2. Peridural saline solution injection performed at site of original puncture, caudal
injections are also effective, relief short lived.
3. Epidural blood patch: first proposed by Gromely in 1960 seals holes or defects
in spinal dura by means of a blood clot “patch”.
- Patient positioned – lumbar area aseptically prepared for epidural puncture.
- Venous blood (10-20 ml) withdrawn from antecubital vein.
- Epidural puncture performed – at original puncture.
- Epidural space identified – autologous blood is slowly injected and needle
removed.
Optimal volume of blood – 10 ml is critical (89% relief). volumes of 12ml or more( 12-
15ml) recommended in adults 96-98% relief.
Rate of injection is – 10 seconds for 10 ml.
1. Patient kept supine for 1 hour.
2. Thereafter movement and ambulation are encouraged.
Epidural spread of blood: spreads homogenously in all directions away from point of
needle – more so cranially extends over 7 to 14 segments. Caudal spread stops at S1 –
S2, cephalad spread between T5 and L1.
Mechanism of relief (1) Immediate “pressure effect” – compresses dura mater –
decrease SAS pressure and restores CSF dynamics. Saline – 15 ml blood – 10 ml critical
volumes. (2) “Sealant effect – 2 to 4 days injected blood forms gelatinous patch in area
of original spinal dural puncture allowing healing of puncture hole.
Other uses (a) after myelography (b) chronic headache.
Adverse responses: Possibility of bacterial contamination, backache, neckache,
vestibular and cerebellar disturbances and nerve root compression.
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Chapter 12 TOTAL SPINAL ANAESTHESIA
1. Total central neurological blockade.
2. This is one of the major hazards to be encountered in performing epidural
anaesthesia.
- It can also occur during interscalene block of Brachial plexus.
- Incidence for the epidural  1 in 1000 cases.
- It is the result of unrecognized spinal puncture and the infection of large
volume of anaesthetic solution  during epidural anaesthesia.
- It usually comes on soon after injection. It may be delayed for 30-45 mins.
Signs and symptoms.

1. Profound bradycardia  because of total sympathectomy and relative increase
in vagal tone.
2. Profound hypotension 
- Vasodilation of capacitance vessels.
- Decrease venous return to heart and
- Decrease systemic vascular resistance
3. Apnoea  for considerable time blockade of C3 – C5. Phrenic nerve block
(Diaphragmatic paralysis).
4. Dilated pupils  due to sympathetic blockade.
5. Loss of consciousness
6. Motor blockade – muscle paralysis.
It can be avoided by:

I. Careful technical application.
II. Aspiration for spinal fluid.
III. Test dose
IV. Incremental doses
Management:
- Turn the patient into supine position.
- Trendelenburg’s position  elevate legs.
- Ventilate with 100% O2.
- It is impt to ventilate the patient by mask before proceeding to ETT intubation.
- If ventilation with 100% O2 by mask is very difficult (or) imposible  rapid
intubation.
- No muscle relaxant (or) hypnotic agent necessary.
- Intravenous fluid blous.
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- Vagolytic dose of atropine  2 – 3 mg.
- Ephedrine  10 – 25 mg.
- Epinephrine  10 – 100 g.→ If hypotension (or) bradycardia not resolved.
- Surgical procedure 
Continued
- Airway is secured
- Hemodynamic response managed and patients is stable.
- Postponed
If there is doubt about hemodynamic (or) CNS status of patients.
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Chapter 13 CAUDA EQUINA SYNDROME
Conus medullaris syndrome:
Cauda equina:
The spinal cord extends normally from foramen magnum to the level of L 1 in adults. In
children the spinal cord ends at L3 but moves up as they grow older.
Anterior and posterior nerve roots at each spinal level join one another and exit
the intervertebral foramina forming the spinal nerves from C1 to S5.
At the cervical level, the nerve arise above their respective vertebre. But starting
at T1 they exit below their vertebrae. But starting at T1, they exit below their
vertebrae. As a result, there are 8 cervical nerve roots but only 7 cervical
vertabra.
At the cervical level and upper thoracic level, the roots, emerge from the spinal
cord and exit the vertebral foramina nearly at the same level. But because the
spinal Cord normally ends at L1, lower nerve roots must travel an increasing
distance from the spinal cord to the interveltebral foramina. These lower spinal
nerves form CAUDA EQUINA. (Horse tail)
Cauda equine syndrome:

Is characterized by (a) urinary and fecal incontinence coupled with. (b) localized
sensory loss in the perineal area with varying degrees of (c) leg weakness due to injury
to cauda equine.
Aetiology: As a rare complication of spinal anaesthesia.
a. Use of microcatheter for repeated dose / continuous infusion of subarchnoid
local anaesthetic.
b. Pooling (maldistribution) of hyperbalic solutions of lidocaine.
c. Neurotoxicity due to chlorprocaine.
d. Damage to conus medullaris
e. Direct injection of local anaesthetic to spinal cord.
f. Accidental injection of alcohol into spinal cord during intrathecal administration.
g. Detergents used clear disposable syringes and their contaminants.
Precautions:
Following are recommended to decrease maldistribution and neurotoxicity of local
anaesthetic:
1. Decreasing dose of lignocaine < 60 mg.
2. Avoid repeated doses
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3. Decreased lidocaine concentration to 1.5%
4. Use of isobaric solutions.
5. Diluting L.A. with aspiration of C.S.F.
6. Substituting bupivacaine for lignocanie / whichever possible.
7. Avoid spinal epinephrine.
Clinical features:
Bowel and bladder dysfunction.
LMN type of injury with peresis of logs.
Anaesthesia in posterior thigh, saddle / great toe perineal area.
Pain characteristic of nerve root compression.
It is suspected, when for fails to regain sensory and motor power within usual
time after spinal anaesthesia
Return of function is usually slow over several months or these effects may be
permanent.
Tidal drainage is recommended as an early form of therapy.
D/D:
Transverse myelitis
Surgical manipulations
Difficulties in evacuation while inbed
Disc prolapse
Tumors or hematomas
Investigations for diagnosis

I. Previous records
II. CT/MRI of spinal cord
III. Myelogram
IV. CSF examination
V. Histology to r/o other systemic disease. (auto antibodies)
Treatment:
1. Bed rest with passive muscle activity.
2. Steroids and antibiotics.
3. Physiotherapy
4. Care of bowel and bladder
5. Surgery if hematoma / tumor
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Chapter 14 DETECTION OF EPIDURAL SPACE
Negative pressure techniques:
a. Hanging drop sign: After the needle has been introduced to the level of
resistance indicating the beginning of ligamentum flavum, a small drop of sterile
distilled water is placed on the hub of the needle. When needle is advanced
through lig flavum  drop will be “sucked into” epidural space.
b. Capillary tube method – odom devised a small capillary tube filled with sterile
saline in which 1 or 2 bubbles of air were placed. These acted as meniscus. As
needle enters epidural space, saline sucked in, and air bubbles advanced into
space.
c. Manometer technique – small ‘U’ shaped glass tube about 3 to 4 inch hieght is
used as a H2O manometer. As the needle advances into the intraspinous lig. the
sterile glass manometer is attached. As it advances into the epidural space –
immediate movement of liquid signifying negative pressure.
1. Lower lumbar area  0.5 cm H2O or less
2. Upper lumbar area  2.0 cm H2O
3. Lower thoracic area  2.0 cm H2O
Disappearance of resistance technique:
1. Syringe technique: Sicard and rorester in 1921. Sudden loss of resistance to a
pressure exerted on the plunger of a syringe filled with H2O.
2. Spring – loaded technique – (Visual technique) when epidural space is entered,
syringe automatically unloaded itself by virtue of the diminished resistance in
the space syringe is heavy.
3. Balloon technique of macintosh – small light balloon mounted on a glass adapter
is attached to the needle when it reaches lig flavum. Balloon inflated with 2-3 ml
of air. As needle advances and penetrates into epidural space balloon collapses.
(Pressure 50 mm Hg).
4. Books device – (Visual technique) odom’s indicator / capillary tube sealed at one
end filled with water or saline and few bubbles are placed in tube part. Attached
to epidural needle when it reaches lig flavum – bulb is heated to create a slight
positive pressure. Needle penetrates epidural space – meniscal bubble advances
into epidural space.
5. Vertical tube of Dawkins – (Visual technique)
A slight positive pressure is created by a short vertical column of H2O in tube less than
10cm high-connected at right angles to needle a bubble of air also may be placed in H 2O.
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Force of gravity on the column of H2O produces pressure. When epidural space is
entered the level of column of H2O drops indicating disappearance of resistance.
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Chapter 15 IVRA (in short)
1908  Bier, local anaesthetic introduced intravenously.
1908  Ramsohoft, introduced agent intraarterially.
Mechanism:
Local anaesthetic administered intravenously have direct action on blood vessel
walls causing vasodilatation.
These agents diffuse into tissues and produces anaesthetic block to small nerve
fibers and nerve trunks.
Greater localization seen towards traumatised tissues (8-10 times)
Indication:
- Below elbow and below knee operations.
- Tendon operation, hand abscess, FB removal, colles fractures, carpal tunnel
release.
- Elderly and children ASA I, II, III
Technique:
- Reassurance to the patient
- I.V. canula is inserted (in the distal vein to operative site).
- Production of ischaemic limb
- Exsanguniation
- Gravity (elevation of limb 2-3 mins)
- Esmarch bandage (distal to proximal)
This enhances the effectiveness of technique. This ischemic period will decrease the
amount of LA.
Tourniquet application:
Cuff placed proximal end of surgical site and inflated 50-100 mg Hg above systolic
pressure. Never deflate cuff 20-30 mins have elapsed ofter injection of LA. No cuff
should be placed > 2 hrs.
Holemar introduced two cuff technique, a second one is placed just distal to primary
one.
Tourniquet discomfort of 1st cuff may be due to tightness and it can be alleviated by
subcutaneous infiltration or appliying a 2nd tourniquet.
Injection of a dilutent solution of LA through the cannula, usually used is
lidocaine (2 hrs).
Bupivacaine (contraindicated because of risk of cardiac toxicity).
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Rapid and intense analgesia  tetracaine.
Prewarming of LA upto 300C lessens patient discomfort.
Ketamine  40 ml of 0.5% limited use (development of unconsiousnes with in
few min).
Pentazocine + pancuronium potentiate action of LA.
Dosage:
A volume dose relationship is involved.
Procaine or lidocaine 1.5 – 3 mg/kg.
Upper limbs 3mg/kg of 0.5% (40-50 ml)
Lower limbs 3 mg/kg of 0.25% (80-100 ml)
Blood volume of upper limbs 3% of total blood volume.
Blood volume of lower limbs 9% of total blood volume.
Responses:
Pale skin  excellent exanguination (Cutis marmorata)
Successful blocks  Complete sensory block.
 Motor paralysis of extremity
 Absence of subjective complaints
 Desirable that patient awake and responsive
Kinetics of distribution of drugs:

Venous system  peripheral superficial veins and fills large superficial veins 
small veins of muscles  deep veins  perforating veins  retrograde filling of venules
 capillaries  extravascular space by diffusion  tissues.
Largest concentration  nerve tissue.
The amount of drug that enters the general circulation on release of tourniquet depends
on
a. Concentration of agent
b. Volume injected
c. Duration of regional vascular containment
When nerves are considered, the fibres for distal distribution are blocked first so that
anaesthesia develops from the finger tip upwards.
Release of tourniquet:
Planned cyclic intermittent release of tourniquet:
Deflation of tourniquet to zero and immediate reinfflation.
After 1 min, 2nd deflation to zero for 10 sec then reinflation.
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After 2 min, 3rd deflation to zero for 30 sec and reinflation.
After 3 min, last deflation to zero and no reinflation.
During deflation we see complaints such as
a) Buzzing b) Dizziness c) Metalite taste
Recovery:
After complete release of tourniquet.
Return of sensory nerve function  1-5 min
Anaesthesia seldom present after  10 min
Reactions occurs when LA enters general circulation
Release of tourniquet too early
Release of proximal cuff when distal one in not fully inflated.
Adverse effects:
CNS: Temporary dizziness, nystagmus, drowsiness, mild seizures and convulsions.
EEG: reduction in alpha activity
Increase in low frequency.
High amplitude waves.
ECG: Mild bradycardia
Decrease in ‘T’ wave amplitude
Effect of NMJ: LA produces a definite pre-junctional block and a curare like attachment
to cholinergic receptors at the muscle end plate.
Advantage: Simple, rapid recovery, rapid onset, muscular relaxation and controllable
extent of anaesthesia,patient awake, oral feeding can be allowed, early ambulation.
It is excellent technique for most procedure (< 90 mins) both for open and closed
reductions of bony fractures.
Complications:
- Toxic reactions after release of tourniquet
- Post operative pain due to rapid recovery
- Tourniquet pain
- Restricts surgery time because of tourniquet
- Oozing of LA into the surgical field of large volume used.
- Nerve injury at edges of tourniquet
- Neuroapraxia
- Axontemesis
- Neurotmesis
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Lower extrimity Beir type blocks (Lehman Jones Block):
A failure rate of about 15% occurs with thigh tourniquet technique. A large volume of
drug is needed and because the concentration is low to use with in 80 ml dose range the
anaesthetic block is often incomplete.
IVRA: - Upper limb – Bier’s blow
- Lower limb – Lehman Jones Block
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Chapter 16 EPIDURAL ANAESTHESIA (in short)
Epidural anaesthesia (peridural or extradural) is anaesthesia obtained by blocking
spinal nerves in the epidural space as the nerves emerge from the dura and then pass
into the intervertebral space foramina.
- Anaesthetic solutions are deposited outside the dura.
- Segmental block – spinal sensory and sympathetic nerve fibers.
- Motor fibers may be partially blocked.
1. Thoracic epidural block or thoracic segmental epidural anaesthesia.
2. Lumbar epidural block or spinal epidural block
Perineal or extremity surgery – 15 ml
Lower abdominal surgery – 20 ml 2% lidocaine
Upper abdominal surgery – 20 ml
Caudal epidural block or caudal anaesthesia sacro coccygeal ligament.
Peridural space:
- Circular space surrounding the dural sac and all its extensions.
- Extends from foramen magnum to coccyx.
- Upper limit foramen where the periosteal layer of spinal vertebral canal fuses
with dural layers.
- Lower limit: sacro coccygeal ligament.
- Posteriorly: more extensive and distensible
- Anteriorly: dura adheres closely to the periosteum of vertebral bodies.
- Lateral: intervertebral foramina and peduncles of verlebrae.
- Potential space – arleolar tissue, fat and spinal nerve roots spinal arteries, and a
capillary network forms a rich venous plexus.
- “Plica mediana dorsalis” of the dura mater connects dura to lig. flavum in
midline.
Midline suggital plane – following structures are penetrated

1. Skin subcutaneous tissues.
2. Supra spinous ligaments
3. Inter spinous ligaments
4. Ligamentum flavum
Epidural space (mm) Thickness of dura (mm)
Cervical 10 – 15 2.0 – 1.5
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Lumbar 5.0 – 6.0 0.66 – 0.33

Overall median distance in normal adult female patients is 4.7 cm at L3 – L4 level.
Factors altering depth:

a) Weight
b) Technique – loss of resistance closer than nanging drop.
c) Angle of needle
d) Position of patient
e) Edema
f) Ethnic origin.
Thoracic  1 to 3 cm H2O (2 cm H2O)
Lower lumbar  0.5 cm H2O
Upper lumbar  1.0 cm H2O
Negative pressure:
- Cone theory – tenting of dura
- Transmission theory – intraplueral negative pressure transmitted through
intervertebral foramina to peridural space.
Described in 1928 by Heldt and Moloney.
Greatest in patients with firm attachments
Greatest at thoracic region
Less in lumbar area
Least or absent in sacral area
Factors that increase negative intra pleura pressure and decrease CSF pressure
 increase negative extra dura pressure.
Marked flexion of spinal columin.
Site of action:
1. On the nerves as they traversal the epidural space.
2. On the nerves as they pass out thru the intervertebral foramina.
3. On the nerves in SAS – by diffusion through dura.
Sensory anaesthesia of all modalities complete sympathetic fibers block partial motor
block incomplete.
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FATE OF EPIDURAL AGENTS.
Epidural injection
Longitudinal spread in epidural space
Leakage by Leakage thru Diffusion thru Diffusion thru

vascular intervertebral dural root dura mater
absorption foramina sleeves
BIPHASIC
Paravertebral block Subdural spread
of nerve trunks
Initial or Slower
rapid absp. absps
Centripetal sub- Spinal root block
Phase phase
perineural spread
CSF
Sub pial spread Peripheral cord block
Factors in extent of EA:

Volume x Force x time
Dispersion = + gravity
Resistance of tissue
1. Volume of solution (10 ml will diffuse over 6-8 segments).
2. Selection of appropriate interspace.
3. Speed of injection – slower rates decrease spread
4. Position of patient
5. Effect of gravity
6. Specific gravity of anaesthetic agent
Detection of epidural space:

Negative pressure techniques Disappearance of resistance technique
1) Hanging drop sign 1) Syringe technique
2) Capillary tube method 2) Spring – loaded syringe
3)Manometer technique 3) Balloon technique
4) Brooks device
5) Vertical tube of Dawkins
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Volume capacity of epidural space:
Volume of solution required for an epidural anaesthestic depends on
- Site of injection
- No of segments to be blocked
Capacity of the lower part of peridural space is larger.
Per segment volume of anaesthetic solution necessary in sacral and lower
lumbar region is greater than in thoracic region.
Segmental dose – “dose spread” vol of analgesic solution injected in ml/no of
dermatomes blocked.
Or
Ml/spinal segment.
Cervical  1.5 ml (each pair of spinal segments)
Thoracic  2.0 ml
Lumbar  2.5 ml
Single injection – 15 to 20 ml
Continous technique – initial dose 8 to 12 ml later 5 to 7 ml every hr.
Poor risk, frial or very old patients – dose volume halved.
Volume of Extent of
Type of surgery Space
injection (ml) anaesthesia
Perineal L3 – L4 10 – 12 4–6
Extremity L2 – L3 12 – 14 8
Lower abdominal L1 or L2 14 – 16 10
Upper abdominal T2 or L1 16 – 18 12
Thorancic T12 20 -22 14
Influence of age on absorption:
Elderly patients:
a. Peak serum level of anaesthetic agent is increased.
b. Time to C5 max is significantly reduced
c. Slower onset of block
d. Increase hydrostatic pressure with age.
Principal determinants of dosage:

