segmental epidural anaesthesia
TRANSCRIPT
i
SEGMENTAL EPIDURAL ANAESTHESIA FORINGUINAL HERNIA REPAIR
ByDr. B.DHARMENDER REDDY
A Dissertation Submitted toThe Rajiv Gandhi University of Health Sciences Karnataka, Bangalore
in partial fulfilmentof the requirements for the degree of
DOCTOR OF MEDICINEIn
ANAESTHESIOLOGY
Under the guidance of
Dr. S. GOWRI KUMARI
Professor and HOD, ANAESTHESIOLOGY.
DEPARTMENT OF ANAESTHESIOLOGY,MVJ MEDICAL COLLEGE AND RESEARCH HOSPITAL,
HOSKOTE, BANGALOREAPRIL 2011
ii
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,KARNATAKA, BANGALORE
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled “SEGMENTAL EPIDURAL
ANAESTHESIA FOR INGUINAL HERNIA REPAIR” is a bonafide and genuine
research work carried out by me under the guidance of Dr. S. GOWRI KUMARI,
Professor and Head, Department of Anaesthesiology, MVJ Medical College and
Research Hospital, Hoskote, Bangalore.
Dr. B.DHARMENDER REDDY,Date: Postgraduate in Anaesthesiology,Place: Hoskote MVJ Medical College and Research
Hospital.Hoskote, Bangalore.
iii
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled “SEGMENTAL EPIDURAL
ANAESTHESIA FOR INGUINAL HERNIA REPAIR” is a bonafide research
work done by Dr. B.DHARMENDER REDDY in partial fulfilment of the
requirement for the degree of Doctor of Medicine in Anaesthesiology.
Date: Dr. S. GOWRI KUMARI.Professor and Head
Place: Hoskote Department of Anaesthsiology,MVJ Medical College andResearch Hospital,Hoskote, Bangalore
iv
ENDORSEMENT BY THE HEAD OF THE DEPARTMENT,
DIRECTOR / DEAN
This is to certify that the dissertation entitled “SEGMENTAL EPIDURAL
ANAESTHESIA FOR INGUINAL HERNIA REPAIR” is a bonafide research
work done by Dr. B.DHARMENDER REDDY, under the guidance of
Dr. S. GOWRI KUMARI, Professor and Head, Department of Anaesthesiology,
MVJ Medical College and Research Hospital, Hoskote, Bangalore.
Dr. S. GOWRI KUMARI. Dr. T. RAJESHWARI.Professor and Head Dean / DirectorDepartment of Anaesthesiology MVJ Medical College andMVJ Medical College and Research Hospital, Research Hospital, HoskoteHoskote, Bangalore. Bangalore.
Date : Date:
Place: Hoskote Place: Hoskote
v
COPYRIGHT
DECLARATION BY THE CANDIDATE
I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka, shall
have the rights to preserve, use and disseminate this dissertation in print or electronic
format for academic/research purpose.
Date: Dr. B.DHARMENDER REDDYPostgraduate in Anaesthesiology,
Place: Hoskote MVJ Medical College andResearch Hospital,Hoskote, Bangalore
@ RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES
vi
ACKNOWLEDGEMENT
It is most appropriate that I begin expressing my indebtedness gratitude to my beloved
parents and family members for being supportive in all my endeavours.
It gives me great pleasure in preparing this dissertation and I take this opportunity to
thank everyone who has made this possible.
It gives me greatest pleasure to express my deep sense of gratitude and profound
thanks to my most revered teacher Dr. S. GOWRI KUMARI, Professor and HOD of
the Department of Anaesthesiology, MVJMC&RH, Hoskote, Bangalore, for her
valuable guidance, constant encouragement, constant efforts in fine tuning my
practical skills, timely expert advice with prospective comments and suggestions,
which she always rendered in every step of my work. Without her valuable guidance,
this dissertation would not have come in its present form. My sincere thanks to her for
being my guide.
I am highly indebted and consider myself very fortunate to have
Dr.T.RAJESHWARI, Dean-cum-Director and the pillar of this MVJMC & RH, for
having inculcated in me a sense of determination and courage, for her constant
support and invaluable guidance with her superb talent and professional expertise
throughout this dissertation work. I find no words to express my heartfelt thanks to
her.
vii
It gives me immense pleasure to extent my sincere thanks to Professors
Dr. A.V. PAI, Dr.PRASAD KULKARNI and Associate Professor
Dr. B. NARASIMHA REDDY whose authoritative knowledge of practical skills has
guided and inculcated in me a sense of confidence. I am thankful to them for their
valuable teaching and guidance.
My sincere thanks are due to Assistant Professor Dr.NIRMALA B.C. for her words
of encouragement and constant and timely support in completing my dissertation
work.
My heartful thanks to other consultants Dr.GAYATHRI, Dr. GIRISH.K.N.,
Dr.GIRISH BABU and Dr.SHASHIDHARA Dept. Of Anaesthesiology,
MVJMC&RH, Hoskote, Bangalore, for their valuable guidance and constant
encouragement.
I thank management MVJ MC & RH for being supportive in every stage of study.
I thank all my post graduate colleagues, members of department of surgery and OT
staff for their whole hearted cooperation.
My heartfelt thanks to all patients who have been the backbone of this study without
whom this study would not have been complete.
Date: Dr. B.DHARMENDER REDDY
Place: Hoskote
viii
ABSTRACT
BACKGROUND AND OBJECTIVES: Inguinal hernia repair is one of the most
commonly encountered surgical corrections in men worldwide. Epidural anaesthesia
is widely used for these surgeries. As inguinal hernia is usually seen in elderly age
group, so as to avoid or reduce the complications which could occur in the
conventional dosages this clinical study of segmental epidural anaesthesia was
undertaken where the extent of block is limited to only few segments involved in the
field of surgery.
METHODS: Study was conducted on 100 patients of ASA I and II posted for
elective inguinal hernia repair. Segmental epidural block was performed with
ing.Bupivacaine 0.5% 5-6ml. Patients were observed for onset, duration and quality
of analgesia. Level of analgesia preoperatively and post operatively. Hemodynamic
stability with heart rate, systolic and diastolic blood pressure.
RESULTS: In the present study, the mean onset of analgesia was 8.08 minutes. The
quality of analgesia was excellent in 53 cases, good in 34 cases, fair in 10cases and
poor in 3 cases. The mean duration of analgesia was 167.42 minutes (120 min to 240
min). All patients were haemodynamically stable throughout the surgery. Shivering
was seen in 5 cases and sweating in 9 cases.
INTERPRETATION AND CONCLUSION: Segmental epidural block with 5-6 ml
of 0.5% Bupivacaine is found to be safe and fulfils the surgical requirement. Could be
successfully employed for inguinal hernia repair with limited spread of analgesia
ix
involving only few segments. Fall in blood pressure and other complications were
very minimal. This technique can be safely used in elderly patients.
KEY WORDS: Epidural anaesthesia; Segmental epidural anaesthesia; Hemodynamic
stability; Excellent alangesia.
x
LIST OF ABBREVIATIONS
Sup : Superior.
Inf : Inferior.
CSE : Combined spinal epidural.
SA : Spinal anaesthesia.
EA : Epidural anaesthesia.
PNOV : Post operative nausea and vomiting.
ECG : Electro cardio graph.
MIN : Minutes.
SAB : Subarachnoid block.
xi
TABLE OF CONTENTS
Sl.No Contents PAGE NO
1 Introduction 1
2 Objectives 4
3 Review of Literature 34
4 Methodology 48
5 Results 57
6 Discussion 77
7 Conclusion 85
8 Summary 86
9 Bibliography 90
10 Annexures
i. Proforma
ii. Consent form
iii. Master Chart
iv. Key to Master Chart
96
98
99
103
xii
LIST OF TABLES
S.NO. TITLE PAGE NO.
1 Characteristics of ligamentum flavum at differentvertebral levels 7
2 Size of epidural space at different vertebral levels 12
3 Pressures in epidural space at different vertebral levels 13
4 Age Distribution 57
5 Sex Incidence 59
6 Weight Distribution 60
7 Height Distribution 61
8 Type of Hernia 62
9 Volume of Drug 63
10 Quality of Analgesia 64
11 Duration of Analgesia 66
12 Level of Analgesia Pre-operatively 68
13 Level of Analgesia Post-operatively 69
14 Side Effects 70
15 Success Rate 71
16 Mean heart rate changes 72
17 Mean blood pressure changes 74
18 Summary of results 76
xiii
LIST OF FIGURES
S.NO TITLE PAGE NO.
1 Vertebral column 8
2 Lateral view of Lumbar vertebrae 9
3 Median section of Lumbar vertebrae 9
4 Fourth Lumbar vertebra ventral view 9
5 Cross section of epidural Space 10
6 Loss of resistance technique 14
7 Site of action of epidural drug 18
8 Anatomy of inguinal canal 21
9 Structure of bupivacaine 27
10 Epidural tray 54
11 Position of the patient 54
12 Loss of Resistance 55
13 Catheter insitu 55
14 Dermatomes 56
xiv
LIST OF GRAPHS
S.NO. TITLE PAGE NO.
1 Age Distribution 58
2 Sex Incidence 59
3 Weight Distribution 60
4 Height Distribution 61
5 Type of Hernia 62
6 Volume of Drug 63
7 Quality of Analgesia 64
8 Duration of Analgesia 67
9 Level of Analgesia Pre-operatively 68
10 Level of Analgesia Post-operatively 69
11 Side Effects 70
12 Success Rate 71
13 Mean heart rate changes 73
14 Mean blood pressure changes 75
1
INTRODUCTION
"I esteem it the office of the physicians not only to restore health, but to mitigate
pain". SIR FRANCIS BACON.
"Divine is the task to relieve pain". HIPPOCRATES.
Most common symptoms for which a patient seeks medical advice are pain and
structural deformity and whatever may be the basic cause they demand a relief.
In general, relief of pain is one of the most tangible roles to be played by the medical
practitioner and as such it merits careful attention. Relief of pain is by far the most
frequent indication of surgical intervention.
The surgeon in his mission induces pain, which at times is more severe than the
original complaint.
Medical profession has attempted various methods of pain relief from ancient times.
The development of epidural analgesia and anaesthesia played a small but significant
role in man’s triumph over pain, which undoubtedly is one of the most fascinating
chapters in the history of medicine.
The rationale of epidural analgesia in surgery is simple. The technique is used to
prevent afferent impulses from reaching the central nervous system and to prevent
transmission of inappropriate efferent signals to the target organs such as muscle,
2
blood vessels and viscera. In doing so, epidural blockade fulfils the central aim of
anaesthesia that is, prevention of pain, overall control of patient and his reflexes and
preservation of physical well being.
Epidural analgesia managed to escape the general decline in regional techniques when
it was given a fresh impetus by introduction of Touhy needle and an indwelling
epidural catheter. With these technical refinements it became possible to maintain
analgesia continuously for even weeks if necessary.
Hernia is the word derived from Greek words “Herons” an offshoot or bulge.
It is defined by Sir Astley Cooper (1804) as “protrusion of any viscous or part of the
viscous through an abnormal opening in the walls of its containing cavity.1
Inguinal hernia repair is one of the most commonly encountered surgical corrections
in men representing 12.5% of total surgical repair in Britain. In the international
classification of diseases 9th division clinical manifestation, the number was 9 for
hernias with relative value guide of 6.2 In providing anaesthesia for inguinal
herniorraphy, the technique chosen must be cost effective with respect to speed of
recovery, patient comfort, and associated incremental costs.3
Inguinal hernia repair is one of the common treatments performed. Which can be
performed under spinal, epidural, general and inguinal field block.
3
Epidural anaesthesia is suitable as a sole agent for lower abdominal surgery and on
lower limbs. It has some definite advantages over spinal anaesthesia like avoidance of
post spinal headache, minimal chances of meningitis, and minimal chances of nausea
and vomiting in post operative period.4 But administration of conventional dosage of
local epidural anaesthetics(15ml and above) for surgical anaesthesia frequently results
in multiple hemodynamic changes, including decreases in chronotropism, inotropism,
dromotropism, systemic vascular resistance, cardiac output, and myocardial oxygen
consumption.5 The economic consequences of these hemodynamic changes are far
from being calculated.
As inguinal hernia is usually seen in elderly age group, the above mentioned
complications will be more severe.
For a simple inguinal hernia repair, which is located at the level of the 12th thoracic
and 1st lumbar dermatomes, an upper analgesic level of the 8th to the 10th thoracic
dermatomes is satisfactory.6
The practice of the technique whereby, the block extends only to the segments
involved in the surgical field is said to have the following advantages.
1. Accurate limitation of the area of analgesia.
2. Minimal or no depression of blood pressure.
3. Small doses of local anaesthetics required and toxic doses are avoided.
4. Minimal incidence of complications.
Hence to meet the above requirements the present study of segmental epidural
anaesthesia for inguinal hernia repair is undertaken.
4
OBJECTIVES
This study is undertaken to evaluate the advantages of segmental epidural anaesthesia
for inguinal hernia repair.
1. To reduce the conventional dosage of epidural anaesthesia to block only the
segments involved in the field of surgery.
2. Hemodynamic effects.
3. To minimise the complications, which could occur in conventional dosage.
5
ANATOMY AND PHYSIOLOGY OF EPIDURAL SPACE
Epidural space is the potential space between the spinal duramater and the periosteum
and ligaments lining the vertebralcanal.7
The duramater is made of two layers, the endosteal and the meningeal layer. The two
layers are closely fused within the cranium. Below the foramen magnum, these two
layers are separate.
The outer layer forms the periosteum lining the spinal canal.
The inner layer forms the spinal duramater. Between these two layers is the epidural
or the peridural space.
The epidural space is widest in the midline posteriorly with an average of 5mm
between ligamentum flavum and the posterior surface of the spinal dura. The depth is
slightly more, proximal to the inferior border of the lamina due to the obliquity of the
vertebral lamina.
Boundaries:8
Above: The foramen magnum, where the periosteal and the spinal layers of the
dura fuse together.
Below: The sacrococcygeal membrane.
In front: The posterior longitudinal ligament covering the posterior aspect of
the vertebral bodies and intervertebral discs.
Behind: The anterior surface of the vertebral lamina and ligamentum flavum.
6
Laterally: The pedicles of the vertebrae and the intervertebral foramina.
The epidural space is not a closed space. It communicates with the paravertebral space
through the intervertebral foramina. It is shallowest anteriorly where it fuses at some
places with the posterior longitudinal ligament. It is deepest posteriorly. The depth
varies as it is obliterated by contact between the duramater and the ligamentum
flavum or vertebral lamina. Laterally, the space is interrupted by contact between
duramater and pedicles.
Thus the epidural space is composed of a series of discontinuous compartments that
become continuous when the potential space separating the compartments is opened
up by injection of air or liquid.
According to a study dorsomedian fibrous tissue connects the duramater and the
ligamentum flavum in the lumbar region fairly frequently.9 Due to these
fibrous strands, the injected fluid distends the space laterally rather than in the
midline.
This has been confirmed anatomically through epiduroscopy and epidurography.
These fibrous strands are responsible for occasionally unilateral anaesthesia following
apparently adequate epidural technique.
Ligamentum flavum: The ligamentum flavum is an important landmark for
technical identification of epidural space during the introduction of epidural
analgesia.
7
It is made of tough elastic fiber disposed in a vertical direction connecting the upper
and lower bodies of adjacent lamina. It is thinnest in the cervical region becoming
progressively thicker down the spine and is thickest in the lumbar region.
Table-1 Characteristics of ligamentum flavum at different vertebral levels10
Site (mm) Skin to ligament (cm)Thickness of ligament
(mm)
Cervical1.5
3.0
Thorasic 3.05.0
Lumbar 3.0-8.0 5.0-6.0
Caudal 2.0-6.0 Variable
The epidural space is entered most safely and easily in the mid lumbar region. The
lumbar spine and the interspinous ligaments are widest in the mid-lumbar
region making an easy land mark for insertion of the epidural needle.
8
Fig-1 Vertebral column
9
Fig-2, 3, 4 4th Lumbar vertebra ventral aspect
10
Fig-5 Cross section of epidural space
Contents of epidural space:
1) Fat: It is a ubiquitous material in the space and is highly vascular. The
fat competes with the nervous tissue of the spinal roots, cord and blood vessels
within the spinal cord for the drug. Drugs with high lipid solubility and lipoprotein
binding characteristics tend to enter the fat phase and remain there for a period of
time, depending on their pharmacodynamics and briskness of local blood flow
competing for uptake. .