1. Volume of anaesthetic solution
- Age / segment factor
- Height factor
2. Selection of interspace
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3. Spread of solutions
4. Speed of injection
5. Position of patient
6. Extra dural pressure and compliance factors of epidural space
7. Sp. gravity of anaesthetic solutions
8. Clinical modifying factors
- Obstetric patient  decrease dose vol by 30%.
- Abdominal distention or extremely obese.
- Arterioscterosis decrease dose vol by 50%.
- Anatomic factors – elderly.
9. Volume of anaesthetic solution
Age/sex factor:
From 4years to 18 years  steady increase from 0.2 to 1.0 ml/seg
20 – 40 years  1.0 to 1.6 ml / seg (plateau)
40 years – 60 years  slight decrease 0.5 to 1.0 ml/seg
> 60 years  0.3 to 0.6 ml/seg.
Height factor – 5 ft (150 cm)  1.0 ml/seg.
6 ft (180 cm)  1.6 ml/seg.
5 ft  + 2 inches (5 cm)  + 0.1 ml/seg.
Selection of interspace:
2nd most important factor
Site of injection should correspond as closely as possible to the middle of the
area to be anaesthetized.
Spread of solutions:
Spread symmetrically to both sides (sitting / lateral position)
Most intense and carliest onset of block at site of injection.
Spread is related 2 anatomic factors
1. Size of epidural space
2. Size of nerve roots
Onset of anaesthesia at L5 and S1 and also other sacral segments – delayed,
intensity and duration – less. (Nerve roots are larger than at other segments).
L1 or L2 lumbar epidural – spread both caudal and craniad L4 T8 equal in the
onset of blockade.
Speed of injection:
- More rapid the injection wider is its spread.
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- Recommended rate of injection 0.5 to 0.7 ml/sec 1.0 ml/1.5 sec is optimal.
- Fast (1.0 ml/sec or more) injection
- Increase ht of dermatome / block
- Discomfort on injection
- Hypobaric activity
- Drainage thru azygos system
- (Bypasses liver) SVC  heart cardiac effects dramatic)
Position of patient:
Epidural space is a potential space, and solutions do not readily flow in this space
because of low compliance, hence gravitational influences minimal.
Lateral position: then to supine  little different in spread or onset of block onset of
sympathetic blockade is olightly more rapid on dependent side.
Retaining lateral position: Intense anaesthesia on dependent side for relatively major
block – approx 15 minutes.
Sitting position:
Obese patients
Perineal anaesthesia
Upper thoracic and cervical region block.
Prone position: cervico-thoracic block with head flexed to chest.
Extradural pressure and compliance factors of epidural space:
- Pressure in epidural space is a specific determent of sprend.
- Pressure is determined by
a. Epidural venous pressure
b. CSF pressure
c. Amount of connective tissue and fat in space.
Breathing pattern: Increase inspiratory negative pressure transmitted to epidural
spread increase cranial spread of solutions.
Specific gravity of anaesthetic solutions:
- Has limited influence as gravitational influences are not a major factor.
- Bupivacaine – dissolved in 10% dextrose and plain bupivacaine – overall
dermatomal spread is similar.
- Rate of injection determine whether sol. Behave as a hyper or hypobaric mixture.
Rapid rate  hypobaric activity.
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Clinical modifying factors:
a. 2 imp clinical conditions require a downward adjustment in dosage
b. Obstetric patient – dose vol. – decrease by 30% (decrease in size of epidural
space from distension of epidural veins – venacaval compression in supine
bosition).
c. Abdominal distension or extremely obese – decrease dose by 30%.
d. Arterioselerosis and / or occlusive vascular disease – decrease dose by 50%.
e. Early diabetes when widespread angiopathy of arterioles.
Anatomic factors – aging process.
With advancing age – the intervertebral foramina are progressively occluded  limits
ontwards spread of solutions  greater vol available to spread in peridural space.
- Dose volume should be reduced in older patients.
- Connective tissue changes – increase permeability of connective tissue.
Complications: - Subarachanoid injection results in unconsciousness.
- Haematoma formation.
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Chapter 17 - CAUDAL EPIDURAL
INTRODUCTION
Caudal epidural analgesia is a popular technique for obtaining pain relief after
urogenital and lower abdominal surgeries. It can be performed after induction of
anaesthesia before surgery, for intraoperative analgesia or anaesthesia or just at the
end of the surgery for postoperative analgesia. Ambulation is faster than any other
conventional techniques.
The single shot caudal blocks are commonly used for ambulatory
procedure; continuous catheter techniques for inpatients undergoing more
extensive procedures.
Advantages of caudal procedure are:

1. Technical simplicity, reliability, safety and rapid performance
2. It permits maintenance of anaesthesia with lower concentration of vapor
anaesthetics.
3. Permits rapid, comfortable recovery from anaesthesia
4. In many cases, use of spontaneous breathing with near normal end tidal CO2 and
minute ventilation are obtained.
5. It reduces the need for endotracheal intubation.
6. May facilitate early discharge from post anaesthetic care unit.
The discovery of caudal epidural analgesia or sacral analgesia, antedated the lumbar
approach by several years; but the technique has not enjoyed consistent popularity and
has been constantly compared with central neural blockade induced at higher level by
both lumbar epidural and subarachnoid spinal techniques.
The reasons for these being

1. There is considerable variation in anatomy near the sacral hiatus, and the bony
sacrum
2. Another reason is also anatomic, relating to the dermatomal distribution of nerve
roots; the site of entry hiatus is at the exit of most terminal nerve roots.
In the lumbar region, spread of anaesthetic solution can occur both cephalad and
caudal, giving rise to wide dermatomal distribution of anaesthesia. Clearly, with
caudal entry, spread can only be cephalad and may be limited by minor bony
obstruction, with the result such that the total number of segments blocked is
bound to be less. To achieve a wide distribution of anaesthesia, predictably with
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marked cephalad spread of solution, a large dose of local anaesthetic drug is
required and there is a risk of drug toxicity.
Some cases are very easy, but cases can be difficult and an overall technical
failure rate of 5-10% is to be expected with experience.
There is an obvious advantage in caudal when compared to lumbar epidural, in
that lumbar epidural analgesia spreads upwards more easily than down wards,
the reluctance to pass the lumbosacral junction is associated with relatively poor
analgesia of L5 and S1 segment subserving the outer border of foot and ankle
unless higher percentage of local anaesthetic agents are used. The alternative
approach to the extradural space through sacral hiatus has the advantage that it
gives precedence to these obstinate segments and allows injected local
anaesthetic solutions to bath the sacral nerves before extending upwards to
areas that are more easily reached by lumbar epidural route.
HISTORY
1901 – Cathelin and Sicard in Paris developed the technique of caudal epidural
injection.
1909 – Stoeckel of Marbug, Germany used caudal injection in obstetrics
1910 – Lawen used caudal injection in lower abdominal surgeries
1940 –Continuous caudal technique was done by Hingson and Edwards. The
result was most gratifying and continuous caudal analgesia was introduced to
relieve pain during labor. They further demonstrated that the level of spinal
segment block through the caudal approach could be raised by increasing the
volume of injected solution.
1942 – First report by Edwards and Hingson on continuous caudal anaesthesia,
Hot Springs, Virginia, September 1942.
1943 – Continuous drop method of caudal analgesia was introduced by
Block.
1943 – Adams, Lundy and Seldon proposed the use of ureteral catheter
instead of malleable needle and this is most practical and efficient
technique.
ANATOMY
The key to success in any regional anaesthetic technique is a clear understanding
of the normal anatomy. This is possibly most relevant to the success of caudal block.
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Wide variation of normality in the region can readily lead the unwary into needle
misplacement; which will result in failed block.
The typical sacrum is a triangular shaped bone dorsally convex formed by
gradual fusion of the lamina of the 5 sacral vertebral segments, which is completed by
the 20th year of life. The bone articulates cephalad with the 5th lumbar vertebra and
caudad with coccyx.
The concave anterior surface is smooth and in part supports many important
structures such as the iliac vessels, rectum and fetal head. This surface features four
pairs of large anterior sacral foramina that are formed consequent to the fusion laterally
of the transverse process of the sacral embryologic segments and provides passage
from the midline sacral canal for the anterior rami of the upper four sacral nerves. The
anterior sacral foramina are typically unsealed and provide a ready passage for escape
of local anaesthetic solution injected into the sacral canal.
The clinically important dorsal surface of the sacrum is variably convex and
irregular with important prominences representing the fused element of sacral
vertebra. In the midline, there is a median crest with three or more, but commonly four
variably prominent tubercules representing the sacral spinal process. Lateral to this
crest and medial to the four posterior sacral foramina is the intermediate sacral crest
with a row of four tubercles, representing the upper four sacral articular processes.
The posterior sacral foramina are smaller than their anterior counter parts and are
sealed effectively by multifidus and sacrospinal muscles.
The sacral foramina’s:

The first foramen is 0.5cm from midline and 2.5cm above the level of the
posterosuperior iliac spine, while the fifth foramina is expected to be 1cm from the
midline. The third foramina is commonly the largest.
Communicating with the foramina are the intervertebral canals connecting with the
spinal canal.
The shape of the sacrum varies with age, sex and race. The remnants of the S5 inferior
articular process are free and prominent and flank the sacral hiatus. They constitute the
sacral cornua, and together with the adjacent coccygeal cornua, which they abut, are key
landmarks for identification of sacral hiatus.
The sacral transverse process give rise to a variably raised lateral sacral crest with
transverse tubercles, the most caudal of which occurs where lateral border of sacrum
deviates more medially at the inferior lateral sacral angle. This is clinically important
because it may be confused with one of the cornua.
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Coccyx:
The coccyx is a small triangular bone consisting of 3 to 5 fused rudimentary
vertebrae, it attaches by means of its upper articular surface to the lower articular
surface of the sacrum. It has two prominent coccygeal cornua that abut their sacral
counterparts.
Sacral hiatus:
It is a defect in the lower part of the posterior wall of sacrum, formed by the
failure of the laminae of S5 and usually part of the S4 to meet and fuse in the median
plane. This leave a space of variable dimensions, often described as being like an
inverted U or V, which is covered by the thick fibrous posterior sacrococcygeal ligament,
part of ligamentum flavum.
Penetration of the sacrococcygeal ligament by a needle yields direct access to the
caudal limit of the epidural space in the sacral canal. It is in this area that there is
considerable variation in normal anatomy. Anatomical studies shows following
findings.
1. The hiatus varies widely in size and shape from normal inverted U or V to
longitudinal or horizontal slits.
2. Sometimes the apex of the hiatus lies higher than the lower 1/3rd of S4.
3. The distance between the tip of dural sac and the apex of hiatus is 2cm – 6cm
usually 4cms. In some cases the dural sac may extend below S2.
4. There is atleast one recorded case of dura directly underlying the hiatus at a
distal level.
5. The hiatus is absent in upto 8% of specimen
In order to predetermine cases that are anatomically unfit for caudal analgesia, X-ray
studies may be carried out. A simple AP view to determine the level of apex and a lateral
view using laminography will reveal significant anatomical defects.
The sacral canal and its contents:

The sacral canal is the continuation of the vertebral canal through the sacrum. It
is curved like the bone and is 3-4 inches long. A cross section of the canal reveals
triangle shape. It communicates laterally with the anterior and posterior sacral
foramina. Inferiorly it terminates at the sacral hiatus. The volume of sacral canal,
including the sacral foraminal extensions vary between 10 to 65ml averaging 30-35ml.
The canal contains

1. Terminal part of dural sac, ending at S2, on a line joining the posterorsuperior
iliac spines.
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2. The 5 sacral nerve roots and the coccygeal nerves.
3. The sacral epidural venous plexus.
4. Filum terminale.
5. Loose areolar fat
6. Lymphatics.
Sacral and Coccygeal nerves:

These give rise to the following nerves –
Posterior cutaneous nerve of thigh,
Perforating cutaneous nerves
Pudendal nerve
Anococcygeal nerves,
Pelvic splanchnic nerves
Various muscular branches
These relay total sensory input from vagina, anorectal region, floor of perineum, anal
and bladder sphincters, urethra and scrotal skin and parts of vulva, penis and a narrow
band of skin extending from the posterior aspect of gluteal region to the plantar lateral
surface of foot. Pelvic organs like uterus, Fallopian tubes, bladder and prostate are
additionally supplied by preaortic and sacrococcygeal nerve groups. Although
unsupplemental caudal blockade may not provide full pain control for surgery on these
structures, it can provide a major component of the combined anaesthetic sequence.
Physiology
The actual site of action of the local anaesthetic is in the intervertebral foramen
where the spinal nerve loses the protective dural sheath.
Anaesthesia usually is first noted on the buttocks about the sacral hiatus. Loss of
sensation proceeds over the buttocks and up the sacrum. It usually occurs after 5
minutes and indicates successful injection. Pain is the first modality of sensation to be
lost, followed by touch and temperature. Pain is usually lost two segments higher than
touch loss. Motor fibers are affected last and some loss of function appears in 10
minutes. Both maximum extent and intensity of anaesthesia is reached in 20 minutes.
Besides the sensory and motor block of sacral roots, one could expect a degree of
autonomic block. The sacral component of the parasympathetic craniosacral outflow
(the pelvic splanchnic nerves) will be blocked, causing loss of visceromotor function in
the bladder and bowel distally from the splenic flexure of the colon. Theoretically there
will be an increase in anal and bladder sphincters tone, but this not seen because of
coexisting sympathetic block. Its always higher than the sensory block. Pooling of
blood in the denervated lower limb and reflex vasoconstriction in the innervated upper
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limbs has been shown to occur. But if an extensive caudal block occur, all consequences
of a high epidural anaesthesia should be expected. These are –
CVS Changes:
1. Hypotension
2. Bradycardia
Respiratory system: Respiration is not affected to that extend by caudal anaesthesia.
Endocrine system: No changes in ACTH, immunoreactive beta-endorphins, ADH,
cortisol, catecholamines, insulin and GH levels.
INDICATIONS
Caudal anaesthesia can be given either as a sole anaesthetic technique or
combined with GA. Operations such as haemarrhoidectomy, anal dilatation,
circumcision when performed under GA alone, can induce laryngospasm and marked
cardiovascular changes, and can be combined with caudal epidural anaesthesia.
Caudal block performed before surgery allows lesser amount of muscles
relaxants and drugs during GA. Post operative analgesia can be provided.
In Paediatrics:
Caudal anaesthesia has been used successfully in children since 1960’s. It is in
this grocy that the caudal technique was found with greatest application. In children, the
sacral hiatus is usually easily palpable, making the procedure simple, quick and reliable.
By the age of 4 to 5 years, the sacral canal is usually large enough to accept 18guage,
thin walled needle for passage of a catheter. In summary, the surgical indications for
the block can be divided into three groups.
a. Sacral block e.g. Circumcision and anal surgery
b. Lower thoracic block e.g., inguinal herniotomy
c. Upper thoracic block e.g., orchidopexy
Middle and upper abdominal surgery is not an indication for conventional caudal
block although, thoracic epidural anaesthesia in children has been achieved with a 24
guage epidural catheter inserted through sacral hiatus. Since young children do not
tolerate the frightening environment of the operating room, GA seems to be the
preferred technique for both induction of caudal block and through out the surgery. In
those patients in whom GA or sedation is not desired Eutectic Mixture of Local
Anaesthetic (EMLA) cream under adhesive plaster can be applied to the skin over the
sacral hiatus 1 hour prior to the procedure.
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Low birth weight and preterm or former preterm neonates constitute a high risk
group of patients for whom the use of regional anaesthesia can obviate the need for GA.
and minimize respiratory complications.
A specific indication for caudal is children is with congenital dystrophia
myotonica. Regional anaesthesia enables the anesthetists to avoid the respiratory
depression associated with GA and minimize use of opiates and muscle relaxants.
Relief of pain in the early postoperative period is probably the major advantage
of caudal anaesthesia in children. Central venous pressure remains low under a
combination of caudal block and general anaesthesia and hence there is minimal
intraoperative bleeding.
In Adults:
Caudal blockade can be used wherever the area of surgery is primarily
innervated by the sacral and lumbar nerve roots. The following procedures are
appropriate indications
Haemorrhoidectomy and anal dilatation.
Vulvectomy.
Circumscision, amputation of penis.
Surgery of lower limbs including amputation, skin grafting debridement etc.
If a caudal catheter is used with its tip positioned higher in the canal, a higher
level of anaesthesia can be assured and more extensive surgery accommodated such as
vaginal hysterectomy and inguinal herninorrhaphy.
Also, postoperative pain following perineal surgery under GA may be relieved by
caudal blockade carried out in the recovery ward.
In Obstetrics:
Caudal analgesia is used for labor analgesia still today. It can also be use for
LSCS
Cervical stitch
Forceps delivery
Advantages:
Pain relief
Most studies showed that caudal anaesthesia has little effect on motor power of
uterus in labor because of higher innervations from T4 and T5.
The cardiovascular changes in labor including tachycardia and increased cardiac
output are minimized.
Decreased blood catecholamine levels
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Decreased chances of deep vein thrombosis
Early ambulation
Disadvantages:
The pathways of pain for 1st stage of labor are by way of T10-L1. Thus a technique that
initially and predominantely block sacral roots are less effective for early labor.
Large doses of LA drugs are required.
All drugs administered to the mother eventually cross the placenta and find their way
into the fetus to a greater or lesser degree. High fetal concentration of LA with opiod
make for a ‘floppy baby’. The caudal route requires more than twice as much LA as does
the lumbar route to achieve adequate analgesia in 1st and 2nd stage of labor.
There is still a place for continuous caudal analgesia in labor in those cases in which
lumbar epidural analgesia is contraindicated because of anatomic abnormalities, or
localized infection. On occasion, sacral analgesia is required either early in labor or
cannot be obtained via a lumbar catheter.
Single shot caudal is useful as an alternative to saddle block spinal anaesthesia for
forceps delivery.
Caudal blockade can be adopted for cesarean section if large enough doses of local
anaesthetics are injected to provide analgesia upto T6 level.
A caudal block is administered only after labor is well established, ie., 4-6cm
cervical dilatation and 60-70% effacement. Caudal block should not be performed if
presenting part is in the perineum. The volume necessary to provide a T10 block varies
from 15-25ml.
Lumbar epidural anaesthesia is preferable to caudal anaesthesia in labor for
several reasons.
1. Segmental T10-L1 dermatome levels can be achieved early
2. Less drug is needed during labor
3. Pelvic muscles retain their tone and rotation of fetal head is more easily
accomplished
A double catheter technique has been described in which a lumbar epidural catheter is
placed for use during the first stage of labor and a caudal catheter is placed for use
during 2nd stage of labor. The technique can be used in patients with cardiac disease in
whom it is desired to avoid the high anaesthetic (i.e. sympathetic) block that sometimes
accompanies attempts to provide complete perineal analgesia with a lumbar epidural
catheter.
Chronic pain management:
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The caudal block can be used to diagnose and to treat low back pain syndromes.
In chronic back pain patients, caudal injection of large volume (upto 60ml) of diluted
lidocaine or bupivacaine, with or without steroids gives symptomatic relief and
sometimes effect an apparent cure.
The caudal route can also be used for extradural injection of neurolytic solutions
for relief of malignant pain confined to the peripheral nerves.
CONTRAINDICATIONS
Specific contraindications include
1. Patient refusal
2. Major malformation of sacrum
3. Myelomeningocoele
4. Infection at puncture site involving skin or deeper tissue
5. Pilonidal sinus
6. Generalized septicemia
7. Blood coagulopathies
8. Meningitis and Active CNS diseases
Techniques
As in preparation for any major regional technique, all equipments must be assembled
and checked including block tray, resuscitation equipments, monitors and suction. An IV
line should be secured. Block tray should contain the following –
a. A pair of sterile gloves
b. Antibacterial solution for cleansing the skin
c. One sterile cup for antibacterial solution
d. Forceps
e. Sterile gauze pads
f. Sterile towels for draping the field
g. One 25g, 1.6-3.8cm needle for skin infiltration
h. One 19g, 7.6cm caudal needle with stylet or one 19g, 3.8cm short bevelled
needle.
i. One 5ml glass syringe
j. One 20ml syringe
k. One disposable caudal catheter
The needle used for this procedure will depend to some extend on clinical
circumstances. For single injection caudal block in a child, a 2 to 3cm disposable 23-25g
needle should be used. The needle should be short beveled, because
1. They give better feel when difficult tissue are punctured
2. They have less tendency to form barbs if bone is struck
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3. The bevel is more likely to fully enter the canal when it is very shallow
4. They may cause less trauma to blood vessels
If a catheter is to be inserted, a short 5 to 7cm 18g Crawford tip needle and a standard
epidural catheter are recommended. Some use plastic IV cannula of small caliber.
Although, this has some advantages, it has a tendency to kink and is less reliable. A large
gauge IV needle can be used to insert a standard epidural catheter.
Three main techniques are available