11
2) Spinal arteries: The arteries that traverse the space arise from the
vertebral, ascending cervical, deep cervical, intercostals, lumbar and ileo-lumbar
arteries. They anastamose with those above and below and across the midline and
lie mainly in the lateral parts of the epidural space
3) Epidural veins: The venous plexus of the vertebral canal which drain the
adjacent structures and the spinal cord lie in the anterolateral parts of the epidural
space. They form a network, which runs vertically within the epidural space. It can
be subdivided into a pair of anterior venous plexus which lie on either side of
the posterior longitudinal ligament into which basivertebral veins empty and
a posterior venous plexus. These are valveless (Batson’s plexus) and afford
a connection between the pelvic veins below with the intracranial veins above. These
veins become distended during coughing and straining and also when the inferior
venacava is obstructed by large abdominal tumors or in late pregnancy. When these
epidural veins engorge, the epidural space is markedly reduced. Aspiration tests may
not always indicate intravenous position of a needle or catheter and subsequent
injections of air or local anaesthetic will be carried directly to the heart. The
appropriate dose of the drug should preclude this problem.
4) Lymphatics: The lymphatics run anteriorly from each intervertebral
foramen. They drain the dural cul-de-sacs of the dural root sleeves and empty in
the longitudinal channels in front of the vertebral column.
Connections between epidural space and paraspinal tissue space:
The epidural space is not a closed space. Many of the tissue planes around the spinal
canal connect to form an extended system of tracks.
12
There are 58 foramina in all. The areolar tissue around these foramina varies in
density according to age. As age advances the soft and tenuous tissue
undergoes increasing condensation to form the fibrous tissue which thickens and
blocks the intervertebral foramina with aging. This confines the solutions injected into
the epidural space within the spinal canal and they escape less rapidly along the
neurovascular bundles into the paravertebral spaces. Thus dosage should be reduced.
The spread is greater in pregnant females.
Size of the epidural space:
The distance across the circular peridural space is variable. It is negligible or almost
non-existent in the anterior region. It is more and readily measurable in the posterior
region, especially in the midline.
Table –2 Size of epidural space at different levels
Level Epidural space (mm) Thickness of dura (mm)
Cervical 1.0-1.5 2.0-1.5
Upper thoracic 2.5-3.0 1.0
Lower thoracic 4.0-5.0 1.0
Lumbar 5.0-6.0 0.66-0.33
13
PHYSIOLOGY
Haldt and Moloney were the first to describe negative pressure in the epidural space
in 1928. This negative pressure is maximum at points of firm attachments. It
is maximum in the thoracic region, less in the lumbar region and least or absent in
the sacral region.
Table 3 Pressures in the epidural space at different levels
Level Pressure (cm H2O)
Lower lumbar - 0.5
Upper lumbar - 1.0
Thoracic -1.0 to - 3.0 (Average -2.0)
Three theories have been put forth to explain the negative pressure.
1) The Cone Theory: 11
Jonzen, 1926, Eaton in 1938 and Lawrence in 1948 put forward this theory.
According to this theory, the needle introduced into the epidural space depresses the
dura, creating a larger space. This theory was reviewed in the studies conducted by
Aitkenhead in 1979 in experiments on dogs.
2) Transmission Theory: 11
According to Macintosh and Bryce-Smith the negative pressure in the epidural space
is caused by the transmission of the intrapleural negative pressure
through intervertebral foramina to the epidural space. It varies with the depth of
14
respiration. i.e., clinically this negative pressure will be diminished or absent if the
patient is not relaxed or straining.
3) Flexion theory: 11
This theory states that the negative pressure is directly proportional to the flexion of
the spine. Marked flexion at the spinal column increases the negative pressure. A rise
in negative pressure may favour the spread of local anaesthetic solution in the
epidural space.
Fig-6 Loss of resistance technique
15
Thus a good knowledge of the anatomy of the epidural space and nearby structures
goes a long way in proper performance of the technique of epidural block.
Identification of epidural space is by:
Negative pressure technique
Hanging drop sign.
Capillary tube method.
Manometer technique.
Disappearance of resistance techniques
Syringe technique.
Spring loaded syringe.
Balloon technique.
Brooke’s device.
Vertical tube of Dawkins.
Local anaesthetic injected into the epidural space acts on the dorsal root ganglia and
spinal roots with their dural cuffs in the extradural space.11
Leakage by vascular absorption.
Leakage through intervertebral foramina.
Diffusion through dural root sleeves.
Diffusion through dura mater.
16
Factors affecting the spread of epidural analgesia:
1. Volume of the solution:
The spread of analgesia in the epidural space depend on the volume of drug injected.
During his experimental study in the dogs and human cadavers by injecting coloured
solution through the sacro coccygeal membrane.12
Larger volumes will travel farther and remains in situ longer than smaller volumes.
When different volume of solution has been used vertical spread has been expressed
as a ratio obtained by dividing the volume of solution injected by the number of
vertical segments involved. The ratio is expressed in millilitres per segment, varies
inversely with the vertical spread, so the lower its value the greater the degree of
spread for a given volume. 13
2. Speed of injection:
spread of solution depend upon the speed of injection.12 With rapid injection fluid is
dispersed widely but thinly throughout the epidural space, so that the resulting block
is extensive and is of short duration. With the slow injection there is time for the
solution to pool evenly in larger amounts in any given area with the result that block
tendts to be more localised and lasts longer.14
3. Gravity:
X-Ray studies of the flow of solution in the epidural space injected via the lumbar
route of living subjects were first carried out by Sicard and Forestier in 1921 using
lipidol. In their study they described the passage of the heavy oil outward through the
17
intervertebral foramina and the influence of gravity in determining the direction of
spread.
Solution flow under the influence of the gravity and will diffuse cephaled in the
trendelenberg position and caudal in sitting up position .13
4. Site of Injection:
The site of injection is one of the extrinsic variables in the spread of analgesic
solution. To keep the dose to minimum, injection should be made at the level
corresponding to the middle of the area to be blocked. The solution injected spreads
equally in cephalad and caudal direction from the site of the injection provided the
solution is injected slowly.13
5. Age:
Small volumes of solution will travel relatively farther in old ages where
intervertebral foraminae are stenosed by calcified processes. Exaggerated spread of
epidural analgesia is seen in patients with atherosclerosis, the degenerative changes in
connective tissue associated with atherosclerosis produce increased permeability of
neural coverings.15 Marked reduction in volume is required clinically in older patients
is due to the much greater degree of neuraxial spread and greater permeability of the
perineurium. The dose requirement decreases as age increases.15
The diffusion gradient is very important when compared to volume because small
volume of high concentration can produce wide spread block, which is due to
18
neuraxial spread which is in turn due to high concentration gradient and greater
permeability of the perineurium.
The mechanism of action of epidural analgesia is complex. The site of action of the
drug injected in the epidural space could be summarised as per figure below. FIG- 7
Longitudinal spread in epiduralspace
Leakage by vascularabsorbtion
Systemic effects
Leakage throughintervertebral
foramina
Paravertebral block innerve trunks
Centripetalsubperineural spread
Subpial spread &uptake in piamatter
18
neuraxial spread which is in turn due to high concentration gradient and greater
permeability of the perineurium.
The mechanism of action of epidural analgesia is complex. The site of action of the
drug injected in the epidural space could be summarised as per figure below. FIG- 7
Epidural injection
Longitudinal spread in epiduralspace
Leakage throughintervertebral
foramina
Paravertebral block innerve trunks
Centripetalsubperineural spread
Subpial spread &uptake in piamatter
diffusion throughduralroot sleeves via
arachnoid villi &perivascularspaces
Sub dural spread
Spinal root block
Uptake in epidural fat
Diffusion in epiduralfat Spinal subdural space
cerebrospinal fluid
18
neuraxial spread which is in turn due to high concentration gradient and greater
permeability of the perineurium.
The mechanism of action of epidural analgesia is complex. The site of action of the
drug injected in the epidural space could be summarised as per figure below. FIG- 7
Diffusion throughspinal cord dura
Spinal subdural space
cerebrospinal fluid
19
Epidural analgesia is not simple as spinal root or ganglion blockade, but rather of
action on several sites after passing through labrynth of diffusion pathways as
outlined in figure.
Solution spread in the epidural space will depend on the volume injected. Within the
extradural space the drug will be taken up and removed by blood flow, or it will be
stored and perhaps spread in the extradural fat.
In young patients with freely patent intervertebral foramina, some solutions will
passout of the spinal canal into the paravertebral spaces and along the spinal nerves,
producing a form of paravertebral block. From these diffusion through the epineurium
and perineurium into subperineural space will allow some degree of centripetal spread
backward towards the neuraxis with subsequent access to the contiguous subpial
space and from these to the surface of the roots and cord.
The epidural neural blockade may affect various systems as described below.
1. Cardiovascular system: The possible cardiovascular influences may be classified
according to the following scheme
a) Neural b) Pharmacological
Neural:
Segmental sympathetic efferent blockade with resultant dilution of resistance
and capacitance vessels.
20
Paralysis of cardiac sympathetic fibers from the upper 4 to 5 thorasic segments
with loss of chronotropic or inotropic drive to the myocardium, resulting in
bradycardia and reduction of ejection force.
Pharmacological:
Vascular absorption of local anaesthetic from the epidural space leading to high
concentration of local anaesthetic in the circulation causes consequent distant effects
on smooth muscle and fall in the cardiac output from beta blockade. The depressant
effects of circulating local anaesthetics are PH dependent and are likely to be most
severe in the presence of renal and respiratory acidosis. If the epidural solution
contained epinephrine, its absorption would lead to increase in cardiac output and fall
in peripheral resistance.
2. Liver: Hepatic flow is largely dependent on mean systemic blood pressure. Under
epidural analgesia hepatic blood flow is significantly decreased if the systolic blood
pressure is allowed to fall below 60-70 mm Hg.
3. Renal system: Decrease in blood pressure causes proportionate decrease in renal
blood flow and GFR effect on bladder.
4. Bladder: Lumbar and sacral epidural anaesthesia results in atonic bladder with
large volume of residual urine, sometimes catheterisation is needed. In segmental
thoracic epidural anaesthesia lower parts of spinal cord are left intact and bladder
function may not be affected.
5. Respiratory System: Depends upon the segmental blockade. There is no effect on
the vital capacity, forced expiratory volume, FRC and gas distribution.
21
ANATOMY OF INGUINAL CANAL
a
bFig-8 Anatomy of inguinal canal
22
No disease of human body, belonging to the province of the surgeon, requires in its
treatment a better combination of accurate anatomical knowledge with surgical skill
than hernia in all its varieties. (Sir Astley Paston Cooper, 1804)16
The inguinal canal is 4cm long and extends from internal inguinal ring laterally to the
external inguinal ring medially. It lies above the inner half of the inguinal ligament.17
The canal gives passage to spermatic cord in male, and the round ligament of the
uterus in the female.18
The deep ring, an oval opening in fascia transversalis, lies about 0.5 inches (1.3cm)
above inguinal ligament midway between the anterior superior iliac spine and the
symphysis pubis. Just medial to it is the inferior epigastric artery. The margin of the
ring gives attachment to the internal spermatic fascia. The superficial inguinal ring, is
a triangular defect in the aponeurosis of the external oblique muscle and lies
immediately above and medial to pubic tubercle. The margins give attachment to the
external spermatic fascia.19
The mid inguinal point is the midpoint of the line between anterior superior iliac spine
and the symphysis pubis. Hence it is just medial to the midpoint of the inguinal
ligament.
23
Boundaries of inguinal canal19 :
1) The anterior wall of the canal: Formed along its entire length by aponeurosis
of the external oblique muscle. It is reinforced in its lateral third by the origin
of the internal oblique.
2) The posterior wall of the canal: Formed along its entire length by fascia
transversalis. It is reinforced in its medial third by conjoint tendon and
reflected part of inguinal ligament.
3) The floor of the canal: It is formed by grooved surface of the inguinal and
lacunar ligaments.
4) The roof of the canal: Formed by arching lowest fibers of the internal oblique
and transversus abdominis muscles.
Contents of inguinal canal:18
1) Spermatic cord in males and round ligament of uterus in female.
2) Ilioinguinal, iliohypogastric and genitofemoral nerves.
24
Protective mechanism for the development of hernia: 18
1) Canal is an oblique passage with weakest areas namely superficial and deep
rings lying some distance apart.
2) Anterior wall is reinforced by the fibers of internal oblique
3) Posterior wall is reinforced by strong conjoint tendon.
4) On coughing and straining, the arching lowest fibers of the internal oblique
and transverses abdominis muscle contracts so the canal is virtually closed.
Nerve supply:
1) Ilioinguinal nerve: 20
Origin: From L1 ventral ramus
Course: It emerges from the lateral border of psoas major, with or just inferior to
iliohypogastric nerve. It passes obliquely across quadratus lumborum and the upper
part of iliacus and enters transversus abdominis near the anterior end of the iliac crest.
It pierces internal oblique and supplies it and then traverses the inguinal canal below
the spermatic cord. It emerges with the cord from the superficial inguinal ring to
supply skin. Occasionally this nerve is completely absent, when the iliohypogastric
nerve supplies its territory.
Motor: Transeversus abdominis and internal oblique.
Sensory: Supplies sensory fibers to transeversus abdominis and internal oblique.
Medial skin of thigh and skin over the root of the penis and upper part of scrotum in
males or skin covering the mons pubis and adjoining labium majus in females.
25
2) Iliohypogastric nerve: 20
Origin: L1 ventral ramus
Course: It emerges from the upper lateral border of psoas major, crosses obliquely
behind the lower renal pole, and in front of quadratus lumborum. Above the iliac
crest, it enters the posterior part of transeversus abdominis. Between transverses
abdominis and internal oblique, it divides into lateral and anterior cutaneous branches.
The lateral cutaneous branch runs through internal and external oblique above the
iliac crest and is distributed to the posterolateral gluteal skin. The anterior cutaneous
branch runs through internal oblique 2cm medial to anterior superior iliac spine, and
through external oblique aponeurosis 3cm above superficial inguinal ring.
Motor: It supplies a small motor contribution to transeversus abdominis and internal
oblique, including conjoint tendon.
Sensory: Supplies sensory fibres to transeversus abdominis, internal oblique and
external oblique, and innervates the posterolateral gluteal and suprapubic skin.
3) Genitofemoral nerve:20
Origin: Ventral rami of L1 and L2
Course: It is formed within the substance of psoas major and descends obliquely
forwards through the muscle to emerge on the abdominal surface near its medial
border, opposite the third or fourth lumbar vertebrae. It descends beneath the
peritoneum on psoas major, crosses obliquely behind the ureter and divides above
inguinal ligament into genital and femoral branches. The genital branch, crosses the
lower part of external iliac artery, enters the inguinal canal by the deep ring. The
femoral branch descends lateral to external iliac artery, then crosses deep circumflex
26
iliac artery passes behind inguinal ligament and enters femoral sheath lateral to
femoral artery.
Motor: Cremaster muscle via genital branch of genitofemoral nerve.
Cutaneous:
Genital branch: skin of scrotum in males or monspubis and labium majus in females
via genital branch.
Femoral branch: Anteromedial skin of thigh.
27
PHARMACOLOGY
Local anaesthetics are chemical compounds which are capable of producing reversible
conduction blockade of impulses along central and peripheral nerve pathways after
regional anaesthesia.
Classification:
Clinically local anaesthetic agents can be classified into two groups depending on the
link between the aromatic portion and the intermediate chain. The amino ester group
have an ester link and include procaine, chloroprocaine and amethocaine. The amino
amides have an amide link between the aromatic head and the intermediate chain and
include lignocaine, bupivacaine, mepivacaine, prilocaine, etidocaine and
ropivacaine21.
Bupivacaine Hydrochloride:
History: Bupivacaine belongs to homologous series of mepivacaine and was
synthesized in Sweden (1957) by Boafekenstan. First reports of its use were made in
1963 by Televard. Since then it has been widely used in Scandinavia.
Structural Formula:
1-N-Butyl-DI-piperidine-2-carboxylicacid-2,6-dimethyl-anilide hydrochioride.
Fig-9 Structure of bupivacaine
28
The only difference from mepivacaine is that the butyl group replaces the methyl
group in piperidine ring. Both are being used as hydrochloride salts.
Bupivacaine, Lignocaine and mepivacaine contain linkages between the aromatic
nucleus and the amino or piperidine group. They differ from procaine, which has an
ester linkage.
Physical and Chemical Properties
It is a poorly water-soluble, long acting amide local anaesthetic. It is a salt of white,
odourless, crystalline powder with a bitter, numbing taste. It is prepared by chemical
synthesis. Its molecular weight is 324.9, freely soluble in water and alcohol in its
hydrochloride form, with its melting point of 258 oc. The pKa is 8.2 and pH is 3.5.
The solution is available in the form of 0.25%, 0.5% and 0.75% in isotonic sodium
solution with or without adrenaline, 1: 200,000 concentrations. A preparation
marketed specifically for intrathecal use contains dextrose.22
Mechanism of action:
Bupivacaine, like other local anaesthetics prevents the generation and the conduction
of the nerve impulse. Their primary site of action is the cell membrane. Conduction
block can be demonstrated in squid giant axons from which the axoplasm has been
removed.
Local anaesthetics block conduction by decreasing or preventing the large transient
increase in the permeability of excitable membranes to Na+ that normally is produced
by a slight depolarization of the membrane. This action of local anaesthetics is due to
their direct interaction with voltage-gated Na+ channels. As the anaesthetic action
29
progressively develops in a nerve, the threshold for electrical excitability gradually
increases the rate of rise of the action potential declines, impulse conduction slows,
and the safety factor for conduction decreases. These factors decrease the probability
of propagation of the action potential, and nerve conduction eventually fails 23.