1. Conventional techniques
2. Simplified technique
3. Continuous technique
Conventional Technique:
The key to successful caudal blockade is the accurate identification of sacral cornua.
The patient may be placed in lateral or in prone position, In the left lateral / lateral
decubitus – the left leg is straightened, right leg or upper leg is flexed with right foot
placed in the popliteal space of left leg. The patients upper buttock is slightly rotated off
the perpendicular plane so that the gluteal fold does not prolapse over the lower middle
portion of the sacrum, where palpation of sacral coccygeal hiatus is performed.
In prone position a pillow is placed under the pelvis, both legs are rotated so that the
toes of both feet are facing medially. This again separates the buttocks and there is no
distortion of landmarks from movement of gluteal cleft, but access to airway is
compromised.
Skin preparation should be done so that all the landmarks can be palpated aseptically.
Confirmation of Landmarks:
Conformation of bony landmarks is the key to success. In a thin, young patients,
the protrusions of sacral cornua can be seen without palpation, and the shallow
depression over the sacral hiatus can be seen between them. Successful needle
placement in the circumstances are exceedingly easy, however the majority of patients
have less obvious surface anatomy and requires palpation of all the bony landmarks.
It is important initially to identify the midline positively.
Considerable variability occurs in the prominence of the cornua, causing problems for
the unwary.
Palpation of the medial sacral crest in a caudal direction will lead to sacral hiatus.
The posterosuperior iliac spines form an equilateral triangle with the sacral hiatus. This
should be used as a confirmatory landmark for correct needle placement. Palpation of
coccyx is avoided due to the possibility of contamination.
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Once the sacrococcygeal membrane is identified between the sacral cornua one
should keep the palpating hand in position. A small wheal of local anaesthetic is raised
over the area
A 19g disposable needle is inserted immediately caudal to the thumb at a cephalad
angle of about 450. Resistance is felt after a few millimeter as the needle engages in the
ligament followed by sudden loss of resistance as it penetrates which is felt as a ‘POP’ as
it enters the sacral extradural space (1st position).
The needle is advanced until bone (dorsal aspect of ventral plate of sacrum) is contacted
then slightly withdrawn and needle is redirected (2nd position) along the long axis of the
sacrum
The needle is advanced 1-2cms (3rd position) into the sacral canal.
An aspiration test should be performed to exclude intravenous or subarachnoid
placement of needle. A caudal, need not be abandoned if blood or CSF is seen on
aspiration, but the needle must be withdrawn or repositioned until test is negative.
If resistance is met, the needle should be rotated through 900, but it should be
removed and reinserted, if there is persistent difficulty.
In children, technique requires some modification. 21G needle is used for all but
the smallest infant in whom a 23g needle is more suitable, the needle is inserted at right
angles to skin. When the needle has penetrated the sacrococcygeal ligament, it should
be reangled at 20-300 skin and the advanced 2-3mm into sacral canal. The LA should be
injected at the rate no more than 10ml/min.
Signs of correct needle placement:

The following are the objective and subjective signs of accurate needle
positioning, and those that appear appropriate should be elicited before completion of
injection. The first four should be regarded as essential (modified by McCaul).
1. Presence of sacral bone on each side, infront and behind the needle at its point of
insertion. This does not exclude the possibility of entry into a decoy hiatus, but
does protect against injection lateral to the sacral or coccygeal margins or into
the presacral tissue or rectum.
2. There should be no subcutaneous bulge or superficial crepitus after injection of
2-3ml of anaesthetic solution or air
3. There should be no tissue resistance to injection, the force required to inject
should not exceed that necessary to overcome syringe and needle resistance and
should be constant throughout. Injection should feel like any other injection into
epidural space
4. “Whoosh test” can be used to predict successful needle placement. This involve
listening with a stethoscope over the midline lumbar spine for a characteristic
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whoosh sound on injection of 2-3ml of air through caudal needle. This test is
more reliable than the “POP” of sacroccygeal ligament penetration or loss of
resistance tests.
5. When correctly positioned, needle should be able to move in the canal, pivoting
at the point of penetration of the sacrococcygeal ligament. Eliciting the sign may
however cause trauma to tissues in the canal particularly blood vessels and
usually is not necessary.
6. There should be no local pain during injection of solution. Pain indicates
misplacement of the needle and injection should stop.
7. Paraesthesia or a feeling of fullness, that extends from the sacrum to the soles of
the feet is common during injection, but ceases on completion and portends
successful blockade
8. The feeling of grating as the needle moves over the anterior wall of sacral canal
indicates accurate positioning, but should not be purposefully elicited lest the
sacral venous plexus be damaged.
9. An epidural catheter or plastic canula should enter the canal freely with the same
or greater ease than in the lumbar epidural space.
10. Evidence of sympathetic paralysis with vasodilatation, flushing, cessation of
sweating and increased skin temperature should be seen following local
anaesthetic injection.
11. If needle is in the caudal epidural space, aspiration with fluid in a 10ml syringe
will show air easily.
The simplified technique:

In this technique, 1.5 inch 21 gauge short bevel needle, is placed through the
sacrococcygeal ligament at 450 angle with the skin as in conventional method, but it is
not advanced from this position. At this time, 25 to 30ml of solution is injected.
This method is indicated in anorectal surgeries. Advantages are
1. A simple manipulation
2. No special needles required
3. Minimal trauma and pain
4. Less chances of subarachnoid injection
5. Sacral anomalies do not limit successful block
6. Bleeding is rare.
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The continuous techniques:
The usefulness of caudal analgesia has been enhanced with the introduction of
the continuous technique by Higson and South Worth. Two variations of continuous
technique are available.
Continuous needle technique:

Here a malleable needle was used which was allowed to remain in place. This technique
is largely of historic interest in the development of caudal/epidural anaesthesia. The
technique has been supplemented by the continuous catheter technique and by lumbar
extradural anaesthesia in obstetrics.
The Continuous catheter technique:

Mainly used in obstetric analgesia and long surgical procedures. A straight tipped, wide
bore needle is used to enter the sacral epidural space. Once the tip has penetrated the
sacrococcygeal ligament, the shaft is depressed and advanced with a rotatory movement
to turn the orifice through 1800 until it faces anteriorly. The rounded tip then glides
easily along the posterior wall of the caudal canal.
Ideally, a catheter equipped with wire stylet is to be used.
The plastic catheter should confirm to bromage characteristics and should be
examined for imperfections.
The catheter is passed through the hub of the needle and is advanced until 2-4
cms project past the bevel of the needle into the caudal space.
If there is difficulty in passage of catheter, 1-2 ml of saline is injected to the
epidural space so that a space is created between the dura and vertebral bodies
through which the catheter could be easily passed.
It is important not to force the passage of the catheter as this could result in
injury of nerve roots, trauma to blood vessels or puncture of the dura.
The distance that the catheter is in the caudal canal can be measured by placing
the plunger of the syringe against the patients back and noting the markings on
the syringe that correlates with the markings on the catheter which is at or near
the hub of the needle.
The needle is removed from the tissues in the following manner. The catheter is
held firmly by the dominant hand 2-3cm from the hub of the needle while the shaft and
hub of the needle are held between the index and middle fingers and thumb of
nondominant hand. While the catheter is held in place with positive forward pressure,
the needle is carefully pulled out so that the thumbs of the two hands meet. Forward
pressure should be applied to the catheter at all times. The maneuver is then repeated
by grasping the tubing another 2-3cm distal to the hub of the needle and repeating the
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same procedure. Finally the tip of the needle will emerge from the skin. The tubing is
prevented from being dislodged by the application of pressure at the point where it
emerges from the skin. The needle is then moved back over the catheter. The thumb
and the index finger may now move some distance up the catheter to hold it firmly to
prevent dislodgement while the needle and stylet are removed from the catheter.
Forward repositioning of the needle is impossible once the catheter advanced
beyond the bevel. If forward repositioning is necessary the needle and catheter are both
completely withdrawn and the procedure is repeated from beginning. Once the catheter
has advanced beyond the bevel any attempt to withdraw it can result in shearing off the
catheter.
An adapter is attached to the end of the catheter or a blunt small gauge needle is
inserted into the tubing. Before the catheter is taped in place, a careful aspiration test is
performed to ensure that the catheter is not in the subarachnoid space or in the epidual
vein. A test dose of 3ml of local anasthetic solution (45mg lidocaine with 15 g
epinephrine or 15 mg bupivacaine) is injected and the patient is observed for CVS
changes sensory/motor alterations or CNS toxicity for not less than 3 minutes.
Sterile gauze pads are placed above and below the catheter as it emerges out of
the skin and the catheter and pads are secured by tapes. The entire catheter is then
taped to the back and over one shoulder for easy access and for repeated injections.
The following modification of the caudal catheter technique has been described
by Owens, Slater and Barritt (1973) and it is recommended because it avoids some of
the difficulties and dangers of the above technique. After the usual landmarks are
identified, caudal puncture is made with a standard 16G intravenous 2.5 inch Teflon
cannula and needle stylet instead of regular epidural needle. The plastic cannula has an
internal bore wide enough to accept a standard epidural catheter. If a continuous
technique is planned, a sterile epidural catheter is threaded through the cannula for a
distance of 2-3cm beyond the tip and then the cannula is removed over the catheter,
leaving the catheter in place in the usual way.
This technique has several advantages:
1. The stylet cannula assembly is advanced for a very short distance of 1-1.5cm and
the main advance into the sacral canal is performed by the soft, blunt cannula, so
that risks of dural puncture or fetal scalp perforation in labor is eliminated.
2. The perforation of sacral cortex and inter cancellous injection is less likely than
with rigid needles.
3. Conformation of correct placement is simplified. The Teflon cannula advance
easily when properly placed within the sacral canal, but is very difficult or
impossible to advance if incorrectly placed in tissues overlying the sacrum.
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If vital signs remain satisfactory and no significant anaesthesia develops after the test
dose, fractional doses of local anaesthesia 3-5ml are administered with a minimal
interval of 60 seconds until full caudal dose is injected.
To obtain continuous anaesthesia from T10-S5, the first intermittent caudal dose may
be the same as in single dose method. When the desired level of anaesthesia has been
achieved with the initial dose, a subsequent “top up” dose of about 2/3rd of initial dose
will maintain this sensory level. Aspiration test must be done prior to each
reinforcements because perforation of duramater or one of the epidural veins by the
catheter has been reported and may have occurred since the last administration of the
anaesthetics.
One school of thought, recommends threading the caudal catheter upward for 8-12cms
until the tip lies at the lumbosacral junction in order to reduce the volume of solution
required to produce a block to the umbilicus. Epidural analgesia effectively controls the
nociceptive receptor from major abdominal procedures and there by favourably modify
the neuroendocrine and metabolic responses intraoperatively and postoperatively.
However, it must be remembered that this incurs a remote risk of perforating the dura
and a careful test dose should always be given before the main dose is injected.
In general, epidural infusions are most effective when catheter tips are in the
dermatomes involved in the surgery.
Several studies have been undertaken regarding advancement of catheter following
caudal needle entry into epidural space with variable results. To ensure high success
with thoracic advancement of catheter tip, two alternatives to blind placement can be
considered. These are (1) Fluoroscopic guidance and (2) nerve stimulation guidance
techniques. Fluoroscopic guidance of cephalad advancement produces high success
rates. Wire wrapped stylleted 20 guage catheter are readily visible with fluoroscopy.
Disadvantages of fluoroscopy includes expense, radiation exposure and lack of ready
availability in many operating rooms.
Recently Tsui and Coworkers have developed the use of electrical nerve stimulation
directly through the catheter. A wire wrapped, styletted, saline filled epidural catheter
is equipped with a special ECG lead connector to permit delivery of current at the tip of
the epidural catheter. They have shown better sensitivity and specificity and improved
success rates in guiding catheters from caudal entry to thoracic tip placement.
The continuous drip technique:

This is a modification in the manner of administration of local anaesthetic
solutions instead of intermittent injections. The continuous system is connected to a
reservoir bottle containing selected local anaesthetic solution. This bottle is suspended
from an infusion stand or rack attached to bed about 7 feet above the floor. A standard
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disposable infusion set with a Murphy drip is connected to the catheter or needle. This
solution is allowed to drip into the caudal canal at an initial rate of 30 drops per minutes
for 2 minutes. However, anaesthesia may be established by single shot injection. Once
anaesthetic level is attained, the rate of drip is established at 12-18 drop/min. This will
maintain anaesthesia upto T10 level.
Drugs and Dosage:

General Considerations:
Through the years many factors have been implicated in influencing the spread
of a standard dose of local anaesthetics injected into caudal canal. The only factors that
have been shown to effect caudal spread in adults are volume, speed of injection and
posture. The other factors whoes influence remains unknown and uncontrollable which
must inevitably give rise to significant unpredictability in caudal anaesthesia includes;
1. The size of caudal epidural space
2. The size and patency of the sacral canal and the anterior sacral foramina
3. The amount of the bony distortion of sacral canal
4. The presence of septa in epidural space
5. The amount and nature of soft tissue in the epidural space especially fatty tissue
6. The permeability of the neural tissue and dural cuffs to the drug
In adults:
The following agents and solutions by virtue of their penetrability, rapid onset,
longer duration and relative safety are recommended.
Analgesic conc Anaesthetic conc

1. Lidocaine 1-% 1-1.5%
2. Bupivacaine 0.125% - 0.25% 0.5%
Doses recommended:
o For low caudal block (analgesia to include T11 segment) – 30ml
o Moderate caudal block (analgesia to include T7 segment) – 45ml
o High caudal block (analgesia to include T4 segment) – 60ml
Paediatrics:
Caudal anaesthesia can be administered safely to infants and children who have
respiratory or renal complications. The application of technique is essentially volume
dependent
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Schulte – Stemberg et al had found that the pattern of caudal spread is
predictable in children upto 12 years of age. The dose required was found to be
0.1ml/segment/year + 0.1ml/segment for 1% lidocaine or 0.25% bupivacaine. This
suggest that the upward spread of caudal solutions is not hampered by the same
anatomical constrains that develop from puberty onwards.
A much more simplified formula was derived by Satayoshi for upper abdominal
surgeries.
V= D-13
Where V is volume in ml
D is distance between C7 to sacral hiatus in cms
Avg D 1-4 months < 22cms
4 months –1 year – 22-30cms
1 year – 8 year - 30-40cms
8 year – 12 year – 40-50cms
1.5 % lidocaine or 0.5% bupivacaine provides satisfactory anaesthesia. Dosage is kept

at 7 mg/kg for lidocaine and 4mg/kg for bupivacaine.
For postoperative analgesia bupivacaine is a commonly employed in pediatric
patients because of its prolonged duration and mild degree of sensory selectivity.
Bupivacaine 0.25% at a dose of 2.5mg/kg produces satisfactory analgesia i.e.,
suppression of autonomic response when used with general anaesthesia and produces
postoperative pain relief after inguinal hernia repair and lower extremity surgery.
Avoid any combination of concentration and volume that yields doses in excess of
2.5mg/kg.
For a level of T10 in children 2-4 years of age, an average volume of 10ml is to be
injected.
In pregnancy:
The sacral canal shares in the general engorgement of extradural veins that
occur during late pregnancy. This leads to a 40-50% increase in segmental spread or a
28-33% decrease in dose requirement in pregnant women.
0.125% - 0.25% bupivacaine is indicated for labor analgesia.
0.25% - 0.5% bupivacaine is indicated if caudal block is provided for LSCS.
Caudal blockade alone needs about 20-25 ml of local anaesthetic for satisfactory
analgesia. In double catheter technique 8ml of local anaesthetic is given through lumbar
catheter and 8-15ml of local anaesthetic is given through caudal catheter in second
stage of labor.
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Epidural spread is most likely exaggerated if injection is made when the mother
is lying on her back.
Continuous epidural dosage:

In view of local anaesthetics accumulation and toxicity, it is advised to keep
infusion rates of 0.125% of bupivacaine below 0.2mg/kg/hr for neonates and infant less
than 6 months and 0.4mg/kg/hr for older infants (> 6 months age) and children.
This can be potentiated by adding fentanyl 2 g/ml
Addition of epinephrine:
Addition of epinephrine to local anaesthetics in concentration of 1: 300,000 has
the following advantages
Causes prolongation of mean duration of analgesia and mean time of first voiding
by 60 minutes.
Decreased placental transfer of lidocaine.
Addition of Bicarbonate:
This increases the concentration of nonionised free base which increases the rate
of diffusion of the drug and speed of onset of action.
1meq of NaHCO3 is added to 10ml of local anaesthetic.
Caudal Opiods:
Morphine and Fentanyl is given with local anaesthetic in caudal analgesia
Advantage:
Lesser doses of opiods are required (approximately half to one fourth of
intravenous dose) as the drug is directly administered to the CNS.
Quality and distribution of blockade is better
Complication of opiods such as respiratory depression, itching, nausea and
urinary retention are minimized.
Dose of morphine – 0.1 mg/kg. Prolonged analgesia of 24-30hrs.
Fentanyl - 2 g/kg. Provide faster onset of analgesia and better quality.
Caudal morphine provides longer analgesia than bupivacaine alone and extends
analgesia beyond the lumbosacral dermatomes. It can also be used in thoracic or
upper abdominal procedures, advantage being it does not cause motor or
autonomic blocks.
Monitoring:
Despite the limited extend of block anticipated with caudal anaesthetics, it is still
mandatory to monitor the patients, including BP, ECG and pulse oximetry. Intravenous
or intraosseous misplacement of caudal needle or excessive block may give rise to
unwanted side effects. Full cardio pulmonary resuscitative equipments must be
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immediately available. Maintaining verbal communication with the patient is the
simplest and in some ways the most reliable method of detecting adverse effects.
In obstetric cases:
Pulse rate
Blood pressure
SaO2
FSH
Cervical dialation
In paediatrics:
Heart rate with pericardial stethoscope
Respiratory rate
SaO2 with pulse oximetry
ECG
Temperature
Urine output
Complications:
The range of complications with caudal anaesthesia is predictable and in
common with other regional technique, decrease markedly with experience and
meticulous attention to details.
1. Failure to identify the sacral hiatus: This may be related to obesity or to distorted
landmarks.
Absent/patchy block
Unilateral or uneven spread of drug
Intravenous or Intraosseous placement
Dural puncture
Inadvertent dural puncture occasionally occurs (1.2%), although the distance
from the hiatus to dural sac is a limiting factor. When unrecognized, high subarachnoid
block may ensue on injecting the large volume of local anaesthetics used.
The patients becomes hypotensive, comatose and paralyzed with dilated pupils
over a period of 2-5 minutes. The condition may last for several hours. Rapid tracheal
intubation, ventilation and fluid resuscitation are required. The obstetric patient is at a
higher risk, because of rapid development of hypoxia and possibility of regurgitation
and aspiration.
Subdural injection:
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This is less likely when the needle is inserted via sacral hiatus. A slow onset, but
extensive block is highly suggestive of subdural injection. A high sympathetic block is
frequent and pupillary dilatation occurs. Hypotension may be seen.
Excessive spread:
Although limited cephalad spread is a more common problem with caudal, on
rare occasions, excessive spread may occur to a high thoracic level, even in absence of
subarachnoid/subdural injection. Although this in itself may not be a major problem, a
decrease in degree of expectation of this situation often results in a lesser degree of
vigilance by anaesthesiologist.
Injection into foetus:
There have been reports of fetal intoxication by local anaesthetic drugs injected
into foetal scalp during attempted caudal injection. This risks exists only when the
presenting part has descended into the perineum and questionable techniques are used.
Hypotension:
It is seen approximately in 6% of patients where caudal block is given.
Catheter problems:
Catheter insertion when the needle is correctly placed is very easy. Early
resistance to insertion is usually an indication that the needle is placed incorrectly. The
catheter should never be withdrawn through the needle because of risk of shearing it
off. Migration of catheter; to intravenous or subarachnoid space has been noted. There
has also been a case report of catheter knotting in the caudal canal requiring
neurosurgical exploration for its removal.
Toxic reactions to local anaesthetics:

Occurs in 0.2% of patients. Includes convulsion, muscular twitching, drowsiness and
depression.
Postoperative Problems:
Pain: At the site of injection or a haematoma may be seen.
Urinary retention:
Infection: Chances of infection at the site of needle entry is more with caudal
approach than with lumbar approach.
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Neurological complications:
A risk of neurological complications do exists with caudal. This includes
Meningismus (aseptic or chemical meningitis)
Adhesive arachinoiditis
Cauda equina syndrome
- Loss of sensory and motor function involving lumbosacral nerves
- Saddle sensory loss
- Fecal incontinence
- Urinary retension
Prolonged headache
Paralytic disturbances
These are caused either by direct trauma from the needle or catheter or toxic neurolytic
action of the agents on the nerve roots. Most of the cases, when thoroughly
investigated, reveal coincidence lesions which tends to be blamed on the block.
Neurological sequelae of traumatic vaginal delivery falls into this group.
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Chapter 18 - ANATOMY AND PHYSIOLOGY OF SPINAL
ANAESTHESIA
SPINAL ANAESTHESIA
Definition:
Spinal anesthesia is a form of regional anesthesia obtained by blocking the spinal nerves
in the subarachnoid space by injection of local anesthetic solution is to CSF, which
mainly act on the spinal nerve roots.
HISTORY OF SPINAL ANESTHESIA:

1885 - J.C. Coming administered cocaine intrathecally for pain.
1981 - Quincke demonstrated technique of lumbar puncture in diagnosis.
1898 - August Bier of Germany produced true spinal anesthesia in man and
introduced the technique as an anesthetic mode.
1904 - Einhorn discovered and synthesized procaine.
1905 - Pitkin popularized the method of introducing agents intrathecally.
1908 - Barker described the use of dextrose to increase and alcohol to decrease
the density of local anesthetic solution.
ANATOMY OF VERTEBRAL COLUMN

33 vertebra – 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, 4 coccygeal.
A typical vertebra is composed of 2 parts.
1. Body – Base anteriorly – bears weight
2. Arch – surrounds the cord laterally and posteriorly consisting of lamina and
pedicles and 7 processes.
3. Muscular – 2 transverse and 1 lesions
4. Articular – 2 upper and 2 lower.
Development: 3 primary ossification centers, 2 lateral for the arch and 1 central for the
body, which first appear at 8th month of embryonic life.
At 16th year of life 5 secondary centres of ossification appear

1 tip of each transverse process
1 tip of spinous process
1 each for upper and lower surface of the body of vertebra.
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Articulation of vertebra is by ligamentous connections and certain gaps between 2
vertebrae can be recognized.
1. Lateral intervertebral gap (or) intervertebral foramen
- Between the adjacent pedicle
- Spinal nerve emerge through this gap
2. Posterior interlaminar gap
- It is the region for conventional technique of spinal puncture,
subarachnoid (or) epidural.
- Normal (or) extended position – small land triangular
Flexion – large diamond shaped opening.
LIGAMENTS: 5 ligaments
1). Supraspinous ligament

2). Interspinous ligament
3). Ligamentum Flavum
4). Posterior longitudinal ligament
5). Anterior longitudinal ligament.
TOPOGRAPHIC LINE OF TUFFIER

Line across the back between the rests of the ilia passes over spine L 4 vertebra –
upright position
Inter space L4 – L5 lateral position
Landmark on the back for identification and numbering of the interspaces
between the spinous process of the vertebrae.
SPINAL CORD
- It is a cylindrical mass of nervous tissue

- Length 42 – 45 cm wt – 30 gm
- Occupies upper 2/3rd of vertebral canal
- Extends from atlas to L1 or L2 vertebra
- The anterior and posterior roots of the most caudal spinal nerves emerge from
the conical terminus of the spinal cord.
- Conus medullaris and form bundle of nerves referred as cauda equine
- Pia mater / continues caudally from conus medullaris as a rudimentary neuron
free structure filum terminate.
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DEVELOPMENT: Spinal cord is derived from the neural tube.
- At 3 months of fetal life the tip of the cord is located at 2nd coccygeal vertebra.
- At birth the tip of cord lies at the level of lower border of 3rd lumbar vertebra and
dural sac at 3rd sacral vertebra.
- After birth the lengthening and growth of the cord as well as meanings lag
behind the growth of bony vertebra. This differential growth rate results in
development of epidural and caudal space.
- Internal structure of spinal cord consists of central grey matter (cell bodies)
covered by outer white matter (nerve fibers)
- There are 31 pair of spinal nerves each emerging from a dorsal and ventral nerve
roots which units in intervertebral formina.
Age Level of tip of spinal cord
3 month fetal life 2nd coccygeal vertebrae
6 month fetal life 1st sacral
Birth Lower border L3
1 year Lower border L2
Adult L1
MEANINGS OF SPINAL CORD

It has 3 coverings - Dura
- Arachnoid
- Pia
Durameter
- Continuation of (meningeal layer) of cerebral dura
- Mode of dense fibrous tissue
- It extends upto second sacral segment and continues as covering of filum
terminate to end by adhering to periosteum of back of coccyx.
Arachnoid mater
- Membranous, lines the dural sheaths and is continuous with cerebral arachnoid.
Piamater
- Vascular connective tissue sheath which closely inverts the brain and spinal cord
and projects into sulci and fissures.
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- Inferiorly it continues as filum terminale.
Compartments related spinal meanings

- Epidural space
- Subdural space
- Subarachnoid space
- Contains innumerable cobweb like trabecular
- Traversed by cranial and spinal nerves
- Contains main blood vessels of CNS
- Contains CSF which functions as lymph
- In the cervical and thoracic region the space is annular below
C1 vertebra the space is circular and has diameters of 15mm.
Curves of the SPINE

In the adult, the normal spinal column has 4 curves
1. The cervical curve – convexity anterior

2. The dorsal curve – convexity posterior
3. Lumbar curve – convexity anterior
4. Sacrococcygeal convexity posterior
In supine and horizontal position
- High point of the spinal curve – 3rd lumbar vertebra

Low point at 5th thoracic vertebra.
BLOOD SUPPLY
Anterior spinal artery – anterior 2/3rd of spinal cord
Posterior spinal artery – posterior 2/3rd of spinal cord
REINFORCEMENT OF ARTERIAL SUPPLY

Spinal radicular branches arising from segmental arteries like vertebral, ascending
cervical, posterior, intercostals and spinal lumbar and lateral sacral arteries enter
through intervertebral foramina.
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They divide into anterior and posterior radicular branches. One of the anterior
radicular branch is larger than others i.e lower thoracic or upper lumbar termed as
ARTERIA RADICULARIS MAGNA (or) ARTERY OF ADAMKEIWICZ. It is responsible for
major blood supply of lower 2/3rd of spinal cord.
VENOUS DRAINAGE OF SPINAL CORD AND VERTEBRAL COLUMN
- External plexus
- Internal plexus Devoid of values
- Basivertebral veins – Large tortuous channels in the body of vertebra
- Intervertebral veins – 1). Accompany the spinal nerves in intervertebral
foramina
2). Contain valves
- Spinal cord veins
PHYSIOLOGY OF CEREBROSPINAL FLUID

- CSF is formed by a process of ultrafiltration through the choroids plexus at a rate
of 0.4 ml / min (25 ml / hr, 600ml / day).
- Total volume of CSF in adults – 120 – 150 ml
- Secretion of CSF is under sympathetic control – by noradrenergic innervation
from sympathetic chain through superior cervical ganglia.
- This secretory innervation is mediated by -adrenergic receptors.
COMPOSITIONS AND CHARACTERISTICS OF CSF
- Specific gravity – 1.003 to 1.009

- Volume 130 – 150 ml
- CSF pressure – 110mm of water
- Protein 15 – 45 mg / dl
- Glucose 50 – 80 mg / dl
- Non protein nitrogen 20 – 30 mg / dl
- Chloride 120 – 130 m eq/L
- Sodium 140 – 150 m eq/L
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- Bicarbonates 25 – 30 mm eq/L
- pH 7.4 – 7.6
CIRCULATIONS OF CSF:
Absorption of CSF:
- Cranial region – mostly supra tentorial through arachnoid villi and pacchionian
bodies (or) granulations.
- Spinal region – through virchow robin spaces into pial venules.
PHYSIOLOGY OF SPINAL ANAESTHESIA:

CNS
LA injected in SAS acts on 3 sites
1). Nerve roots
2). Dorsal nerve root ganglion, posterior and anterior horn synapses.
3). Limited and incomplete spinal cord parenchyma on ascending and descending
tracts.
Determinants of nerve fiber susceptibility
- Fibre size
- Degree of myelination and distance between the nodes of remover.
- Functional
Difference of levels of block according to fibre type

Sympathetic block 2-4 segments above sensory motor block 2-4 segments below
sensory.
SEQUENCE OF NERVE BLOCK
1). Vasomorot block – dilatation of skin vessels and increase cutaneous blood flow.
2). Block of cold temperature fibres
3). Sensation of warmth by the patient – due to above
4). Temperature discrimination
5). Slow pain
6). Fast Pain
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7). Tactile sense
8). Motor paralysis
9). Pressure sense
10). Propiroception and MTJ sense
Pulmonary effects of high thoracic blockade:

Parameter Effect
Lung volumes and spirometry
VC, TLC, FEV 1 ↓ ≈ 5%
FEV1 / FVC →
TV →
PEFR, PEP ↓b
Gas exchange, ABG →
Ventilatory response to hypoxemia, hypercarbia →
Bronchial tone →
Influence of neuraxial blockade on the endocrine response to lower abdominal or

lower extremity surgery
Plasma hormone Intraoperative response
Growth hormone ↓
ACTH ↓
ADH ↑
TSH ↓
- Endorphin ↓
Cortisol ↓
Aldosterone ↓
Renin ↓
Epinephrine ↓
Norepinephrine ↓
Insulin 
Glucagon →
T3 and T4 →
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Influence of neuraxial blockade on the metabolic response to lower abdominal or
lower extremity surgery
Metabolic parameter Response
Plasma glucose ↓
Glucose tolerance ↑
Insulin clearance ↓
FFA and glycerol ↓
Plasma Ketones ↓
Plasma lactate ↓
Liver glycogen ↓
Muscle amino acids ?
Nitrogen balance ?
Plasma acute phase proteins →
IL-6 →
Oxygen consumption →
Neuraxial anesthesia effects of bladder function
Local anesthetics
Block efferent and afferent signals to / from the detrusor muscle.
Decrease sensation / urge to void
Decrease detrusor contractility
Block efferent and afferent signals to / from the internal urethral sphincter a.
Block efferent and afferent sigansl to / from the external urethral sphincter
Opioids
Decrease detrusor contractility
Decrease sensation, urge to void
Epinephrine
Potentiate actions of local anesthetics
The male bladder neck has amore developed middle muscle layer compared to the
female and this layer is richly innervated with adrenergic nerve fibers.
Risk factors for bradycardia following spinal technique
Moderate bradycardia (40 – 50 bpm)

Baseline HR < 60 bpm
Male gender
Age < 37 years
Non emergency surgical status
Beta blockade use
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Case duration
Severe bradycardia (< 40 bpm)

Baseline HR <60 bpm
Male gender
DIFFERENTIAL NEURAL BLOCKADE: DNB

Phenomenon in which nerve fibers subserving different functions display varying
sensitivity to LA blockade.
PROBABLE MECHANISMS OF DIFFERENTIAL BLOCK:

a. Different diameter of axons
b. Time available for diffusion
c. Number of nodes blocked
d. Decremental conduction.
e. Different agents have different ED50 values for different axon types.
PHARMACOLOGICAL BASIS;
EXPOSURE LENGTH OF NERVE FIBER – may explain differential nerve block.
“Decremental conduction block” of a critical length of a nerve.
Describes the decreased ability of successive nodes of Ranvier to propagate an impulse
in presence of LA.
Thicker nerves concentrate more LA – when compared with high volumes of low
concentration and low volumes of high concentration.
Concentration of LA in nerve roots is a function of distance from site of highest
concentration of LA in CSF. This combined with the fact that different types of nerve
fibers have different sensitivities.
ZONES OF DIFFERENTIAL BLOCKADE

Most apparently measured above i.e.. cephalad to site of highest concentration of LA in
CSF.
This zone of differential blockade remains constant in extent during maintenance and
regression of the level of anesthesia as anesthesia wears off.
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Order of blockade
Sympathetic -> Temp -> Pinprick -> Touch-> Pressure -> motor -> vibration ->
proprioception
Central neuraxial block - spatial separation.

Sympathetic - 2-6 segment higher than sensory level.
Sensory - 2-3 segment higher than motor block.
SPATIAL SEPARATION: results from gradual decrease in LA concentration within CSF

as a Function of distance from site of injection. Clinically important for determining the
level of
- Sympathetic block -> CVS effects

- Sensory analgesia -> surgical relaxation.
Most troublesome sequelae of differential neural blockade is the patient who has intact
touch and proprioception at the surgical site despite adequate sensory block
EFFECT ON CVS:
Hemodynamic effects of neuraxial anesthesia:
Parameter Effect
Blood pressure ↓
Central venous pressure ↓
Heart rate ↓, →, ↑
Cardiac output ↓
Stroke volume ↓
SVR ↓
Risk factors for neuraxial Anaesthesia – associated bradycardia

Block height higher than T5
Younger age
ASA PS I
Baseline hearet rate < 60 bpm
Prolonged PR interval
-blocker therapy
Most important physiological responses to SAB involve CVS.
Mediated by combined effects of

Autonomic denervation
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Higher levels of neural block
In partial sympathetic block reflex increase in sympathetic activity in unblocked areas
leads to vasoconstriction above the level of block.
ARTERIAL CIRCULATION:
Sympathetic denervation produces arterial and more physiologically important
arteriolar vasodilation although it is not maximal.
Vascular smooth muscle on arterial side has an intrinsic tone and vasodilatation is not
maximal.
PVR decreases only modestly about 15 – 18% in normovolemic subjects even with total
symp block provided C.O. and other determinants of BP are maintained. In elderly and
cardiac patients. PVR decreases by 25% and cardiac output by 10%.
VENOUS CIRCULATION:
MAXIMAL VASODILATION UNLIKE ARTERIAL SIDE. Veins and venules have few
smooth muscles in their walls and they retain no significant residual tone following
acute pharmacological denervation.
Venous circulation becomes gravity dependent. PRELOAD i.e. venous return to heart
depends on position of patient, especially during high spinal anaesthesia.
HEART RATE
Charcteristically decreases during SAB in the absence of autonomically active drugs.
Predictors of bradycardia during SAB.
1 Baseline heart rate of less than 60 beats per minute
2. Prolonged PR interval
3. Use of beta blockers
4. Block height T5 or higher.
Bradycardia is due mainly to the blockade of preganglionic cardio accelerator fibers.
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Cardiac reflexes:
Are faster acting reflex loops between the heart and the CNS that contribute to the
regulation of cardiac function an maintenance of physiologic hemostasis.
Baroreceptor reflex (carotid sinus reflex):

Maintains BP through a negative feedback loop
Stimulus: increase in systemic BP > 170 mmHg
↓+
Stretch receptors in the carotid sinus and aortic arch
↓
Glossopharyngeal and vagus nerves
↓
Nucleus of tractus solitarius in medulla
+
Inhibits sympathetic discharge Parasympathetic NS
↓ In vascular tone, bradycardia, ↓ Myocardial contractility
↓ BP
Reverse effects are elicited with onset of hypotension.
It plays an important role during acute blood loss and shock.
The reflex are loses its functional capacity at a BP < 50mm Hg.
Volatile anaesthetics inhibit the reflex.
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Patients with chronic hypertension also had a decreased baroreceptor reflex
response.
Bainbridge reflex:
Increase in right-sided filling pressure (eg. Hypervolemia)

↓+
Stretch receptors in the RA wall and cavoatrial junction
↓ Vagal afferents
Rt.
Cardiovascular centre in medulla
Atrial
↓
stretch
Inhibit parasympathetic system
↓+ SAN
↓
↑ HR
Bezole – Jarisch reflex:

Noxcious ventricular stimuli
↓
Mechanoreceptors in ventricle
↓ + Vagal afferent C-fibers
PNS
↓
Bradycardia, hypotension, coronary dilation
CARDIAC OUTPUT
Preload is an important determinant of co.
Normovolemic with total symp block – CO. is maintained as long as they are
positioned with legs elevated above the level of heart.
Head up position leads to severe decreases in venous return to the heart and
thus to significant decreases in cardiac output.
MAP / HYPOTENSION
Risk factors for neuraxial anesthesia – associated hypotension
Block height higher than T5.
Older age
Baseline systolic blood pressure < 120mm Hg.
Combined neuraxial – general anesthesia
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Dural puncture higher than L3-L4 interspace
Predictors of hypotension during SAB:

1. Sensory block at T5 or higher.
2. Age over 40 years.
3. Systolic BP < 120mm Hg.
4. Combined spinal / general anesthesia.
5. Dural puncture at interspace between 2nd or 3rd lumbar
vertebrae or higher.
6. Chronic alcohol consumption.
7. Emergency surgery
8. Hypertension.
Slight decreases in BP - @ 15 – 18% in normovolemic patients can be ascribed to
decrease in afterload (PVR).
Severe hypotension – can only be due to decreases in CO – Secondary to decrease in
preload associated with peripheral pooling of blood.
Indications for treatment of hypotension – considered in terms of myocardial
oxygenation and cerebral oxygenation.
MYOCARDIAL OXYGENATION:
Directly proportional to perfusion pressure in coronary vasculature.
↓ In MAP - ↓ in CoBF
But it is countered by a decrease in the myocardial O2 requirement. Myocardial
O. demand decreases due to,
- Decreased after load - > decreased LV minute work.
- Decreased preload - > decreased work of LV and RV.
- Decreased HR - > decreased frequency of contraction, hence ventricular
workload is diminished.
CEREBRAL BLOOD FLOW:

Cerebrovascular autoregulatory mechanisms maintain CBF at constant levels even in
presence of wide fluctuations in MAP because cerebrovascular resistance decreases
proportionately. Therefore treatment needs to be initiated at higher level of BP.
PULMONARY EFFECTS:
Central neuraxial block considered safer than GA but may have S/E
VT, Max. inspiratory volumes, RR, ABG – unchaged
VC, ERV, Peak negative and positive airway pressure – 4-
↓ in PEFR, FVC, FEV1, Max. exp. Pressure, MBC.
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ERV decrease is due to paralysis of abdominal muscles rather than a decrease in
phrenic or diaphragmatic function.
Paralysis of external intercostals

Compensated by diaphragm – function actually improves with central neuraxial block,
abdominal wall paralysis allows easier displacement of abdominal viscera.
EXPIRATION
Anterior abdominal muscles, internal intercostals – regularly affected by SAB –
maximum intrapleural pressures during forced exhalation is diminished.
Implications: Active expiration – necessary for coughing, in asthmatic and COPD – to
overcome resistance which is partially lost in SAB. Therefore when administering SAB
to respiratory cripples.
- Inspiratory function must be satisfactory
- Caution of its affect on expiration esp is asthmatics / COPD.
BRONCHOSPASM:
6.4% - GA with ETT
1.9% - Central neuraxial block
1.6% - GA without ETT.
Probable mechanism:
1. Direct blockade of pulmonary Sym. Fibers.
2. Circulating catecholamine levels – block of adrenal medulla. Transient
respiratory arrest is due to ischemia of, medullary respiratory neurons
secondary to decrease in blood pressure and CO, severe enough to impair CBF.
It is advisable to let patients breathe spontaneously during high spinal rather than to
control ventilation. Elimination of the negative intrapleural pressure of spontaneous
inhalation by positive pressure ventilation not only removes a valuable indication of the
adequacy of CBF, but also may further decrease venous return, cardiac output and
arterial BP.
GASTRO INTESTINAL TRACT