Pharmacokinetics of Bupivacaine:
Bupivacaine is rapidly absorbed from the site of injection, the rate of rise in plasma
concentration and the peak plasma concentration depending on the particular local
anaesthetic technique being used. There is also some inter individual variation, and
peak systemic concentrations may occur between 5 and 30 min after administration.
1. Absorption:
The site of injection, dose, age of the patient and addition of a vasoconstrictor
determine systemic absorption of bupivacaine. The maximum blood level of
bupivacaine is related to the total dose of the drug administered from any particular
site.
2. Distribution:
This can be described by a two compartment model. The rapid distribution (phase A)
is believed to be related to uptake by rapid equilibrating tissue (i.e., tissues that have
high vascular perfusion). The slow distribution (phase B) is mainly a function of
distribution to slowly equilibrating tissue, biotransformation and excretion of the
compound.
30
More highly perfused organs show higher concentrations of the drug. Bupivacaine is
rapidly extracted by lung tissue. Though skeletal muscle does not show particular
affinity for bupivacaine it is the largest reservoir of the drug.
Distribution characteristics of Bupivacaine.
1. T1/2 A (min) – 2.7
2. T1/2 B (min) – 28
3. Volume of distribution at steady state (ltrs) – 72.
4. Clearance (ltrs/min) – 0.47.
3. Biotransformation and excretion:
Bupivacaine undergoes enzymatic degradation primarily in the liver. The excretion
occurs via the kidney. Renal perfusion and factors affecting urinary PH affect its
excretion. Less than 5 percent of unchanged drug is excreted via the kidney through
urine. The major portion of injected agent appears in urine in the form of 2, 6,
pipecolyloxylidine (PPx) which is an N-dealkylated metabolite of bupivacaine. Renal
clearance of this drug is related inversely to its protein binding capacity and pH of
urine.
Dosage:
The dosage varies upon the area to be anaesthetised.
1. The vascularity of the tissue
2. The number of segments to be blocked
3. The individual tolerance
4. Site of injection
31
In recommended doses, bupivacaine produces complete sensory block, but the motor
block depends on the concentration.
1) 0.25% incomplete motor blockade
2) 0.5% motor blockade is produced but muscle relaxation may be inadequate for
surgery.
3) 0.75% causes complete motor blockade.
Maximal dose is 2mg/kg body weight (25-30 ml 0.5% solution) and the strength used
is 0.125% - 0.75%. 24, 25
Advantages:
1. More powerful drug.
2. Prolonged duration, 4-5 times that of lignocaine or mepivacaine.
Toxicity of Bupivacaine:
It is relatively free of side effects if administered in an appropriate dosage. It is more
cardiotoxic than lignocaine and this is made worse by hypoxia, hypercapnia and by
pregnancy.
1. Central nervous system toxicity:
CNS is more susceptible to bupivacaine. The initial symptom involves feeling of light
headedness and dizziness followed by visual and auditory disturbance. Disorientation
perioral numbness and occasional feeling of drowsiness may occur. Objective signs
are usually excitatory in nature which includes shivering, muscular twitching and
tremors; initially involving muscles of the face and part of extremities. At still higher
32
doses cardiovascular or respiratory arrest may occur. Acidosis increases the risk of
CNS toxicity from bupivacaine, since an elevation of PaCO2 enhances cerebral blood
flow, so that more anaesthetic is delivered rapidly to the brain.
2. Cardiovascular system toxicity:
Bupivacaine depresses rapid phases of depolarization (Vmax) in purkinge fibres and
ventricular musculature to a greater extent than lignocaine. It also decreases the rate
of recovery from a dependent block than that of lignocaine. This leads to incomplete
restoration of Vmax between action potential at high rates, in contrast to complete
recovery by lignocaine. This explains why lignocaine has antiarrhythmic property
while bupivacaine has arrhythmogenic potential. High level of bupivacaine prolongs
conduction time through various parts of heart and extremely high concentration will
depress spontaneous pacemaker activity, resulting in bradycardia and arrest. Cardiac
resuscitation is more difficult following bupivacaine induced cardiovascular collapse
and hypoxia along with acidosis which markedly potentiates cardiac toxicity.
Bretylium but not lignocaine could raise the ventricular tachycardiac threshold that
was lowered by bupivacaine.
3. Respiratory system:
Respiratory depression may be caused if excessive plasma level is reached which in
turn results in depression of medullary respiratory center. Respiratory depression may
also be caused by paralysis of respiratory muscles as may occur in high spinal or total
spinal anaesthesia.
33
4. Autonomic nervous system:
Myelinated preganglionic beta fibres have a faster conduction time and are more
sensitive to the action of local anaesthetic including bupivacaine. Involvement of
preganglionic sympathetic fibres is the cause of widespread vasodilatation and
consequent hypotension that occurs in epidural and paravertebral block. When used
for conduction blockade all local anaesthetic particularly bupivacaine produces higher
incidence of sensory blockade than motor fibres.
Adverse effects and precautions
The safety and effectiveness of local anaesthetic depend upon proper dosage, correct
technique, adequate precautions and readiness for emergencies. The lowest dosages
that produce effective anaesthesia should be used, to avoid high plasma levels and
serious systemic side effects. Injection of repeated doses of bupivacaine may cause
significant increase in blood levels with each dose, due to accumulation of the drug or
its metabolites or due to slow degradation. Tolerance varies with the general condition
of the patient. Debilitated elderly patients and acutely ill patients should be given
reduced doses commensurate with age and physical condition.
34
REVIEW OF LITRETURE
Corning has been credited with being the first to use epidural analgesia in 1885.26
In 1901 Jean Enthuse Sicard and Fernand Cathelin independently introduced cocaine
through the sacral hiatus, becoming the first practitioners of caudal epidural analgesia.
They popularised this caudal approach for epidural analgesia.27
Arthur Lawen successfully used caudal anaesthesia with large volumes of procaine for
pelvic surgery.28
After the favourable reports of Sicard and Cathelin, Tuffier attempted epidural analgesia
by lumbar approach. But his lack of success and natural difficulties of locating a narrow
space of 2-4 mm width at a depth of 20 times that amount discouraged all further
attempts for many years.
In 1906 Forestier independently described the interspinous approach to the peridural
space utilizing a loss of resistance technique and thus, is considered as the co-originator
of the method of locating the peridural space with Sicard, who in 1906 demonstrated the
feasibility of the interspinous approach to the epidural space.28
In 1921 Fidel Pages, a Spanish military surgeon devised a technique to introduce
epidural procaine at all the levels of neuraxis. His method was to use a blunt needle and
then feel and hear the entry of the needle through the ligamentum flavum. He had
produced a segmental anaesthesia through epidural injections, avoiding some of the side
35
effects of complete neuraxial block, which occurred after high subarachnoid
administration of local anaesthetics. He published an article “Anaesthesia Metamerica”
in which he described satisfactory anaesthesia for abdominal surgery obtained by
utilising the interspinous approach to the peridural space.27, 28
In 1926 Janzen first described existence of negative pressure in the epidural space.29
A catheter passed through a needle into epidural space was first used in obstetrics by
Aburel in 1931.
In 1931 Achille Mario Dogliotti described epidural injections of local anaesthetics,
apparently without prior knowledge of the work of Pages. In 1933 in his article “A new
method of block anaesthesia” has mentioned about anatomy, physiology and
identification of epidural space by loss of resistance technique by using a continuous
pressure on the plunger of a saline filled syringe as the needle advanced through the
ligamentous structures. Subsequently this method became known to be as Dogliotti
method.27
A.Gutierrez of Argentina developed the hanging drop sign, which is still being used by
some anaesthesiologists to identify the epidural space.30
In 1936 B.Odom of New Orleans published 285 cases of lumbar epidural anaesthesia
and introduced the concept of test dose to detect intrathecal injection.31
36
William Lemmon used a 17-gauge, malleable, silver needle that was connected through
a hole in the operating table to rubber tubing and a syringe. Injections could then be
made at intervals to maintain the block for several hours.32
Edward Tuohy in 1945 used a ureteral catheter threaded through a large Huber-tipped
spinal needle to provide continuous anaesthesia.33 Later in 1949 this was modified to
give continuous epidural analgesia by Martinez Curbelo.34 A fresh impetus was given
by the introduction of Tuohy’s needle for epidural analgesia.
The marked increase in the use of epidural analgesia followed the introduction of
reliable, relatively non-toxic and fast acting local anaesthetics.
Philip Bromage and John Bonica performed several studies on epidural dose-response
relationships and the hemodynamic changes that followed initiation of the block. Whose
text books on the subject have made them thus the world’s authority of epidural
space.35,36
In 1951 Rudin D.O. working upon live dogs found that it is possible to recover in
CSF up to 10percent of local analgesic drug placed in the epidural space and behaves
as a true spinal analgesic acting either on nerve roots or dorsal root ganglia and that
the drug spreads from the epidural space through the intervertebral foramina and
produces block at the paravertebral space.
37
In 1966 Ekblon and Widman during 640 extradural lumbar blocks gave on an average
1.29+/- 0.03 mg/kg body weight of local anaesthetic without the appearance of any
appreciable side effects.37
In 1972 a study on the relation of age and length of vertebral column and volume of
solution for lumbar epidural anaesthesia was done by Dr. Mandappa. Approximately
up to age of 60 years the relationship between dose in volume to length of vertebral
column could be established. For higher age group a volume to age relationship is
observed which could be due to narrowing of the inter vertebral foramina limiting the
flow of injected fluid away into paravertebral space and also atherosclerosis of blood
vessels which limits absorption of injected fluid. The procedure of approximating
length of the vertebral column, age of the patient has greatly reduced the
complications. Further it is interesting to note that older age group requires only about
half the volume of drug required for younger age group for same operation. Sticking
to this regime, many protect the aged patients from complications.
In 1972, Philip R.Bromage Studied the incidence of missed, unblocked segments
during continuous epidural analgesia for relief of pain in labour and vaginal delivery
in 433 patients. Six different local anaesthetic agents were tested: the carbonated salts
of lignocaine and prilocaine, and the hydrochloride salts of lignocaine, prilocaine,
bupivacaine and amethocaine. The incidence of painful or unblocked segments ranged
from 1 per cent with carbonated lignocaine, to 12.8 per cent with amethocaine
hydrochloride, and it was four times higher with lignocaine hydrochloride than with
carbonated lignocaine.38
38
In 1974 P. R. Bromage studied lower limb reflex changes in segmental epidural
analgesia where sensory changes and lower limb reflexes were observed in 35 patients
receiving segmental epidural analgesia in the mid-thoracic region. Sensory blockade
was confined to the thoracic and upper lumbar segments. The lower limb reflexes
changed to an "upper motor neurone" pattern, with the onset and development of
segmental blockade. With regression of analgesia the reflexes returned to normal in
the reverse order. The significance of these findings is discussed in relation to the
anatomy of descending spinal pathways, and to the pattern of penetration of local
anaesthetics into the substance of the spinal cord.39
In1975 Maltau JM, gave selective lumbar epidural anaesthesia with 0.25% or 0.5%
bupivacaine without adrenaline in doses of 5 ml to 8 ml in 35 patients and monitored
the foetal heart rate changes. In 33 parturients the FHR changes observed were
insignificant. In one case a period of marked bradycardia was seen. One parturient
developed acute hypotension with a synchronous foetal bradycardia while lying in the
supine position. He concluded that continuous lumbar epidural anaesthesia with low
dose bupivacaine without adrenaline does not precipitate foetal bradycardia during the
first stage when care is taken to avoid maternal hypotension.40
In 1977, Hollman A, Jouppila R, Pihlajaniemi R, Karvonen P and Sjostedt conducted
a study of segmental (T10-T12) epidural analgesia in 418 parturient, using 4-6 ml
dose of 0.5% bupivacaine with or without adrenaline. Seventy percent of parturients
were primi paras and 30% had history or signs of possible uteroplacental
insufficiency. The analgesia during the opening phase was of good quality in 89% of
primiparas and 84% of multi. The onset of analgesia was rapid (3-5min) and duration
39
was on average 2 ½ hr. Slight but rapidly correctable hypotension occurred in 16.5%,
and in 2 cases the hypotension led to more serious complications. There was no
maternal or neonatal mortalities.41
In 1978 Jouppila R, Pihlajaniemi R, Hollman A and Jouppila P conducted a study
‘Segmental epidural analgesia and postpartum sequel’. Where the incidence of the
postpartum sequel of headache, backache, pain in the legs and difficulties in
micturition, was studied in 219 normal vaginal deliveries after segmental epidural
analgesia at the level of T10-T12 for pain relief during the first stage of labour. The
results showed that segmental epidural analgesia did not increase the occurrence of
postpartum sequel either in primiparous or in multiparous parturients.42
In 1979 Jouppila R, Jouppila P, Karinen JM and Hollman studied the effect of low-
dose continuous segmental epidural analgesia given during the first stage of labour on
the progress of labour, the frequency of foetal malpositions and the rate of vacuum
extractions was studied in 100 parturients (epidural group). The results were
compared with 100 parturients given none or conventional analgesia (control group).
The results showed that in the primiparous epidural group the progress of labour was
slower than in the control group. After the block, however, the subsequent course of
the labour was of equal duration in both groups. The duration of the second stage of
labour did not differ significantly between the groups. The differences in foetal
malpositions at delivery were statistically insignificant. Nor did the rate of vacuum
extractions, 8% in the primiparous and 0% in the multiparous epidural group, differ
statistically from the corresponding rate in the control groups. The results signify a
normal progress and outcome of labour after low-dose segmental epidural analgesia.43
40
In 1979 Willdeck-Lund G, Lindmark G and Nilsson BA, conducted segmental
epidural block for vaginal delivery to 242 women. Of these, 178 with a spontaneous
start of labour and vaginal delivery were studied with respect to the effect of epidural
block with bupivacaine-adrenaline on the course of labour and the condition of the
infant in women with normal uterine activity and women with primary uterine inertia
treated with oxytocin infusion. On an average, the 178 women had already had a
longer course of labour before the block was applied than women in control groups.
The block per se had only a slight effect on the first stage of labour, but the effect on
the second stage was more obvious, leading to outlet extraction in 50% of the
primiparous women, compared to 12% of the controls.44
In 1979 Gal D, Choudhry R, Ung KA, Abadir A and Tancer ML conducted a study to
evaluate segmental epidural analgesia . Bupivacaine (0.25 per cent) was used during
the first stage of labor and for the second stage, either 3 per cent - Chloroprocaine
delivered through the catheter (Group I) or 1 per cent Lidocaine as a perineal infiltrate
(Group II) was used. There were 124 full term patients of whom, 36 were nulliparous
and 88 were multiparous. The effects of segmental epidural analgesia on maternal
blood pressure, pain relief, preservation of lower limb motor power, duration and
progress of labor, and foetal outcome were evaluated. Pain relief during the first stage
of labor was satisfactory in 114 (92 per cent) of the patients. There were no significant
changes in maternal blood pressure, motor power in lower limbs, efficiency of uterine
contractions and internal rotation of the presenting part when analgesia was effective.
The use of 2-Chloroprocaine for second stage pain relief required low forceps
delivery in 84 (91 per cent) patients, as compared to 14 (44 per cent) patients that had
1 per cent Lidocaine local infiltration. Foetal outcome, was excellent in all cases.45
41
In 1982,Pentti Jouppila, RiittaJouppila, Arno Hollman and Antero Koivula measured
intervillous blood flow using a Xe133 clearance technique during the first stage of
labour in 9 parturients with severe preeclampsia before and after lumbar epidural
analgesia. Analgesia was produced with 10 ml of 0.25% bupivacaine. After the lumbar
epidural block the intervillous blood flow significantly improved, suggesting that
epidural analgesia is the obstetric analgesic method of choice in cases of severe
preeclampsia.46
In 1983 Kanto J, Erkkola R, Mansikka M and Aärimaa L, Studied the effect and
safety of segmental epidural analgesia (SEA) in three groups of parturients totalling
250. In 50 primigravidae, the analgesic effect was good in 90%, moderate in 8%, and
poor in only 2%. The SEA did not lead to more malpositions than were present in the
nonepidural groups. Nevertheless, the rate of instrumental deliveries was
approximately three times higher in the SEA groups than in nonepidural groups.47
In 1993 Anthony C. Webster, J. D. McKishnie, J. T. Watson and W. Donald Reid
evaluated lumbar epidural anaesthesia (LEA) to assess its technical feasibility,
effectiveness and incidence of complications in infants. Using a standard loss of
resistance technique and a 4.0 cm 20 G epidural needle. Epidural analgesia was
achieved in all 16 cases with bupivacaine 0–25% with and without 1:200,000
epinephrine, 0.75 ml/ kg for the first two cases, and subsequently 1.0 ml/ kg. In 15
patients, good operating conditions were achieved with epidural analgesia alone.