Preqanqlionic fibres are (T5-L1) inhibitory to the gut therefore small intestine contracts
during midthoracic levels of spinal anaesthesia, owing to unopposed activity of vagus
nerves. Provides excellent surgical conditions because of contracted gut.
However, splanchnic sympathetic blockade may have deleterious hemodynamic
consequences. Gut hypo perfusion may compromise gut mucosal integrity as well as
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myocardial blood flow. Translocation of endotoxin from the gut lumen and release of
inflammatory mediators for the basis of SIRS.
Laser Doppler imaging has shown correction of mean perfusion pressure by
inotropes is more likely to correct bowel blood flow than is excessive fluid resuscitation.
RENAL:
Urinary retention can occur. Lower concentrations of LA are only necessary for the
paralysis of bladder function than for motor nerves to lower extremities. It is prudent
to avoid administration of excessive volumes of crystalloid solutions intravenously to
patients undergoing spinal anaesthesia.
Renal blood flow is maintained by autoregulatory mechanisms through a wide
range of pressures. When MAP is below 50mm Hg transient decrease in RBF and urine
output can occur.
HEPATIC
The decrease in hepatic blood flow is associated with an increase in the difference
between systemic arterial and hepatic venous oxygen content. This reflects an increase
in hepatic CL extraction, not hepatic hypoxia.
Spinal anaesthesia when possible could avoid hepatoxicity caused by halogenated
anaesthetics if susceptible patients were able to be identified preoperatively.
FACTORS AFFECTING BLOCK HEIGHT

WITH PROVEN EFFECTS WITH NO PROVEN EFFECTS
Controllable factors Patient weight
Site of injection, Angulation of needle Age Gender
Characteristics of LA CSF composition
Density of LA Circulation of CSF
S.G, Baricity Concentration of LA in solution injected
Dose of LA, Volume of LA Diffusion in CSF,
Position of patient – during injection & After Addition of vasoconstrictors
injections Rate of Injection (except hypodermic)
Factors not controllable Direction of needle bevel
Anatomic configuration of spinal column Turbulence in CSF Eg. Barbotage
Patient height (At extremes) Coughing
Volume CSF
CSF volume with intra abd press, e.g. Pregnancy
Distribution of LA in subarachanoid space determines the extent of neural blockade.
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CONC OF LA IN CSF DECREASES AS A FUNCTION, NOT OF DISTANCE FROM SITE OF
INJECTION, BUT OF DISTANCE FROM the epicenter at which the concentration of LA is
greatest.
PROCEDURAL CONSIDERATION
Preparation and monitoring
- Functional intervenous line

- Premedication
- Preloading the patient
- Blood pressure monitoring, pulse oximeter
- Equipments for airway management and oxygen administration
- Emergency drugs
Position of patient:
Lateral flexed position – Most commonly used
Sitting: used in surgeries where low lower and sacral levels of sensory anaesthesia are
adequate such as perineal and urologic operations.
Obese patient and scoliosis where identification of midline anatomy is difficult in lateral
position.
Prone position: Used for hypobaric technique for procedure on rectum, sacrum, lower
vertebral column.
Equipment:
Standard spinal needle has 3 parts – Hub, cannula, stylet.
Size – 18 gauge to 30 gauge
Length – 3.5 to 4 inches
Cutting edge – quincke babcock, Pitkin
Non Cutting edge – Greene, whitacre
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TECHNIQUE OF LUMBAR PUNCTURE:
- Preparation of equipment and puncture site.
- Testing spinal needle for flexibility, resiliency, spine sstylet fits properly into
cannula.
Midline approach
- Spinal canal should be horizontal plane
- Identifying the space using iliac crest as landmark the skin and subcutaneous
tissue are infiltrated with local anaesthestic.
- The spinal needle is inserted in the midline of the interspace with a slight
cephalad angulation 10 – 15. Following structures are pierced before reaching
the SAS.
- Skin – subcutaneous tissue – interspinous ligament – ligamentum flavum –
epidural space – dura – SAS.
- There is a characteristic change I resistance as the needle transverses the
ligamentum flavum and dura give way sensation.
- Stylet is removed and CSF allowed to appear at the hub of the needle.
- Attach syringe containing the therapeutic dose firmly to the needle, CSF is gently
aspirated to confirm the space and the local anaesthetic is slowly injected.
- Patient is placed in position
- CVS and RS functions are monitored.
- Analgesic level to pinprick or temperature level is checked.
b). Paramedian (or) lateral approach
- Performed in any position
- Ideal positioning of the patient cannot be achieved owing to pain (fracture,
dislocation involving lip and lower extremities)
- Arthritic (or) deformed spine
- Narrow (or) calcified interspinous space is elderly due to degenerative changes.
- 1.5 cm lateral to midline
- Direction 25o C to midline and without deviation cephalad or caudad.
- The first significant structures encountered will be ligamentum falvum.
TOYLOR technique:
- Useful method in case of spine fusion, arthritic spine, opisthotones, skin infection
in lumbar region.
- Enter the L5 S1 interspace (largest inter laminar space)
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- Needle is inserted at a point 1 cm medial and 1 cm above to lowest prominence
of the posterior superior iliac spine and directed upward, medially and forward
at an angle of 50o.
FACTORS AFFECTING THE SPREAD OF LA IN THE SAS:
Major factors affecting CSF spread
Patient age
Patient height
Patient position
Configuration of spine
Volume of CSF
Site of Injection
Speed of injection
Direction of needle
Local anaesthetic baricity
Local anaesthetic dose and volume
Factors not affecting CSF spread

Patient weight
Patient gender
CSF composition
Vasoconstrictors
DRUGS USED IN SA:

Lignocaine Bupivacaine
Dosage L4 25 – 50 mg 4- 8 mg
T 10 50 – 75 8 – 12
T4 75 – 100 14 – 20
Onset 3-5 min 5-8 min
Duration 60 to 90 min 2-4 hrs
STOUT’S PRINCIPLES FOR SPREAD OF SOLUTIONS: TESTING FOR LEVELS OF BLOCK

FOR DIFFERENT NERVE MODALITIES:
Testing for sensory level

Loss of sensation to pin brick
2-4 segments below the sympathetic block
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Assessment of motor block
2-4 segments lower than sensory block
assessed by logan – wildsmith modification of bromage scale
Test for sympathetic block
2-4 segments higher than sensory block

Due to blockade of preganglionic sympathetic B fibres
LEVEL OF SPINAL ANAESTHESIA FOR COMMON SURGICAL

PROCEDURES
Level Surgical procedure
T4 – T5 (nipple) Upper abdominal surgery
T6 – T8 (xiphoid) Intestinal surgery, appendicectomy gyn pelvic surgery,
ureter and renal pelvic surgery
T10 umbilicus Transurethral resection, obstetric, vaginal delivery, hip
surgery
L1 (inguinal ligament) Transurethral resection, if no bladder distension thigh
surgery
L2 – L3 Lower limb amputations foot surgery
(knee and below)
S2 – S5 (perineal) Perineal surgery, hemorrhoidectomy anal dilatation
INDICATIONS / ADVANTAGES
Anatomical distortion of upper airway
Rectal Procedures
TURP – Consciousness maintained
Obstetrics and Lower extremity surgery
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Absolute C/I: Relative C/I
Infection at site of injection Major surgery above umbilicus
Dermatological conditions – e.g. Psoriasis Deformities of spinal column
Septicemia / bacteremia Chr. Severe headache.
Shock / severe hypovolemia Blood in CSF that fails to clear after
Pre-existing diseases involving spinal cord 5 – 10 ml of CSF has been aspirated.
ICT Failure with 3 attempts
Severe aortic stenosis, mitral stenosis Cardiac disease – Myocardial, valvular,
Coagulation abnormalities ischaemic
Patient refusal
Lack of skill by personnel
Uncertainly of duration of procedure
COMPLICATIONS:
Adverse or exaggerated physiological responses
Urinary retention
High block
Total spinal anesthesia
Cardiac arrest
Anterior spinal artery syndrome
Horner’s syndrome
Complications related to needle / catheter placement
Trauma
Back ache
Dural puncture / leak
- Postdural puncture headache
- Diploma
- Tinnitus
Neural injury
Nerve root damage
Spinal cord damage
Cauda equine syndrome
Bleeding
Intraspinal / epidural hematoma
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Misplacement
No effect / inadequate anesthesia
Subdural block
Inadvertent subarachnoid block
Inadvertent intravascular injection
Catheter shearing / retention
Inflammation
Arachnoditis
Infection
Meningitis
Epidural abscess
Drug Toxicity
Systemic local anesthetic toxicity
Transient neurological symptoms
Caudal equine syndrome
HYPOTENSION
Associated with high thoracic levels of spinal blockage
Age more than 40 years
Obesity
Concurrent general and neuraxial anaesthesia
Coexisting beta adrenergic blockage
Hypovolemia
Prevention and treatment of neuraxial blockade induced hypotension

Prophylaxis Treatment
Intravascular volume Intravascular volume
Expansion (colloid > crystalloid) Expansion (colloid > crystalloid)
Vasopressor IV dose (ephedrine 5 – 10 mg, Vasopressor IV dose (ephedrine 5-10 mg,
phenylephrine 40 – 80 µg) phenylephrine 40 – 80 µg, epinephrine 0.1 µg
/ kg)
Smaller dose of intrathecal / epidural LA
Substitution of opioid for LA
Slow titration of epidural LA
Wrapping the legs (thromboembolic
stockings, inflatable splints or boots or
elevating the legs
Beach chair position Trend elenberg or “Leg up” position to
improve blood flow to heart / brain.
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Hypotension treatment algorithm:
HR
MAP Symptom Treatment
(bpm)
< 45 Within 20% of baseline Asymptomatic Atrophine 0.4 mg IV or ephedrine
5 – 10 mg
< 100 Within 20% of baseline Symptomatic Ephedrine 5-10 mg IV
< 100 Below 20% of baseline Asymptomatic Ephedrine 5-10 mg IV
> 100 Below 20% of baseline Symptomatic Phenylephrine 40 – 80 µg IV
PONV
Stimulation of CTZ
Risk factors for PONV:

Patient factor:
Female gender
History of PONV
History of motion sickness
Pain
Anxiety
Nonsmoking status
Gastric distention
Increased intracranial pressure
Hypoglycemia
Surgical factor
Long surgical duration
Specific surgeries (intra – abdominal, major gynecologic, laparoscopic, breast,
ENT, Strabismus)
Anesthetic factor:
Volatile anesthetics
Nitrous oxide
Opioids
Neostigmine
Hypotension (especially following neuraxial techniques)
Hypoxemia
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POSTDURAL PUNCTURE HEADACHE
Delayed complication
Incidence
2nd or 3rd post op. day (75% of cases)
By the end of 1st week 75% cases will have subsided
Occurs soon after assumption of head up position
Location – Occipital or at vertex with nuchal rigidity (spasm due to headache)
Mechanism:
Dural puncture – loss is greater than rate of CSF production
↓ 10 ml / hr loss, 30 – 50 ml – critical
Fall in spinal fluid pressure
↓ Loss of water cushion effect
Traction on pain sensitive supporting structure including blood vessels
↓
PDPH
Risk factors for PDPH

Category Risk factor
Practitioner Limited neuraxial technique experience
Fatigue (higher incidence on night shifts)
Technique Larger – gauge needle
Cutting needle (vs. pencil – point needle)
Loss of resistance to air (Vs. saline)
Cephalad or caudal (vs. lateral) orientation of needle
Midline approach (vs. paramedian) approach (controversial)
Patient Younger age
Female gender
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Treatment options for PDPH:
Therapy Agent / dose Comment
Phychologic support Validation of symptoms and
involvements in resolution
important
Bed rest Symptomatic relief, not
preventative or therapeutic
Abdominal binder Impractical and limited benefit
Hydration Oral or IV fluids Avoid alcohol, limited benefit
Caffeine 1). Caffeine sodium benzoate IV Promotes constriction of
500mg in lactated ringers IL over 4 dilated cerebral vessels
h
2). Caffeinated beverages
3). Floricet and florinal
Analgesics 1). Floricet 1-2 tabes q 4h, not
be exceed 6 tabs q 24h
2). Fliorinal 1-2 tabs q 4 h, not
to exceed 6 tabs q 24 h
3). Percocet
4). NSAIDs
Alternative medications 1). Aminophyline 100mg PO bid Works by vasoconstriction
(extended release) or 225mg q8 h x Experience limited, may not be
3-5 d uniformly effective
2). Sumatriptan 10 mg PO tid
for up to 96 h
3). Adrenocorticotropic
hormone
EBP Autologous blood, 10 – 20 Ml, drawn Pprophylactic use
aseptically controversial performed with
loss of resistance to saline (to
avoid pneumocephalus).
Decubitus position for 1-2 h
following EBP may be of
benefit
Epidural saline injection Preservative free saline. 30-40ml ; May offer transient relief
some follow with infusion of 40 ml/h
over 12-14 h.
Epidural albumin, dextran, Experience limited, may
fibrin glue, or gelatin require placement under direct
powder (gelfoam) observation
Shivering: 20 – 60%
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Differential inhibition of spinal cord afferent thermoreceptors and redistribution of
body heat.
Urinary retention
Blockade of the sacral nerve roots of which mainly S2
Signs and symptoms of a subdural blockade:

Nerve Sign or symptom
Sympathetic Minimal to moderate degree of hypotension
Sensory Higher than expected level of sensory blockade
Blockade often bilateral, but can be asymmetric
Sensory changes occur over 10 – 20 min
Patchy, variable quality of blockade
Poor caudal spread with sacral sparing
Horner syndrome, facial and corneal anesthesia
Sense of dyspnea
Motor Higher than expected level of motor blockade, including upper
extremities
Motor blockade of variable density
Signs and symptoms of total spinal blockade:

Rapid sympathetic, sensory, and motor blockade
Bradycardia and hypotension
Dyspnea with difficulty swallowing
Limited ability to phonate
Unconsciousness
Respiratory depression with respiratory muscle and diaphragm paralysis.
Brainstem and cerebral hypoperfusion.
MANAGEMENT OF HYPOTENSION
Treatment is needed only when the critical point is reached when these organs
suffer hypoxia.
Arbitrarily set at 30 – 33% below resting control levels. (In HT-20 – 25% of
resting levels)
Increasing FiO2.
Physiological treatment:
Internal auto transfusion

Slight head down (not > 20%) or leg up position.
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Restoration of preload and CO
Extreme Trendelenberg
Counterproductive – by t IJV pr.
Cerebral perfusion and CBF.
FLUID LOADING
Rapid infusion of large volume. Vaso pressors have been found to be more effective
after fluid loading.
VASO PRESSORS
Routine use in not recommended
Cause of hypotension – is not a decrease in PVR – but due to decrease in preload and CO.
IDEAL VASOPRESSOR
Must produce selective vasoconstriction, without affecting after load, HR or
contractility, but not available.
Ephedrine and mephenetermine may be used (ephedrine – tachyphvlaxis)
Dopamine may be used for infusions. Epinephrine is used in refractory cases.
Search for cause- e.g. Blood loss, retractors. The best initial means for treating
hypotension during SAB is this PHYSIOLOGICAL AND NOT PHARMACOLOGICAL
SPINAL ANAESTHESIA IN CHILDREN

Spinal anaesthesia is increasing being used in children of all age groups. The
excellent block within a few minutes is compatible with light sedation levels
which maintain defensive reflexes of the airway.
1. Anatomical considerations
The termination of spinal cord in neonates is at L3, hence the lumbar puncture is
commonly carried out at L4-5/S1-2.
Neonates and infants have a proportionately smaller pelvis than adults and the
sacrum is located more cephalad relative to the iliac crests.
Therefore, intercristal line crosses the midline of the vertebral column t at the
L4-5 or L5-S1 interspace, well below the termination of the spinal cord making
this landmark applicable.
The cerebrospinal fluid (CSF) volume (almost double than adults) and the
reduced CSF hydrostatic pressure.
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Cerebrospinal fluid (CSF) volume is larger on an mL/kg basis in infants and
neonates (4mL/kg) compared to their adult counterparts (2mL/kg).
This may, in part, account for the higher local anaesthetic dose requirements and
shorter duration of action of spinal anaesthesia in this population.
Techniques
Spinal anaesthesia is either administered in the lateral or sitting position in

children. It is imperative to keep the neck extended in sitting position so as to
prevent airway obstruction.
POSITIONING OF THE PATIENT

Spinal anaesthesia is customarily administered in the lateral or sitting position in
children. Hypobaric solutions are not commonly utilized infants. If the sitting
position is preferred, special attention must be paid in the infants to ensure that
the neck in not flexed, which may result in airway obstruction.
A short beveled 22 or 25 G spinal needle is advanced slowly until CSF flows back
when the drug is injected slowly.
Local anesthetic choice and doses
Hyperbaric bupivacaine 0.5% is the most commonly used agent.
Clinical uses
Preterm infants at high risk of apnea following GA form the commonest
indication of spinal anaesthesia in paediatric patients.
Particularly high in ex-preterm infants with a history of apnea of pre-maturity.
Complications
The haemodynamic changes are less frequent in children when compared to

adults.
The sympathetic block produced in children more than 5 years of age may be
particularly profound as to cause hypotension and bradycardia.
Respiratory failure and apnea may manifest if the level is above T1.
Young children may also develop post dural puncture headache.
Toms are usually relieved with bed rest and mild analgesics.
Dosage regime of 0.5% spinal bupivacaine in children (10)

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0-5 Kg 5 – 15 >15 Kg
Dose (mg / kg) 0.5 0.4 0.3
Volume (ml/kg) 0.1 0.08 0.06
Duration (min) 65-75 70-80 75-85
DEVELOPMENT OF A DIFFICULTY SCORE FOR SPINAL ANAESTHESIA:

Possible determinants of spread of Local anesthetic solutions with in the subarachnoid
space
Patient characteristics 0 1 2 3
Age (Year) 20 – 40 41 – 60 > 60
BMI (Kgm-2) < 22 22 – 27 > 27 – 34 > 34
Spinal bony landmarks Clear Unclear
Spinal bony deformity No Yes
Radiological characteristics of Easy Difficulty
lumbar vertebrae
SPINAL ANAESTHESIA FOR SPECIAL CATEGORIES OF

PATIENTS
SPINAL ANAESTHESIA IN GERIATRIC AGE GROUP
Problems faced with geriatric age group:
- Positioning of the patients for spinal anesthesia because of osteo arthritis and
osteoporosis.
- Associated hearing problems may make. Patients un-cooperative for procedure.
- The calcified ligaments in elderly may create problems with the median
approach difficult. Hence paramedian approach is suitable.
- Even though aging appears to have minimal effects on vasoconstriction, the aged
heart does not respond to baroreceptor stimulation as effectively as young heart so
there will be less of an increase in heart rate and contractility mechanisms through
baroreceptor mediated sympathetic stimulation for increasing cardiac output will be
less effective than in young adults, in aged groups.
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SPINAL ANESTHESIA IN OBESE PATIENTS
Proper positioning of the patient for lumbar puncture is a problem.
Because of increased subcutaneous fat, identification of the space may pose a
major problem and anesthetist may end up with a repeated attempts at lumbar
puncture.
Many of these patients cannot lie down, because of decreased respiratory
capacity that ensures as functional residual capacity is decreased and closing
capacity increased in obese patients.
SPINAL ANESTHESIA IN PREGNANCY
Spinal anesthesia can be initiated with the patient in either the sitting or the
lateral position. The sitting position however appears to be the optimal for the
placement of neuraxial block in obese parturient.
Hyperbaric solutions have the advantages of greater predictability of the block
height than plain solutions do and they allow the anesthesiologist the ability to
adjust block height by adjusting the table position.
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Chapter 19 - ANATOMY AND PHYSIOLOGY OF
EPIDURAL ANAESTHESIA
History
1885 -Corning first performed peridural anaesthesia with cocaine for relief of pain in
an extremity. It was apparently accidental.
1895 -Cathelin first used epidural anaesthesia in sacral region. This is now called
caudal analgesia.
1910 -Lawen investigated the anatomy of the spinal and epidural areas, he found that
injections into the sacral canal did not reach the sub-arachnoid space.
1949 -Curbelo first performed continuous peridural anaesthesia by means of a
ureteral catheter.
1951 -Crawford used peridural anaesthesia for thoracic surgery.
Definition
Epidural anaesthesia (peridural or extradural) is anaesthesia obtained by blocking
spinal nerves in the epidural space as the nerves emerge from the dura and then pass
into the intervertebral foramina. The anaesthetic solution is deposited outside the dura
and therefore differs from spinal or subdural anaesthesia, where the solution is
deposited in the subarachnoid space. A segmental block is produced chiefly of spinal
sensory and sympathetic nerve fibers. Motor fibers may be partially blocked.
Deposition of anaesthetic solutions may be accomplished at the thoracic, lumbar, or
caudal area.
ANATOMIC CONSIDERATIONS:
The peridural space is a circular space surrounding the dural sac and all of its
extensions. It extends from the foramen magnum to the coccyx.
BOUNDARIES
Superior: At foramen magnum where the periosteal layer vertebral canal fuses with
spinal dura.
Inferior: Up to sacrococcygeal membrane
Lateral: Intervertebral foramen and peduncles of vertebra. Interconnected with

paravertebral space
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Posterior: Ligamentum flaum
The space is more extensive and easily distensible posteriorly, while anteriorly, the
dura adheres closely to the periosteum of vertebral bodies. Lateral extensions of the
space accompany the spinal nerves through the intervertebral foramina into the
paravertebral tissue up to the angle of the ribs.
To reach the peridural space in a midline sagittal plane, the following structures are
penetrated.
1. Skin and subcutaneous tissues.