Inhalational anaesthesia supplementation was necessary in three cases. In the first two
patients, the level of analgesia (T8) was insufficient to control the response to traction
on the hernial sac. In one infant, analgesic to T4, whose surgery was inadvertently
42
delayed for four hours, inhalation anaesthesia was needed to control restlessness
rather than pain. Ten infants were analgesic to T2, four to T4, two to T9 and two to
T9. No adverse hemodynamic effects were seen. And there were no postoperative
complications. They concluded that lumbar epidural anaesthesia was technically easy,
and provided good operating conditions for most neonates in this study.48
In 1993 Peutrell JM and Hughes DG, in order to avoid complications of high doses of
local anaesthetics, injected the local anaesthetics at appropriate segmental level
through epidural catheter in awake ex-premature babies who were undergoing
inguinal herniotomies. The anaesthesia was excellent in six babies. Two babies cried
briefly with peritoneal or spermatic cord traction. One other baby needed
supplementation with nitrous oxide in oxygen in order to complete the surgery. The
majority of babies slept throughout surgery. There was no reported postoperative
complications.49
Studies conducted by Dr.M.H.Rao, Prof. Dept. Of Anaesthesiology, Thirupathi and
Dr.Phani Thota, Head Dept. Of Anaesthesiology KMC Mangalore in 1995 on
segmental dose requirement of epidural lignocaine and the effects on age, height,
body weight and body surface area. In their study a negative correlation is seen
between the age and segmental dose requirement of epidural lignocaine in adults.
Correlated moderately with height and body weight but correlated best with body
surface area. Dose required to block each segment in males was about 22.3
mg/segment and in females about 19.7 mg/segment.50
43
In 1995 William M. Splinter, Juan Bass and Lydia Komocar conducted a study where
they compared the effect of local anaesthesia with that of caudal anaesthesia on
postoperative care of children undergoing inguinal hernia repair. This was a
randomized, single-blind investigation of 202 children aged 1–13 yr. Anaesthesia was
induced with N2O/O2 and halothane or propofol and maintained with
N2O/O2/halothane. Local anaesthesia included ilioinguinal and iliohypogastric nerve
block plus subcutaneous injection by the surgeon of up to 0.3 ml/kg bupivacaine
0.25% with 5 μg/kg adrenaline. The dose for caudal anaesthesia was 1 ml/kg up to
20 ml bupivacaine 0.2% with 5 μg/kg adrenaline. Postoperative pain was assessed in
the anaesthesia recovery room. The postoperative pain scores and opioid usage were
similar; however, the local anaesthesia group required more acetaminophen in the day
care surgical unit. The local anaesthesia patients had a shorter recovery room stay.
The postoperative stay was prolonged in the caudal anaesthesia group. They conclude
that Local anaesthesia and caudal anaesthesia have similar effects on postoperative
care with only slight differences.51
In 1996 Cedric Prys-Roberts and Andrew M.S.Black stated that segmental epidural
block with local anaesthetic is far more satisfactory when placed at correct vertebral
level and in more than 90% patients undergoing lower abdominal surgeries where
block required is between T10-L2 the volume of local anaesthetic required is 5ml.
Duration of block with Bupivacaine 5ml (0.5%) is limited to 3-4 hours, whereas
continuous infusion, with 0.25%(3-7ml/hr) after bolus dose of 5ml maintains
satisfactory analgesia for a variable period of time.52
44
In 2000 Della Rocca G, Giampalmo M, Giorni C, Di Marco PA, Monaco S, Romboli
D, Gossetti F, Negro P, Carboni M and Pietropaoli P conducted a study comparing
different anaesthetising techniques for inguinal hernia repair, where 405 patients
undergoing inguinal hernioplasty were studied. Four different anaesthetic techniques
were used: (i) surgical field infiltration (SFI) with 0.5% carbonated lidocaine +
0.125% bupivacaine (193 pts.) in which monitored anaesthesia care was administered
with propofol (3 to 4 mg/kg/h) when necessary; (ii) epidural anaesthesia with 2%
lidocaine + fentanyl 100 mcg (137 pts.); (iii) general anesthesia with isoflurane and
fentanyl in N2O:O2 (48 pts.); and (iv) intrathecal anaesthesia with 1% hyperbaric
bupivacaine 1-2 ml (25 pts.). Intra- and postoperative complications, intraoperative
sedation, postoperative supplemental drugs for analgesia and postoperative length of
hospital stay were recorded. Intraoperative hypotension/bradycardia were observed in
4 patients (2%) in the SFI group and in 6 patients (4%) in the epidural group. Sedation
was required in 29.5% of patients in the SFI group and in 15.3% in the epidural group
(P < 0.05). Postoperative supplemental analgesic drugs administered and length of
hospital stay were similar in the 4 groups. No difference in intra- and postoperative
complications was observed among the 4 groups. In conclusion, both SFI and epidural
anaesthesia are safe and suitable for the inguinal hernioplasty procedure, without
intra- or postoperative complications.53
In 2002 Günal O, Arikan Y and Celikel conducted a study where they compared the
effect of spinal and epidural anaesthesia on surgical outcome measures of inguinal
herniorrhaphy. Ninety-eight male patients undergoing inguinal hernia repair were
randomized to either spinal or epidural anaesthesia. Anaesthesia onset time (AOT),
postoperative stand-up time (SUT), first pain sensation time (FPT), operation time
45
(OT), analgesic requirement (AR), hospital stay (HS), visual analogue scores of pain
(VAS), per- and postoperative complications, and post anaesthesia complications
were recorded and compared with each other. No statistically significant difference
was found between the SA and EA groups with respect to the other outcome measures
that were considered. Concluded as spinal and epidural anaesthesia show some
differences from each other with respect to outcome measures such as OT, SUT, FPT,
and 12- and 24-h VAS scores.54
In 2005,Todorovic Dragana, Konstatinovic Slavko, Jankovic Radmilo studied the
efficiency and safety of administration of minor anaesthetic concentrations in epidural
anaesthesia for operations of inguinal hernia .Half of the patients were given 20 ml
2% lidocaine and half patients were given 20 ml 1.5% lidocaine. In patients with 2%
lidocaine motor blockade occurred after 14.37+-1.04 mins and duration
110.45min.Only 20 % of the patients on whom 1.5% lidocaine was given had motor
blockade after 11.16+-2.02 mins and duration 100.3 mins. Systolic pressure
significantly decreased after 20ml of 2% lidocaine administration compared to the
group to whom 1.5% was given. The first group had to stay longer in the post
operative ward than the second group, and concluded stating that minor
concentrations of anaesthetics can be efficient and safe in epidural analgesia and they
achieve adequate amount of analgesia for surgical interventions.55
In 2007 Srivastava U, Kumar A, Saxena S, Neeraj and Sehgal conducted a
prospective randomized study in 92 adult male patients to compare the local
anaesthesia with conventional spinal and general anaesthesia for elective unilateral
inguinal hernia repair. The operative conditions were excellent in majority of the
46
patients in local anaesthesia group similar to other two groups. The main disadvantage
of local anaesthesia was dome pain or discomfort at the operative site during
dissection of sac but this did not affect the satisfaction by the patients and its use
again. 87 percent of surgeons and 90 percent of patients were satisfied with the local
anaesthesia. The main advantages of this method were excellent operative conditions,
quick recovery, long analgesia and minimal postoperative complications.56
In 2007 A. A. J. Van zundert, G. Stultiens, J. J. Jakimowicz, D. Peek, W. G. J. M.
Van der ham, H. H. M. Korsten and J. A. W. Wildsmith studied laparoscopic
cholecystectomy under segmental thoracic spinal anaesthesia where twenty ASA I or
II patients undergoing elective laparoscopic cholecystectomy received a segmental
(T10 injection) spinal anaesthetic using 1 ml of bupivacaine 5 mg/ml mixed with 0.5
ml of sufentanyl 5 µg/ml. Other drugs were only given to manage patient anxiety,
pain, nausea, hypotension, or pruritus during or after surgery. The block was effective
for surgery in all 20 patients, six experiencing some discomfort which was readily
treated with small doses of fentanyl, but none requiring conversion to general
anaesthesia. Two patients required midazolam for anxiety and two ephedrine for
hypotension. Recovery was uneventful and without sequelae, only three patients (all
for surgical reasons) not being discharged home on the day of operation. This
preliminary study has shown that segmental spinal anaesthesia can be used
successfully and effectively for laparoscopic surgery in healthy patients.57
In 2008 Yang B, Liang MJ and Zhang Y, conducted a randomized trial to investigate
the efficacy and safety of local anaesthesia and epidural anaesthesia in tension-free
repair of inguinal hernia. 269 patients underwent inguinal hernia repair were
47
randomly divided into two groups, receiving local anaesthesia (143 cases) and
epidural anaesthesia (126 cases). The clinical data from the two groups were analyzed
retrospectively. The operation time, ambulation time, length of hospital stay and cost
of hospitalization in local anaesthesia group were significantly less than those in
epidural anaesthesia group. No significant differences were found in intra-operative
use of ancillary sedation drugs, postoperative recovery situation, pain scores and
operation-correlated complications between the two groups. 58
48
METHODOLOGY
A clinical study was undertaken for anaesthetising 100 patients aged between 18-70
years posted for elective inguinal hernia repair, agreeing and co-operative for epidural
anaesthesia. Study was conducted at MVJ Medical College and Research Hospital
Hosakote, Bengaluru during the period of September 2008 to August 2010.