2. Supraspinous ligaments
3. Interspinous ligaments
4. Ligamentum flavum
The vertebral column provides anatomic factors important in inserting the epidural
needle. In the cervical and lumbar area, the spinous processes are more horizontal.
However, in the thoracic region, they are oblique. In the mid – region from T4 – T7 this
is marked and the tips of the spines usually overlie the next lower vertebrae or
interspace.
CONTENTS
1). Connective tissue
Significant amount present ventrally connecting dura with posterior longitudinal

ligament.
Dorsally a distinct midline fold of connective tissue called ‘plica mediana
dorsalis’ connects the dura to ligamentum flavum. These midline band divide the
epidural space into right and left sides and narrow the space in midline.
Clinical correlation:
The insertion of an epidural needle of necessity must separate the dorsomedian fold or
strands of connective tissue. It is possible that when a true dorsomedian band or
membrane exists, a spotty and / or unilateral type of block may result.
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Epidural Fat
Varying amount distributed in random fashion more so lateral and posterior
region.
Has affinity for lipid soluble drugs (Bupivacaine and etidocaine) thus competes
with vascular and neural uptake – the drug remains in fat for longer duration.
The compliance of the epidural fat varies with persons and with increasing age –
low compliance may result in “Drip back” of injected local anaesthetic.
3). Areolar tissue
4). Spinal nerve roots with their dural sleeves
5). Spinal arteries
The spinal branches of aortic, subclavian and iliac artery crosses the epidural
space in the region of dural cuff.
6). Epidural veins
Large valveless veins which are part of internal vertebral venous plexus.
They lie in the anterolateral part thus epidural needles should pierce the
ligamentum flavum in midline.
Marked increase in intra abdominal pressure (pregnancy, abdominal mass) thus
obstruction of IVC results in re routing of the venous return by way of epidural
veins and then to azygous vein above the level of obstruction. This leads to
Increased chance of accidental puncture or catheter insertion into the veins.
Increased surface area – more absorption of local anaesthetics.
Decreased epidural space volume thus requiring reduction of dose.
7). Epidural Lymphatics:
Dural cuff region is supplied with rich lymphatic network.
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SIZE OF PERIDURAL SPACE
Regional epidural space width and dural thickness
Epidural Space (mm) Thickness of Dura (mm)

Cervical 1.0 – 1.5 1.5 – 2.0
Lumbar 5.0 – 6.0 0.33 – 0.66

The distance of the epidural space from the skin in the midline of the lumbar region on
insertion of an epidural needle has been measured with subjects in the lateral position.
The overall median distance in normal adults female patients is 4.7 cm at the L 3 – L4
level. In only 5% of patients is the distance greater than 7.0 cm. In 60% of patients, the
epidural space is to be found within 5.0 cm of the skin in the midline. In about 10% of
patients, it may be necessary to insert a needle to a depth of 6.0 cm or more. On the
other hand, a loss of resistance at a depth of less than 3.0 cm probably does not identify
the epidural space.
Factors altering depth are as follows:

Distance increases with increasing adipose tissue as seen in obese patients.
Angle of the needle. If the needle is not perpendicular, the space will be located
at a greater distance.
Position of the patient – with the patient in the lateral position, the skin may sag
imperceptibly and the distance increase. With the patient in the sitting position,
the depth of the epidural space is slightly less.
One must attempt to maintain the skin in a normal anatomic position i.e., in the
midline, since there may be some slippage to the dependent side when patients
are in the lateral decubitus position.
Ethnic origin – Asian women have an average depth to the epidural space of 4.33
cm which is less than that of Caucasian women with a depth of 4.89 cm.
Edema – Clinically recognized edema in patients will increase the distance from
the skin to the epidural space by an average of 0.75 cm.
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EPIDURAL SPACE IN CHILDREN
In children under six years of age, the epidural space has spongy, gelatinous lobules and
distinct spaces. This is in contrast to the densely packed fat globules and fibrous stands
characteristic of the mature epidural space. Because of this difference, there is a more
rapid longitudinal spread of drugs within the juvenile epidural space.
PHYSIOLOGIC CONSIDERATIONS
Originally, a negative extradural pressure was described in 1928 by Hedlt and Moloney.
This so called negative pressure in the peridural space is greatest at points of firm
attachments and also in the thoracic region, less in the lumbar area, and least or absent
in the sacral area.
There are two theories explaining this negative pressure:
1. The Cone Theory considers that the needle introduced into the peridural space
depresses the dura, consequently creating a larger epidural space. It thus is
considered an artifact caused by the identification of the dura by the advancing
needle.
2. The Transmission Theory considers that the negative pressure in the epidural
space is caused by the transmission of the intrapleural negative pressure
through the intervertebral foramina to the peridural space.
Anatomically, there is free communication of the extradural space with the
paravertebral space and in turn, the tissue pressure in this area is influenced by the
intrapleural pressure. Factors that decrease the negative intrapleural pressure or raise
the subarachnoid pressure will decrease the negative peridural pressure.
Marked flexion of the spinal column reduces the length of the anterior wall and
elongates the posterior wall. Consequently, the capacity of the vertebral canal proper
increases and results in a greater negative pressure. The negative pressure is greater in
young people. In older patients with ligamentous changes and ankylosis of
articulations, anterior flexion is limited.
The extradural pressure has been carefully measured in the relaxed patients. In the
lower lumbar region, it amounts to about 0.5 cm H2O. In the upper lumbar, it amounts
to 1.0 cm H2O and in thoracic region, it varies from 1 to 3 cm H2O with an average of 2.0
cm.
SITE OF ACTION
Three sites of action of the local anaesthetic agents have been identified:
1. On the nerves as they traverse the epidural space
2. On the nerves as they pass out through the intervertebral foramina
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3. On the nerves in the subarachnoid space – the agent having reached this area
by diffusion through the dura.
After administration of 2% lidocaine solution, anaesthesia appears in about 10 minutes
and is complete in 20 minutes. Sensory anaesthesia of all modalities is complete ; block
of sympathetic fibers is partial, while motor paralysis is incomplete. The anaesthesia
lasts up to two hours and gradually disappears during the following two hours.
FATE OF EPIDURAL AGENTS
Epidural Injection
Longitudinal Spread in Epidural space
Leakage by Leakage through Diffusion through Diffusion through

vascular intervertebral dual root sleeves dura mater
absorption Foramina
Paravertebral block Subdural spread

of nerve trunks in
young subjects
Centripetal sub
Perineural spread Spinal root block
Subpial spread CSF

Peripheral cord block
Sites of action
The actual site of action is in intervertebral foramen where the spinal nerve loses the
protective dural sheath
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VASCULAR ABSORPTION PHARMACOKINETICS:
Absorption of local anaesthesia from the peridural space is biphasic. The intial or rapid
absorption phase is characterized by short peak plasma times, rapidly attained and high
peak concentrations. As the peak levels decline there continues a slower second phase
of absorption, lating up to 3 hours. This slow absorption phase extends into the
elimination half life phase, which appears to be prolonged.
EFFECT OF ADRENALINE ON ABSORPTION

The addition of adrenaline to the local anaesthetic mixture provides definite protective
effects. In Mather’s study, the addition of adrenaline to lidocaine or etidocaine epidural
anesthetic solutions reduces the venous concentrations as measured by about 60%.
This represents an added safety factor.
INFLUENCE OF AGE ON ABSORPTION:

Study of absorption of local anaesthetic solution sin the elderly patient reveals the
following:
The peak serum level of anaesthetic agent is increased.
The time to CS max is significantly reduced. Older patients achieved a peak level
faster (less than 10 minutes), while those under 30 years required up to 20
minutes to reach a peak serum level.
Onset time to loss of pinprick sensation is not significantly different in the young
compared to the elderly.
Hydrostatic pressure in the epidural space increases with age after injection of
an epidural anesthetic solution. This should partially explain the more rapid
intravascular and higher peaking of serum concentrations.
The increased rate of absorption and of the attainment of high serum levels of
local anesthetics from the epidural space may be modified by the usual decline in
cardiac output with increasing age.
FACTORS IN EXTENT OF EPIDURAL ANESTHESIA

Volume of solution
Selection of appropriate interspace
Speed of injection - slow rates diminish spread, and interrupted injection minimizes
spread.
Position of patient
Effect of gravity - solutions tend to gravitate to dependent parts of the epidural space.
This is not significant as in SAB.
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Specific gravity of Dispersion =Volume x Force x Time + gravity
Resistance of tissue to anesthetic agent.
In summary, one may write an equation for spread:
VOLUME CAPACITY OF EPIDURAL SPACE

The volume of solution required for an epidural anesthetic depends on the number of
segments to be blocked and the site of injection. Spread or extent of anesthesia is
commonly expressed as the segmental dose. That is, the "dose spread" is the volume of
analgesic solution injected in milliliters per number of dermatomes blocked or
milliliters per spinal segment. For each pair of segments the following volumes are
recommended.
Cervical - 1.5 Ml
Thoracic - 2.0 mL
Lumbar - 2.5 mL
PRINCIPAL DETERMINANTS OF DOSAGE

Volume of anesthetic solution:
The dose of epidural local anesthetic agent is largely determined by the number of
spinal segments to be blocked and the volume necessary to reach and effectively bathe
those segments. Both, patients height and age factors must be considered, as well as
anatomic, clinical, and pharmacokinetic aspects, to arrive at a safe anesthetic volume-
dose.
Age / Segment Factor:

From an age of about 4 years to 18 years, there is a steady increase in dose requirement
per segment from 0.2 mL to 1.0 mL per segment; from 20 to 40 years, the dose
requirement is at a plateau in the range of 1.0 to 1.6 mL per segment, modified
according to height.
From 40 to 60 years, there is a slight decrease in dose requirement, with a range of 0.5
to 1.0 mL/segment, adjusted to height. After 60 years of age, the volume per segment is
decreased further and should be set at 0.3 to 0.6mL segment.
Generally, after 40 years of age, there is a linear relationship between a given single set
dose and the number of segments blocked.
Height factor:
The segment volume should be modified according to the patient's height. For patients
who are 5 feet in height (150 cm), a volume of 1.0 mL/segment will be appropriate; for
patients who are 6 feet tall (180 cm), the dose-volume of 1.6 mL is sufficient. For
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intermediate heights, an increase in the volume to be injected is based on an increase of
0.1 mL of the anesthetic solution for each 5.0 em (2 inches).
Selection of interspace:
The site of injection should correspond as closely as possible to the middle of the area to
be anesthetized. Entry into the epidural space in the lumbar and lower thoracic region is
easiest because of the following:
1. The angle of the slopes of the spinous process is less acute.
2. The interspinous ligaments and ligamentum flavum are thicker in the lumbar
region and more easily sensed or appreciated by the operator.
3. The epidural space is wider in the lumbar area.
4. The negative pressure is significant in the lower thoracic region.
Spread of solutions
An anaesthetic solution injected extradurally spreads widely through the extradural
space. The resistance is less in this space than in the intervertebral foramina.
The most intense block and earliest onset of blockade occurs at the site of injection. The
spread is related to two anatomic features:
1) The size of the epidural space
2) The size of the nerve roots.
Speed of injection:
The more rapid the injection, the wider is its spread. Conversely, when the need for
extensive epidural anaesthesia is not great, the anaesthetic should be injected slowly.
It is recommended that the rate of injection should be approximately 0.5 to 0.7
mL/second. A rate of about 1.0 mL/1.5 second is optimal. The disadvantages of a rate of
1.0 mL/second or greater are as follows: there is usually an increase in the height of the
dermatomal block, which may not be desirable, but it is accompanied by a shorter
duration of action of the anaesthetic.
CLINICAL MODIFYING FACTORS

Two important clinical conditions require a downward adjustment in dosage.
Obstetric patient: In obstetric patient, when administered the usual dosevolume, will
have an extensive spread of about 20 segments instead of 12. Therefore, the dose-
volume is reduced by 30%. This is explained by a decrease in the size of the epidural
space from distention of the epidural veins; hence, a given volume will spread over
more segments. This is considered to be the result of the vena-caval compression in the
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supine position. Similarly, the patients with abdominal distention or who is extremely
obese should have a reduction in dose of about 30%.
Arteriosclerosis: Depending on the degree of arteriosclerosis, and/or occlusive

vascular disease, there is an exaggerated spread of epidurally administered anaesthetic
solutions. Generally, the segmental dosevolume should be reduced by 50%.
Anatomic Factors: Anatomic factors are more precisely related to the aging process.
The patency of the intervertebral foramina and the number of arachnoid villi in the
spinal roots are altered with age. With advancing age, the intervertebral foramina are
progressively occluded. This limits the outward spread of solutions injected into the
peridural space. Hence, a greater volume is available to spread in the peridural space.
This partially explains why the dosevolume should be reduced in the older patient.
POSITION OF PATIENT
The epidural space is a potential space, and solutions do not readily flow in this space
because of relatively low compliance; hence, gravitational influences are minimal. The
lateral decubitus position is widely used, especially in the pregnant patient.
The sitting position is indicated in obese patients for technical ease of introducing the
epidural needle. It is also desirable when perineal anesthesia is desired, since blockade
of the sacral nerves is more complete and reliable.
For upper thoracic and cervical region block, the sitting position also provides greater
ease of insertion of the needle into the epidural space, and the level at C7, and T1, is a
recommended space.
DETECTION OF EPIDURAL SPACE:

To recognize the position of a needle in the epidural space, several methods have been
recommended. These methods either: take advantage of the potential negative
pressure, or use the sudden disappearance of resistance when the ligamentum flavum is
penetrated.
NEGATIVE PRESSURE TECHNIQUES

1. Hanging Drop Sign: A small drop of sterile distilled water is placed on the hub
of the needle after it has been introduced to the level of resistance indicating the
beginning of the ligamentum falvum. When the needle is advanced through the yellow
fibrous tissue, this drop will be "sucked into" the epidural space. This is called the "sign
of the drop".
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2. Capillary Tube Method: Odom devised a small capillary tube filled with sterile
saline in which one or two bubbles of air were placed. These acted as a meniscus. As
soon as the needle entered the epidural space, the saline was sucked in, and the air
bubbles could be seen to advance into the space.
An air bubble can be placed in a syringe filled with saline, and when the attached needle
enters the epidural space, the bubble will double in size.
3. Manometer Technique: A small "U-shaped" glass tube about 3 to 4 inches high
is used as a water manometer. After the needle has been introduced into the
interspinous ligaments, the sterile glass manometer is attached to the needle. As it is
advanced through the ligamentum flavum and enters the epidural space, there is an
immediate movement of the liquid, signifying a negative pressure.
DISPPEARANCE OF RESISTANCE TECHNIQUES:

1. Syringe Technique: Sudden loss of resistance to a pressure exerted on the
plunger of a syringe filled with water as a needle advances through the ligamentum
flavum was first recognized by Sicard and Forestier in 1921. It was introduced by them
into clinical practice. Liquids transmit pressure changes more quickly and accurately
than air. A small syringe is chosen as more efficient. The presence or absence of
resistance is noted during advancement of the needle by exerting continuous firm
pressure on the plunger of a 2 mL syringe filled with fluid and attached to the needle.
The disadvantage to this technique is that it may be clumsy; the anaesthetist must
divide attention between exerting pressure and introducing needle.
2. Spring -Loaded Syringe: A Visual Technique. Although the syringe is heavy,
when the peridural space is entered, the syringe automatically unloads itself by virtue of
the diminished resistance in the space.
3. Balloon Technique: A small light balloon mounted on a glass adapter is
attached to the epidural needle when this needle has reached the yellow ligament. The
balloon is just inflated with 2 or 3 mL of air. When so fully inflated the pressure within
the balloon is approximately 50 mm Hg. As the needle is advanced and penetrates into
the epidural space, the balloon will collapse.
4. Brook's Device: A Visual Technique. An Odom's indicator or capillary tube can
be sealed at one end and a glass bubble crated there. This is filled with water or saline,
and few bubbles of air placed in the tube part. It is attached to the epidural needle when
the needle reaches the Iigamentum flavum. At this point.the bulb is heated to create a
slight positive pressure. When the needle penetrates to the epidural space the positive
pressure of the heated water advances, the meniscal bubble toward the epidural space.
5. Vertical Tube of Dawkins: A Visual Technique. In this method, a slight positive
pressure is created by a short vertical column of water in a tubeless than 10 cm high
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connected at right angles to the hub of the epidural needle. A bubble of air also may be
placed in the water. The force of gravity on the column of water produces the pressure.
When the epidural space is entered, the level of the column of water drops indicating a
disappearance of resistance.
PREPARATION OF SYRINGE FOR LOSS OF RESISTANCE TECHNIQUES

Accurate location of the epidural space is commonly determined by the loss of
resistance techniques using a new 5 mL glass syringe. The quality and functioning of the
syringe is key to success.
The intrinsic resistance of the plunger moving into the syringe barrel must be minimal.
Bromage recommends that the plunger be lubricated by wetting with saline before
insertion into the barrel, assuring that this lessens resistance to plunger movement in
the barrel.
TECHNICAL PROCEDURE
1) Preparation and monitoring of patient:
Functional intravenous line and emergency drugs.

Blood pressure monitoring, pulse oxymeter
Equipment for airway management and O2 administration
2) Position of patient
Lateral decubitus position - more commonly used for lumbar epidural

Sitting position - obese patient, thoracic approach
- cervical approach
Site of injection:
A spinal interspaces chosen one to two segments below the middle of the area to be
anesthetized.
Site of puncture for epidural anesthesia ;

Operation Spine level Needle bevel
Perineum Sacral caudal Up
Lower extremities L3 Down
Perineum L4 Down
Inguinal L2 Up
Lower abdomen T1 – L1 Up
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T8 – T10 down
Upper abdomen T6 – T8, T10 Up down
T8 – T10
T6 – T8
Chest T4 – T6 Down up
T6 – T8
PREPARATION:
Skin is cleaned, an antiseptic applied, and the area draped, a skin wheal is made and
deeper tissues infiltrated with 2% lidocaine.
Choice of needles and catheters:

Epidural needle Catheters
Crawford point needle 18, 19, 20 G, 16 G
Touhy needle Huber point Nylon, polyurethane and Teflon
Hustead needle Single lumen (open end)
Other: Weiss, cheng, Crawley Multi orifice (blunt tip)
INSERTION OF NEEDLE:
The needle should be inserted slowly and gradually. The needle passes through the skin
and interspinous ligament which offers a light resistance. When this is pierced, no
further resistance is felt until the ligamentum favum is engaged.
A glass syringe or a low resistance, plastic syringe is filled with 2-3 ml saline / air
and attached to the hub of epidural needle, after removing the stylet.
Maintain a constant pressure on testing syringe with the dominant hand.
Controlled needle advancement in vice like grip (bromage grip) is made with the
non dominant hand.
As the needle enters the epidural space there is a sudden and dramatic loss of
resistance as the saline or air is rapidly injected.
ASPIRATION TEST
When the needle is considered to be in the epidural space, a syringe is attached to the
needle and by gentle aspiration evidence of CSF or of blood is sought. The anaesthetic
needle is then rotated and aspiration attempted in four planes, 90° apart. If neither fluid
nor blood is obtained, the operator may proceed.
It free blood is found in the epidural space, the technique should be modified or
abandoned. Another interspace may be chosen.
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TEST DOSE TECHNIQUE:
A test dose, consisting of a fraction of the full dose of the anaesthetic solution, was
recommended by Foldes to be injected before the full or loading dose to reveal
accidental subarachnoid and/or intravenous injection. The incidence of intravenous
injection is estimated at 0.01 % to 0.2% Moore studied the components of an effective
test dose and recommended that a single test dose should consist of a 3.0 mL volume of
a local anaesthetic, to which 15 µg of epinephrine (5.0 µg/mL solution) is added, making
a concentration of 1: 200,000.
Value and Limitations:

The test dose is of particular value in recognizing a subarachnoid injection of the
anaesthetic mixture.
Appraisal of Test Dose:

Despite some false-positive results and other failures, the lead dose reveals a large
percentage of misplaced needles. And the test dose can reveal two potentially lethal
complications, namely, total spinal block and accidental intravascular injection of local
anaesthetics.
TOTAL SPINAL BLOCK: Total spinal block can occur with large volumes of local
anaesthetic intended for the epidural space when accidentally infected into the
subarachnoid space. The patient becomes hypotensive, comatose, and paralyzed, with
dilated pupils, over a period of 2 to 5 minutes; the condition may last for several hours.
Management:
Rapid tracheal intubation, ventilation, and fluid resuscitation are required. The obstetric
patient is at a higher risk because of rapid development of hypoxia and the possibility of
regurgitation and aspiration.
ACCIDENTAL INTRAVASCULAR INJECTION:

Accidental intravascular injection of local anaesthetic is revealed by a transient
tachycardia - an increase of about 30 beats/min - and an increase in systolic pressure of
about 20 mm Hg within 20 to 40 seconds. Jitteriness, tinnitus, and circumoral pallor are
readily seen, and patients will complain of palpitation; this effect usually lasts for 3 to 4
minutes. However, hypoxia, acidosis and aspiration, or convulsions may follow.
Treatment and resuscitation must be immediate. The high lipid solubility and protein
binding of bupivacaine and etidocaine make them cardiotoxic when injected as a bolus
intravenously. 0.5% bupivacaine, which is commonly used, when injected into an
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epidural vein, can also cause ventricular arrhythmias, cardiac decompensation, and
death in an obstetric patient.
Recommended Safety Procedure Before Injection

1. Perform an aspiration test
2. A 2-rnL test dose of 1.5% to 2% lidocaine for labor pain without epinephrine
3. For cesarean section, use 3 mL of 1.5-2% lidocaine with 1: 200,000 epinephrine
4. In patients with preeclampsia diabetes, intrauterine growth retardation, or fetal
distress avoid epinephrine. Give bupivacaine in 5-mL increments.
5. Test - dose failure and total spinal occasionally can occur. Deaths can be
prevented by prompt intubation and resuscitation.
Continuous epidural anaesthesia:

Use of a catheter for epidural anaesthesia affords much greater flexibility than the single
shot technique because they can be used
To prolong a block that is short
To extend a block that is low
To provide postoperative analgesia.
Bromage ideal charact6eristics of an epidural catheter:

Biochemical inertness
Low coefficient of friction
High tensile strength
Maneuverable rigidity
Kink resistant
Atraumatic tip
Depth indicators
Radio opacity
An appropriate catheter is chosen and verified that passes easily through the epidural
needle before the needle is placed in the epidural space. The needle bevel should be
directed either cephalad or caudal. If the catheter does not pass beyond the needle tip
the needle can be carefully advanced 1-2mm more or rotated 180° and catheter
reinserted.
If the catheter advances only a short distance past the needle tip, it is unlikely to be in
epidural space and needs to be repositioned. In such cases catheter and needle should
be pulled out in tandem, lest the catheter tip will be sheared off by the bevel's sharp
edge.
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The catheter should be advanced only 3-5 cm into the epidural space. Placing a longer
length increases the risk of -
Entering an epidural vein
Puncture the spinal meninges
Exit through intervertebral foramen
Wrap around a nerve root.
POST – INJECTION POSITION:

If spinal lumbar epidural approach is used, position aids to some extent in obtaining
proper extent of anaesthesia: head-down position of 10° tilt for upper abdominal
surgery, supine horizontal position for lower abdominal surgery; and head-up position
of 5° tilt for perineal surgery.
Choice of agent for epidural block:

Surgical Analgesia:
Sensory +++ 2% lidocaine Rapid onset, excellent analgesia and
motor block medium duration
Motor +++ 0.5% bupivacaine Slow onset, good analgesia moderate
motor block, long duration
Postoperative pain 0.125% 0.25%
sensory +++ bupivacaine
Motor O
Lignocaine 2% with Bupivacaine 0.5%
epinephrine
Latency 5 min – 16 min 10-20
Motor blockad 38% 20% 28.95%
Duration by 2 segments 97 19 min 164 46 min
regression
Top dose:
A single repeat dose (20% of initial dose) given 20 min. After main dose
- Consolidates the level of block thus missed segments are filled up.
In conscious patient - monitoring for sins of segmental regression will indicate the need
for top up dose.
In others the approximate time of regression of analgesia as determined by clinical
study is used for top up dose.
Lignocaine - 60 min
Bupivacaine - 120 min
If the initial blockade is too high top up dose should be appropriately delayed.
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CLINICAL CONSIDERATIONS:
Indications:
The guide to the use of any technique is whether it will provide satisfactory working
conditions for the contemplated procedure. If epidural anaesthesia meets this
specification, then it may be used in the flowing circumstances:
1. Poor risk patients

2. Cardiac disease
3. Pulmonary disease
4. Metabolic disturbances
5. When general anaesthesia is contraindicated
6. Obstetric analgesia
Contraindications:
Many of these are similar to the contraindications for spinal anaesthesia. These may be
relative or absolute. In general, the technique is not administered in the following:
1. Severe hemorrhage or shock

2. Uncooperative or apprehensive patients
3. Previous laminectomy
4. Coagulation defects: patients on anticoagulants or hemophiliacs
5. Local inflammation.
Advantages and Disadvantages:

Among the advantages of epidural anaesthesia, the following are to be noted:
1. The area of anaesthesia is well defined.
2. The duration of anaesthesia is longer than spinal.
3. The more severe disturbances of spinal anaesthesia (headaches, meningitis,
arachnoiditis) are minimized.
4. GI complaints are minimal. Nausea and vomiting are minimal.
5. Catheterization incidence is small, urinary retention averages 1.5%.
The disadvantages ar:

1. Technical difficulty resulting from the need for accurate placement of needle
2. Incomplete muscle relaxation
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3. Need for larger volumes of fluid and hence large quantities of drug to achieve
anaesthesia especially for abdominal surgery.
4. Danger of entering subarachnoid space
5. Bleeding in epidural space by catheter injuring venous plexus
6. Spotty segmental block not infrequent
7. Occasional back pain
Criteria for Correct Position of Needle and Successful Block:

1. Onset of analgesia and loss of sensation in 10 minutes after injection of initial
dose of 8 mL.
2. No aspiration of spinal fluid or blood.
3. No palpable swelling superficial to the sacrum
4. Sense of fullness or tingling in legs or rectum
5. Progressive spread of anaesthesia
6. Evidence of sympathetic paralysis with vasodilatation, flushing, cessation of
sweating, and increased skin temperature.
7. In obstetric patients, relief of uterine cramps.
COMPLICATIONS – TECHNICAL
1) Inadvertent Dural Puncture: During attempts at placing the needle in the

epidural space, the dura is occasionally punctured. It has been recommended
that when this occurs, plans for epidural anaesthesia be abandoned and simple
spinal or a general anaesthetic be administered.
2) Total subarachnoid block
3) Subdural injection: In placing an epidural needle (and subsequently a catheter),

the needle may not be epidural (or peridural or extradural), but in the immediate
subdural space, which can be referred to as the extraarachnoid space, i.e., the
space between the dura and the pia-arachnoid. Injection into this area may result
in "spotty" anaesthesia, extensive delayed anaestehsia, or failed anaestehsia. This
subdural space was described clearly in 1963 by Sechzer. Characteristics of a
subdural (extra-arachnoid) block have been further elucidated in the Lubenow
report. The following clinical picture emerges:
1. Unexpected extensive sensory block

2. Unexpected motor block in about 60% of patients
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3. High sympathetic block with frequent papillary block and exaggerated
hypotension.
4. Slow but variable onset of block, from 5 to 30 minutes, usually 10 to 20 minutes.
5. Use of small volumes of dilute local anaesthetics (i.e., 6-8 ml- 0.125 - 0.25%
bupivacaine).
COMPLICATIONS RELATED TO EPIDURAL CANNULATION:

Bleeding caused by the needle or catheter, 18%
Failure to insert catheter, 3%
Discomfort on insertion of catheter, 2%
COMPLICATIONS – CATHETERS:
1. Misplacement
2. Kinking or Curling
3. Occlusion
4. Defects in Construction
5. Damage of Catheter at Insertion
6. Severance and Breaks on Removal
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Chapter 20 - INTRAVENOUS REGIONAL ANESTHESIA
(IVRA)
INTRODUCTION:
Intravenous regional anesthesia is a method of producing analgesia of the distal part of
a limb by intravenous injection, while circulation to the limb is occluded.
HISTORY
"AUGUST BIER" in 1908, first described a satisfactory technique of venous anesthesia
using procaine hydrochloride and injecting together with methylene blue tried to study
the distribution of the injecting dilute solution of procaine intravenously between two
tourniquets which were inflated above the systolic pressure to isolate the circulation.
The resulting analgesia was adequate to perform all surgical procedures distal to the
tourniquet. But surprisingly this technique did not achieve any amount of popularity
except for passing mention in anesthesia text books.
After Bier's initial report of 134 cases, some reports followed for a year or two:
- Catz. J. 1909
- Hartal 1909
- Hirzrot 1909
- Pag and Mac Donald 1909
- In 1919 Eggleson and Hatcher published their results of intravenous procaine,

but its clinical use remained stand still mid 1930's.
Later, the technique was almost completely forgotten. The main reasons for the lack.of
general acceptance are as follows.
The technique was - cumber some
Require wrapping and unwrapping of eschmarch bandage in precise manner.
Special equipment was needed.
It necessitated an operative procedure (cut down) to deliver the anesthetic
solution.
Up to 1925, all the investigators of this technique used procaine, it might be
assumed that adverse reaction to the anesthetic agent played some role in its
lack of acceptance.
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In 1931, Morrison gave a detailed account of this method in England. It was he
who first suggested the use of venipuncture and this made the technique more
practicable.
Ritter was the first to use cocaine intravenously to produce anesthesia without
side effects.
Harrisons used 0.3gm of cocaine as 2% solution intravenously over a period of
30 minutes. At the end of the injection; a deep skin incision produced only
moderate discomfort. The amount of cocaine used was. considered to be an
extremely toxic dose, but produced only imperfect and short duration analgesia.
The technique of intravenous regional analgesia was largely forgotten until
february, 1963, when Holmes (UK) reported a modification of Bier's technique of
intravenous regional analgesia using Lidocaine.
The revival in this technique created enthusiasm in many parts of the world and
attempts have been made to master the technique and find its effectiveness and
advantages over the other nerve blocks.
INDICATIONS IN SURGERY:
1. Operations below Elbow.
2. Operations below knee
3. Tendon operations, scar removal, ganglion excision, hand abscesses, removal of
foreign bodies, lacerations, Colle's fracture.
Leg ; toe nails removal, bunions excision, amputations.
4. Useful in elderly patients and acceptable in children. Patients of ASA I to III can
be safely managed.
CONTRAINDICATIONS:
1) Mainly related to tourniquet use - Absolute contraindications include sickle cell
disease, Raynoud's disease or scleroderma, allergy to local anesthetics and patient
refusal.
2) Relative contraindications include severe hypertensive or PVD, local infection,
skeletal muscle disorders. Paget's disease (local anesthetics may spread to the systemic
circulation via venous channels in bone).
3) In addition, patients with untreated heart block is a particular contraindication,
since sudden release of local anesthetics into circulation may convert a partial heart
block to a complete heart block or may precipitate asystole. Brady cardia has been
recorded following cuff release when lidocaine was used even in normal patients.
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4) Patients in physical status ASA - IV are not usually anesthetized by intravenous
regional anesthesia. The method is not recommended in semistuporous or
uncooperative patients; infections of the extremity are a contraindication.
CHOICE OF LOCAL ANESTHETIC AGENTS

Most commonly used local anesthetic agent is lidocaine. This was the local
anesthetic advocated by Holmes. This agent can be used for short procedures
and for those procedures lasting over 2 hrs by applying the intermittent or
continuous technique.
Bupivaeaine 0.25% to 0.5% has been used for prolonged surgical procedures. An
increase in post deflation sedation and anesthesia occur. Potential serious
complication have been reported.
Other agents have been used but have undesirable actions. Chlorprocaine is
associated with high incidence of thrombophlebitis (5% to 10%)
Prilocaine is associated with methemoglobinemia.
Mepivacaine 0.5% has been used but has no advantage over lidocaine.
Tetracaine provides rapid and intense anesthesia.
CHARACTERISTICS OF THE DIFFERENT LOCAL ANESTHETIC AGENTS USED FOR

UPPER EXTREMITY INTRAVENOUS REGIONAL ANESTHESIA:
Drug Usual Total dose Time to surgical Loss volition
concentration (mg/kg) anaesthesia (min) motor activity
(%) (min)
1. Procaine 0.5 3-4 2 8
2. Chlorprocaine 0.25 – 2 Upto 8 5 15
3. Tetracaine 0.2 1 – 1.5 3–6 8
4. Lidocaine 0.25 – 0.5 3–4 3–5 15
5. Mepivacaine 0.5 – 0.6 2–8 3–4 13
6. bupivacaine 0.2 – 0.5 1. 5 – 3 2–8 10
7. Prilocaine 0.5 – 1.0 3 4–5 10
DOSAGE:
A volume – dose relationship is involved in obtaining anaesthesia by this method.
There must be a volume of solution sufficient to fill the vascular bed and the
concentration must be sufficient to produce anaesthesia. The latter is limited by
the factor of toxicity.
With regard to regional intravascular anesthesia of the extremities, a large
volume of low concentration of the local anesthetic agent is employed. The
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anesthetic solution is used to replace the blood in the vascular area to be
anesthetized. It is thus a volume technique and depends on knowing the vascular
volume of the extremites.
To replace the blood volume of an area and also to eliminate the dilutional effect
of the blood on the anesthetic solution, the selected extremity must be made
ischemic.
For the upper extremity, a dose of 3 mg / kg is used in a 0.5% solution. In most adults a
volume of 40 to 50 ml is thus injected. If a preinjection period of ischemic is used, then a
smaller volume may be used based on a dose of 1.5mg / kg or a volume of 20 to 24 ml of
an 0.5% solution.
For the lower extremity, the dose is also 3 mg / kg but a solution of 0.25% is used, hence
the volume is doubled.
BLOOD VOLUME IN THE EXTREMITIES:

It has, been found that in an average man weighing 70 kg, the upper extremity has a
blood volume of about 170 ml, and lower extremity has volume of about 300 ml.
MECHANISM
Because the venous system is a one way flow system on account of valves, an
anesthetic solution injected into a peripheral superficial vein travels proximally
from the site of injection to the level of the applied inflated tourniquet (Holmes
technique).
Initially, the solution fills the large superficial veins. As the full volume of
solution is introduced, it concentrates in the region of the elbow, particularly in
the anterior part, filling the antecubital veins (basilic, cephalic and median
cubital vein). This is reasonable, because there are large veins around the elbow
with minimal resistance (especially in the collapsed or milked state) to the
injection of solutions.
After filling the venous channels around the elbow, which are in proximity to
main nerve trunks, smaller vascular channels take the agent to the core of the
nerve trunks.
Once in the core, the anesthetic diffuses toward the periphery of the nerve.
Because fibres to the distal part of the extremity are in the core of the nerve
trunk and those to the proximal part of the arm are in the outer nerve layers, it
would be expected that the fibers for distal distribution would be blocked first.
This is in agreement with the clinical observation that anesthesia develops from
the finger tip upward.
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Alternatively small veins in muscles, deep veins, and perforating veins are also
filled. As these veins are filled, there is a rapid retrograde filling of venules and
capillaries. Once in the capillaries; there is diffusion of the drug through the
capillary walls in to the extravascular space and to the tissues. So, anaesthetics
may act directly.
Hence two sites of action for local anesthetics have been proposed.
1) At the nerve trunks.
2) At the small sensory nerves and the sensory nerve endings (and, presumably, at
the neuromusctor junction)
TECHNIQUE:
STANDARD METHOD FOR THE ARM:
Premeditation - premeditation usually is not required particularly if the proposed

operation is likely to be of short duration. How ever, some form of sedation may be used
for longer operations. Just prior to the performance of the block, an appropriate dose of
a sedative, such as diazepom, midazolam or a neurolept analgesic may be given
intravenously. This will help to reduce the patients awareness of the operation and
allow better tolerance of the inflated cuff, and it may raise the threshold for toxic effects.
Preparation of the patient:

The patient should, normally have fasted in the same manner as for those who have
general anesthesia, since vomiting could represent a hazard. Having ascertained that the
patient accepts this form of analgesia and has no history of allergic reactions to local
anesthetic agents or has other contraindications, the anesthesiologist should explain the
technique and should check the pulse occlusion pressure. As with any anesthetic
administration, it should be routine to secure a route for intravenous fluids and
supplemental drugs, usually in the other arm.
Choice of vein:
1) An intravenous Cannula or catheter is inserted into a -vein distal to the operative

site, usually on the back of the hand or at an ankle vein. However, if no veins are
visible there, a vein on the forearm or even at the antecubital fossa may be
choosen. There is however, some evidence that failure to obtain analgesia, or
"patchy" analgesia, is more likely to occur when proximal veins are used. A
plastic Cannula is preferred for the venipuncture, through a "butterfly" needle
with a short extension tube may be used. A long intravenous catheter should not
be used, because there is at least one recorded case in which the end of such a
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catheter was actually above the inflated cuff, resulting in the injection directly in
to the general circulation. The Cannula or needle is placed in the vein, flushed
with saline and taped securely. Care must be taken not to dislodge it during the
exsanguination or subsequent injection. As with any venipuncture, there should
be careful palpation of superficial arteries, to avoid intra arterial injection.
Production of an ischemic limb:

The completeness of exsanguinations of the extremity to be anesthetized will provide
more complete anesthesia with a more rapid onset. It can be done by 2 ways:
a) By milking or expressing the blood by means of an Esmarch or a Martin bandage
wrapped from the distal portion of the limb toward the proximal part.
b) Elevation of the arm or use of an air inflated splint is an acceptable alternative.
Tourniquet application:
a) The tourniquet cuff is placed at the proximal end of a limb well above the
surgical site.
b) The tourniquet is inflated to a pressure above the patients pulse occlusion value.
Although high pressures might be assumed to confer greater safety from leakage past
the cuff. Discomfort is also likely to be related to the pressure. The exact amount by
which the tourniquet pressure should exceed the systolic pressure cannot clearly be
stated, because the patient's blood pressure may rise during the injection or during the
operation. Some authors advise a tournique pressure of 200 to 250 mmHg, while a
pressure of 150 mmHg above systolic or 50 to 100 mmHg above pulse occlusion
pressure has also been recommended. In all cases, disappearance of the radial pulse
should be checked.
The practice of cross clamping the tubing of the cuff after inflation is not recommended;
should the cuff have a small leak, it might not be detected. It is better to observe the cuff
pressure at all times on the aneroid dial.
c) Note that in the two cuff technique a secondary tourniquet is placed just distal to
the primary cuff, contiguous to the primary cuff.
Drug administration:
Injection of a dilute solution of a local anesthetic through the paced needle or catheter is
accomplished. Using a 50ml syringe, 40m] of 0.5% lidocaine without preservative or
vasoconstrictor is injected slowly. The quantity must be varied according to the
estimated mass. of tissue below the tourniquet even though that mass may not correlate
well with patient's overall weight. For example, if maybe necessary to use 50ml for a
muscular forearm of a 70 kg patient, whereas a thin forearm of a 110 kg patient may be
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satisfactorily anesthetized with a smaller amount. As the drug is injected, the skin
usually becomes mottled, and analgesia develops rapidly. Muscular relaxation, usually
quite profound, appears at the same time. If sufficient analgesia is not present 5 minutes
after the injection of 40 ml, further 10ml should be given before removing the needle.
After the onset of anesthesia and before the onset of tourniquet discomfort, the
secondary or distal cuff is inflated (the area is now anesthetized) and primary or
proximal cuff is deflated.
Tourniquet discomfort:
During the operation the tourniquet must be kept inflated above the previously
determined valve. After a time, particularly in the unseadated patient, discomfort may
develop at the site of the tourniquet. This may respond to a small intravenous dose of
diazepam or an analgesic drug. An alternative or additional maneuver is to place
another cuff below the first and to inflate it over the analgesic part of the arm, after
which the upper cuff is deflated.
Tourniquet release:
Never deflate the tourniquet until at least 20-30 minutes have elapsed from the time of
injection when lidocaine or procaine has been used. A longer time is advised if
bupivacaine is employed.
No tourniquet should remain continuously in place for more than 2 hours. For
prolonged surgery, the continuous or intermittent technique can be employed.
The tourniquet is released at the end of the operation, and not before, since sensation
returns rapidly. It is at this time that adverse reactions may occur. So the patient's pulse,
oxygen saturation, blood pressure and ECG should be monitored closely during the first
few minutes after tourniquet release. Appropriate resuscitation equipment should be
available, and the patient should be warned to expect transient generalized paresthesia
and sometimes tinnitus. There appears to be no risk of delayed after effects.
MODIFIED METHOD FOR THE HAND

The cuff is placed on the forearm taking care to keep it below the head of the
radius.
About 10 ml of solution will usually provide complete analgesia i.e., 1.5mg/kg of
0.5% lidocaine will provide excellent anesthesia.
Since the quantity of solution is so small, the tourniquet could be released safely
at any time, so a short procedure is quiet feasible.
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A difficulty some times encountered with this method is that blood flow through
the radius and ulna causes gradual vascular congestion of the hand if the
operation is other than quiet short.
For a longer operation, a second tourniquet on the upper arm may be needed to
prevent this congestion.
Many papers now attest to the value of this method for hand surgery, including
one report of a series of out patient operation for dupuytren's disease.
An interesting variation of this is the method of digital regional anesthesia
described by Ryding. He showed that if a vein on the dorsum of a finger can be
connulated with a fine needle, a very good analgesia of the finger can be achieved
with a small quantity of anesthetic, using a rubber tourniquet around the base of
the finger. This method is quiet appropriate for the treatment of conditions such
as paronychia.
LOWER EXTREMITY IVRA:
Lehmon – Jones block:

Establish iv line in an upper extremity for fluids and drugs.
Two standard arterial thigh pneumatic tourniquet are pretested (300 mg Hg for
adults, 250 mmHg for children).
Tourniquets are placed adjacent to each other around the thigh as far proximal
as possible.
An intravenous route is established with a 22 guage plastic needle in the lower
extremity at the levels of the foot or ankle. The needle is severed with tape.
Dorsum of foot-veins adjacent to dorsal is pedis artery.
Greater saphenous vein just anterior to medial malleolus is the most satisfactory.
The lower extremity is elevated for 3 minutes to achieve venous drainage.
Exsanguination of the extremity is completed by wrapping the leg from the toes
to the level of the tourniquet with an esmarch bandage. The lower leg should be
placed on a pillow.
Inflate the upper tourniquet to the preset pressure of 300 mmHg. Check arterial
occlusion by palpating the tibial artery.
A lidocine anesthetic solution of 0.25% or 0.5% concentration is injected into the
intravenous line in the lower limb. For the lower concentration, a dose of 3.3 mg
/ kg of body weight is administered. For a 70 kg man, this amounts to a volume
of about 90 ml. This volume should be infused over a period of) minutes.
Sensory anesthesia develops in 15 to 20 minutes.
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At this time, the lower tourniquet is inflated and the upper one deflated.
MODIFICATION FOR ANKLE OR FOOT SURGERY:

Establish an intravenous line in an arm for fluids and drugs.
Place a standard arterial arm tourniquet around the calf at its widest
circumference but at least 3 inches below the head of the fibula to avoid peroneal
nerve compression. A double tourniquet on the calf of the lower leg does not
evenly fit the curvature of the calf and frequently. fails; therefore, it is not used.
A standard arterial thigh tourniquet is placed at the midpoint of the thigh as a
"back up". This provides an additional means to prevent the anesthetic from
entering the systemic circulation in the event of lower tourniquet failure. Both
cuffs are connected to a separate oxygen - powered variable pressure inflation
regulator.
A 22 gauge plastic needle is inserted into the greater saphenous vein at the ankle
just anterior to the medial malleolus for administration of the intravenous
anesthetic.
The lower extremity is elevated for 3 minutes to achieve venous drainage.
Exsanguination of the extremity is completed by wrapping the leg from the toes
to the level of the tourniquet with an esmarch bandage. The lower leg should be
placed on a pillow.
Inflate the calf tourniquet to 300 mmHg by a pressure powered regulator.
A 0.5% lidocaine anesthetic solution is administered via the ankle plastic needle.
The dose of lidocaine is based on the size of the limb and not the patients weight;
it is a volume dose ranging from 40 to 50 ml.
A test dose of 10 ml of 0.5% lidocaine anesthetic solution is injected The patient
is observed for systemic toxicity over a period of 1 minute. In the absence of
adverse reactions, the remaining volume is injected.
The plastic needle is removed and the extremity surgically prepared. During this
time, the adequacy of anesthesia is tested.
PROLONGED INTRAVENOUS REGIONAL ANESTHESIA

As mentioned earlier IVRA is better suited for short procedures.
It may be used for prolonged operations if the patient is well sedated.
The technique was described by Brown and Weissman and this consists of
inserting an indwelling plastic catheter into a suitable vein away from the
operation site and leaving it in site during the operation.
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After about one hour, the tourniquet is deflated and bleeding vessels may be
secured during the short interval before sensation returns.
The arm is then elevated, the tourniquet reinflated and another dose of local
anesthetic injected.
They found that to produce adequate analgesia, this dose may be only one half
the volume of the first.
The procedure may be repeated if necessary.
However, it is not proven that this short tourniquet release affects the incidence
of tourniquet complications and generally the governing factor in long
operations is the time for which it is considered safe to leave a tourniquet
inflated.
SUPPLEMENTAL ANESTHESIA:
Some nerves to the arm are poorly anesthetized, namely the intercostobrachial, the
lower lateral, the posterior cutaneous nerves of the arm. For surgeries in these areas of
innervation, the nerve must be blocked by local injection to supplement the intravenous
regional anesthesia.
TOURNIQUET DISCOMFORT:
This may appear in 15 to 20 minutes often as an ache, tightness or paresthesia.
If significant, one of the following steps alleviates the condition.
1) The subcutaneous infiltration of a local anesthetic (0.25% lidocaine or
mepivacaine) above the tourniquet as a band or armlet around the arm.
2) Application of a second tourniquet cuff just below the first and in the area
already anesthetized. The second cuff is applied at the inception of the
procedure.
LEAKAGE OF ANESTHETIC SOLUTIONS:

Leakage of anesthetic solutions into the systemic circulation during IVRA does occur.
It has been associated with high. plasma levels of local anesthetic on occasion, which
have resulted in significant morbidity and mortality. Seizure phenomena, convulsions,
and the cardiopulmonary arrest have been reported. The safety of the technique
depends on the ability to prevent escape of anesthetic solution into the general
circulation by means of an effective tourniquet pressure.
It depends on two factors
Effective tourniquet (occlusion) pressure
Maximum venous pressure
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An effective tourniquet pressure is one that minimally balances the maximum pressure
that is generated in the region of injection of the anesthetic agent into the various
system of the region being anesthetized. An effective tourniquet pressure is not
necessarily the gauge pressure.
The commonly used tourniquet for this procedure consists of two adjacent cuffs of 6 cm
width. When either cuff is inflated alone of a gauge pressure of 300mm HG, the effective
required tourniquet pressure may only be 200 mg Hg.
One more factor governing the leakage is related to the maximally developed venous
pressure as the anesthetic solution is injected.
Maximum venous pressure that can be developed without leakage has been defined as
the venous pressure above which level there is an associated leakage.
Among the factors affecting venous pressure are the following:
1) Venous pressure developed depends on the site of injection - higher venous
pressures are developed when injections are made in the proximal veins. Thus, it
is recommended that injections be made in a distal vein at the wrist or in the
hand.
2) Higher pressure develops in the venous system if exsanguinations of the arm is
incomplete. The.filling pressure of the injectate is thus added to the residual
venous blood volume and together they provide a greater venous pressure.
3) Higher pressures are developed when the rate of injection is rapid.
4) Injections at the elbow results in the passage of the anesthetic solution into the
deep venous system in the elbow. It does not traverse readily distally into the
distal superficial venous system; there is a limitation by the venous value system
and high syringe pressures are often used. Therefore, at the proximal site, the
venous pressure can exceed cuff pressure and produce leakage.
5) Further, the venous system is continuous with the circulation of the forearm
bony system, and leakage can occur from the radius to humerus. It is noted that
cuff pressure will not prevent fluid passage through such a pathway.
Recommendation:
1) The tourniquet pressure should be minimally set at 300 mmHg.
2) The arm should be exsanguinated by means of an Esmarch bandage,
3) The injection site should be limited to the distal hand or forearm veins.
4) A slow rate of injection is recommended to be approximately 90 seconds.
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RELEASE OF TOURNIQUET:
At the conclusion of surgery, the confining tourniquet is released according to a set plan
to avoid high systemic levels of the local anesthetic. A planned "cyclic" intermittent
technique of release is usually recommended.
1) Deflation of tourniquet pressure to zero and immediate reinflation.
2) After 1 minute, a second deflation to zero pressure for 10 seconds and
immediate reinflation.
3) After 2 minutes, deflation to zero for 30 seconds and reinflation.
4) After 3 minutes, another deflation to zero and no reinflation.
During the deflation phases, the operator must observe for signs of local anaesthetic
toxicity. These indicate a significant blood level and warrant shorter periods of
deflation.
SYSTEMIC PLASMA LEVELS OF AGENT AFTER TOURNIQUET RELEASE:

Effect of duration of vascular occlusion
The duration of vascular occlusion and regional vascular containment of the anesthetic
solution significantly affects the concentration of the agent that enters the general
circulation on release of the tourniquet. As the time of vascular occlusion increases,
there is a steady decrease in the peak systemic arterial plasma concentration.
Venous levels (Injected arm):

After 20 minutes of vascular occlusion, plasma levels of different anesthetic agents in
the venous drainage of the injected arm were observed to be 15 to 40 pg/ml two
minutes after release of the tourniquet (non cyclic).
Lidocaine = 40 µg/ml
Etiodocaine and prilocaine = 15 µg/ml
Bupivacaine = 20 µg/ml
After 45minutes of anesthesia, release of tourniquet results in peak venous plasma
levels which was estimated to be
Lidocaine 7.5 µg/ml, for
Prilocaine = 5 µg /ml
Etidocaine and bupivacaine = 2 µg/ml
Arterial levels:
The plasma levels in the venous drainage of the injected arm represents the amount
that reach the pulmonary artery and lung. A large proportion of this local anesthetic is
taken up by the lung tissue and is also diluted by venous return from other parts of the
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body. Thus, the arterial level of the anesthetics will be greatly reduced. Peak systemic
arterial concentrations are only 3% of the pulmonary arterial plasma levels.
After 10 to 20 minutes of vascular containment using a 1% lidocaine solution (3 mg/kg),
the peak arterial plasma concentration of lidocaine was determined at 10.3 µg/ml on
the release of tourniquet.
After 45 minutes of occlusion the plasma arterial concentration of lidocaine is
approximately 2.5 µg/ml on the release of tourniquet.
Venous level (contralateral arm):

On release of atourniquet 5 to 10 minutes after the injection of 20 ml of lidocaine 1%
anesthetic solution, peak venous concentrations of the local anesthetic are found in the
opposite arm of approximately 1 to 2 pg/ml at 1 to 2 minutes after release.
By 10 to 20 minutes after regional injection, the peak venous blood level in the opposite
arm is less than 1 pg/ml on release of the tourniquet.
It is evident that not all of the anesthetic is released immediately from the anesthetized
region on deflation of the tourniquet but that there is a gradual release from tissues.
Thus, tissues tend to retain the anesthetic drug.
ADJUNCTS USED FOR IVRA:

Although these adjuncts can be used, but since there is lacking consensus on their
dosages, these are of limited utility.
Adjuncts used are
1) Opioids (fentanyl, mepiridine, morphine, sufentonil)

2) Tramadol
3) NSAIDs, ketoralac, tenoxicam, acetyl salicylate
4) Clonidine
5) Muscle relaxants (atracorium, pancuronium, mivacurium)
6) Alkalinization with sodium bicarbranate
7) Potassium
NSAIDs in general and ketoralac in particular, help in improving post operative

analgesia.
Clonidine 1 mg/kg also appears to improve post operative analgesia and prolong
tourniquet tolerance.
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Opioids are poor by this route, only meperidine 30 mg or more has substantial
postoperative benefit but at the expense of post deflation nausea, vomiting and
dizziness.
Muscle relaxants improve intraoperative motor block and aid fracture reduction.
Advantages:
1) Reliability: Technique has high success rate.
2) Ease of performance:
3) Safety: The reported incidence of adverse side effects is low.
4) Muscle relaxation: Appropriate relaxation is obtained so fractures of

dislocation can be reduced.
5) Controllable duration of action: The duration of action of the block is governed

not by the duration of action of the local anesthetic agent being used, but rather
by the time for which the tourniquet is kept inflated. Operations as long as 6
hours has been described and it would seem that there is no diminution of block
until the tourniquet is released.
6) Controllable extent of analgesia: The extent of the analgesia is limited

proximally by the position of the tourniquet. The closer the tourniquet is to the
periphery, the smaller the quantity of local anesthetic solution is required.
7) Rapidity of Recovery: Normal sensation and motor power returns rapidly after
cuff release, even if it is released well before the expiration of the agent's usual
duration of nerve blocking action this rapid return to normal function is
important because it helps to re-evaluate neurologic signs after fracture
reduction. The patient who has had outpatient surgery will not be leaving the
hospital with an anesthetized limb, and thus will not risk accidental injury, burns
etc.
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DISADVANTAGES:
1) A tourniquet must be used
This means that the method cannot produce analgesia of the entire limb but only of that
portion of the limb distal to the tourniquet.
The tourniquet must be kept inflated continuously, it is not possible to release it to
enable bleeding vessels to be identified, unless more local anesthetic is injected after the
tourniquet is reinflated.
The tourniquet may cause pain.
Duration of surgery is limited by the time for which an arterial tourniquet is safe.
The tourniquet itself may cause complications and at least one case of tourniquet
paralysis is on record.
2) Toxic reactions
There is possibility of a systemic reaction to the local anesthetic when it is released into
the general circulation. The risk tends to be greater when large quantities of local
anesthetic agent are used, especially in lower limb IVRA.
3) Inability to provide a blood less field: (modified IVRA technique)
When analgesia of the hand or foot is produced with a tourniquet on the forearm or
lower leg, there is likely to be gradual vascular engorgement, because of interosscous
blood flow not controlled by the tourniquet.
4) Rapidity of recovery with loss of analgesia may be considered a
disadvantage in major surgical cases, and parenteral pain relief may be required
early in the postoperative period.
230

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2011

Dr Azam's Notes in Anesthesiology

Regional Anesthesia & Nerve

Dr. Mohammed Azam Danish

Dr Azam’s Notes in Anesthesiology

Regional Anesthesia& Nerve Blocks

Graphic representation of data is an excellent form of data compression; figures or

I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate

Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more

The format is designed to provide easy access to information presented in a concise

Anesthesiology is an ever-changing field. Standard safety precautions must be

However, in view of the possibility of human error or changes in medical sciences,

To Mohammed Shafiulla, my father, my oxygen,

I also would like to thank my mom (Naaz Shafi), my wife

I also thank my Colleagues Dr Rajshekar Reddy & Dr Sachin for

Finally, I would like to thank my teachers. The dream begins

CHAPTER 1 PRINCIPLES OF REGIONAL ANAESTHESIA ..................................................................................... 12

CHAPTER 2 - LOCAL ANESTHETICS .................................................................................................................. 19

DESIRABLE PROPERTIES: ......................................................................................................................................... 19

CHAPTER 3 BLOCK OF CRANIAL NERVES ......................................................................................................... 33

GASSERAIN GANGLION BLOCK: (MECKEL’S CAVE) ............................................................................................... 33

CHAPTER 4 BLOCKS OF UPPER EXTREMITY..................................................................................................... 44

BRACHIAL PLEXUS BLOCK ................................................................................................................................. 44

CHAPTER 5 FIELD BLOCKS .............................................................................................................................. 64

FIELD BLOCK FOR TONSILLECTOMY .................................................................................................................. 64

CHAPTER 6 - PERINEAL ANAESTHESIA ............................................................................................................ 69

PUDENDAL NERVE BLOCK ................................................................................................................................ 69

CHAPTER 7 - NERVE BLOCKS OF THE LOWER EXTREMITY ............................................................................... 72

ADVANTAGES OF NERVE BLOCKADE OF THE EXTREMITY: ............................................................................................... 72

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TOPOGRAPHIC LINE OF TUFFIER:............................................................................................................................... 94

CHAPTER 9 SPINAL NEEDLES ........................................................................................................................ 112

TYPES ............................................................................................................................................................... 113

CHAPTER 10 COMPLICATIONS OF SPINAL ANAESTHESIA& EPIDURAL ANESTHESIA ...................................... 115

COMPLICATIONS OF EPIDURAL ANAESTHESIA ............................................................................................... 115

CHAPTER 11 POST DURAL PUNCTURE HEADACHE (PDPH) ............................................................................ 118

AETIOLOGY: .................................................................................................................................................... 118

CHAPTER 12 TOTAL SPINAL ANAESTHESIA ................................................................................................... 123

CHAPTER 13 CAUDA EQUINA SYNDROME .................................................................................................... 126

CAUDA EQUINA: ................................................................................................................................................. 126

CHAPTER 14 DETECTION OF EPIDURAL SPACE .............................................................................................. 128

NEGATIVE PRESSURE TECHNIQUES: ......................................................................................................................... 128

CHAPTER 15 IVRA (IN SHORT) ...................................................................................................................... 130

CHAPTER 16 EPIDURAL ANAESTHESIA (IN SHORT) ....................................................................................... 135

FATE OF EPIDURAL AGENTS. .......................................................................................................................... 137

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CHAPTER 18 - ANATOMY AND PHYSIOLOGY OF SPINAL ANAESTHESIA ........................................................ 165

SPINAL ANAESTHESIA ..................................................................................................................................... 165

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CHAPTER 19 - ANATOMY AND PHYSIOLOGY OF EPIDURAL ANAESTHESIA.................................................... 196

CHAPTER 20 - INTRAVENOUS REGIONAL ANESTHESIA (IVRA) ...................................................................... 216

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Iodine Tincture of iodine (1%) provides 300 ppm free

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Differential block (Cm):

Transitional block (Wedensky block ):

Glucose in L.A impair its action due to hypo-osmotic effect.

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If pKa – pH of medium is > 1, percentage of ionized will be almost complete 

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Nerve stimulator: 1913 by Perthes.

Endoneural injection: Nerve damage