Selection of patients:
Inclusion criteria:
1. Patients undergoing inguinal hernia repair.
2. Age 18– 70 years.
3. Normal adults belonging to ASA Grade I and ASA Grade II
Exclusion criteria:
1. Patients below 18 and above 70 years.
2. Patients with ASA Grade III and ASA Grade IV.
3. Patients allergic to local anaesthetics.
4. Presence of ischemic heart diseases, hypertension, symptomatic asthma,
inability to climb a flight of stairs, uncontrolled diabetes, epilepsy, renal
problems, bleeding disorders, patients on chronic drug medications such as
MAO inhibitors, acute substance abuse, previous problem with anaesthesia,
obesity, neurological deficit, infection at injection site and patients unwilling
to comply with instructions.
49
Pre-anaesthetic evaluation:
Pre-anaesthetic evaluation was done a day prior to the elective surgery. History of
present complaints, duration of swelling and any co-existing disease, previous surgery
were noted. A thorough physical, systemic examination was done which included the
size of the swelling, type of hernia, weight of the patient, vital signs and airway
assessment.
The following investigations were carried out in all patients:
BLOOD: Haemoglobin percentage, bleeding time, clotting time and random blood
sugar.
URINE: Urine for routine examination, urine albumin and urine sugar were done.
ECG & chest x-ray for patient above 45 years.
All patients were assessed and they were graded according to the ASA physical status
I and II. They were educated regarding the anaesthetic technique. Consent for the
same was obtained. Local anaesthetic test dose was carried out on the previous day of
surgery. Patients were premedicated with oral Alprazolam 0.5 mg and Oral Ranitidine
150 mg on the night prior to surgery and 2 hours before the surgery.
Regional anaesthetic equipment:
There are several important requisites for optimal results in regional anaesthesia. In
order to have consistently good results, the anaesthesiologists must have a genuine
interest in and be convinced of the advantages of regional anaesthesia. After attaining
the necessary skill and clinical application, thorough knowledge of the pertinent
anatomy and landmarks, familiarising with the pharmacology of the local anaesthetic
50
agents as well as the physiological changes that accompany these anaesthetics. He can
thus anticipate any changes and be prepared to institute immediate treatment if
necessary (i.e. intravenous fluids, vagolytics and possible vasopressors). Equally
important is the careful preparation and management of the individual patient and the
availability of appropriate anaesthesia equipment, as well as equipment for
resuscitation and the treatment of adverse reactions.
The department of anaesthesiology in which regional anaesthesia is to be performed
in a sophisticated fashion must have a significant inventory of regional anaesthetic
technique must be kept ready.
Needles:
A wide selection of high quality disposable epidural (Tuohy) needles 16 and 18G.
Syringe:
Disposable and glass barrel syringes with close fitting plungers and various sizes
ranging from 2ml, 5ml, 10ml, 20ml are kept ready.
Drugs:
Inj.Bupivacaine 0.5% isotonic.
Resuscitation:
To perform epidural analgesia, equipments and drugs for resuscitation and treatment
of complications should be kept ready.
51
This should include a means of administering oxygen by positive pressure, such as an
anaesthesia machine or an resuscitation bag and mask connected to a source of
oxygen, airway equipment, working laryngoscope, oro-pharyngeal airways of several
sizes, cuffed endotracheal tubes of appropriate sizes, a suction apparatus and labelled
syringes that contain atropine and a dilute solution of vasopressors.
Monitors:
In the operation theatre an IV line was secured with no. 18 or 20 G IV cannula.
The monitors – pulse oxymeter, ECG, NIBP were connected.
Segmental epidural block denotes the use of local anaesthetic solution enough to
cover only the segments involved in the field of surgery by injecting a low volume
and selecting site of puncture of epidural space, so it becomes the midpoint of
segments involved.
Procedure:
Each patients selected for the study was positioned laterally (on affected side) on the
operation theatre table. With all aseptic precautions the epidural space was identified
at L1-L2 space , with 18G epidural needle 5ml of 0.5% Bupivacaine is injected very
slowly only to block the segments(T12-L2) involved in the field of surgery. Later
epidural catheter was inserted and secured and patient positioned back to supine
position.
Level of analgesia was checked by needle prick. After conforming the adequacy and
level of analgesia, the surgery was commenced. If the patient complained of pain
52
during needle prick, then injected local anaesthetic (0.5% Bupivacaine) with an
incremental dosage of 1ml at a time, till the complete onset of analgesia.
Pulse Rate and Blood Pressure were recorded at an interval of 1 minute for first 5
minutes and then every 5 minutes till the end of the surgery. Oxygen saturation and
ECG monitoring was done continuously.
Onset of analgesia, level of analgesia (pre & post operatively), duration of analgesia,
total dosage of local anaesthetic used were recorded.
Complications like bradycardia, hypotension, respiratory depression, shivering,
nausea and vomiting, sweating and inadvertent dural puncture were recorded.
Criteria for hypotension was taken as a fall in systolic Blood pressure more than 20%
of patients basal reading and treated with vasopressors like Inj.Ephedrine 3-5 mg IV.
Bradycardia as heart rate less than 60 and treated with Inj.Atropine 0.6 mg IV.
If any inadvertent dural puncture occured, those cases were excluded from the study
and was given homologous epidural blood patch to prevent post dural puncture
headache.
After confirming the onset of analgesia patient was sedated with Inj.midazolam 1 mg
IV.
53
In the present study the following scale was adopted to grade quality of analgesia and
relaxation.
1. Excellent: Patient comfortable, analgesia and surgical relaxation adequate, no
supplementation required during surgery.
2. Good: Analgesia and relaxation adequate, minimal discomfort present during
surgical procedure. Additional top-ups of local anaesthetic at an incremental
dose of 1 ml are given.
3. Fair: Analgesia and relaxation adequate, discomfort present even after
additional top-up of epidural local anaesthetic, this was alleviated by analgesic
dose of Ing.Fentanyl 1 Mcg/kg IV.
4. Poor: Patients complaining of severe intolerable pain during surgery without
relaxation. These cases were supplemented with general anaesthesia.
Statistical analysis:
Descriptive data included mean, standard deviation and percentage which were
determined for the study group.
54
Fig-10 Epidural Tray
Fig-11 Postion of The Patient
55
Fig-12 Loss of Resistance
Fig-13 Epidural Catheter Insitu
56
a
b
Fig-14 a, b Dermatomes
57
RESULTS
Segmental epidural anaesthesia was given to one hundred patients undergoing
inguinal hernia repair at MVJ Medical College and Research Hospital, during the
period of September 2008 to August 2010 and these cases were taken up for study as
outlined in the methodology.
AGE DISTRIBUTION:
TABLE – 4
Age Group No. Of Cases
18-30 21
31-40 30
41-50 22
51-60 17
61-70 10
Total 100
58
GRAPH - 1
Age of these patients ranged from 18 to 70 years and this incidence is shown in Table
– IV.
Mean Age 42.65 years
STD Deviation 12.85
Majority of the patients were in 31-40 Age group.
0
5
10
15
20
25
30
18-30 31-40
21
30
58
GRAPH - 1
Age of these patients ranged from 18 to 70 years and this incidence is shown in Table
– IV.
Mean Age 42.65 years
STD Deviation 12.85
Majority of the patients were in 31-40 Age group.
31-40 41-50 51-60 61-70
30
2217
10
58
GRAPH - 1
Age of these patients ranged from 18 to 70 years and this incidence is shown in Table
– IV.
Mean Age 42.65 years
STD Deviation 12.85
Majority of the patients were in 31-40 Age group.
61-70
10
59
SEX INCIDENCE:
TABLE – 5
Sex No. of Cases
Male 97
Female 3
Total 100
GRAPH – 2
Regarding the sex incidence it is the male who predominates as compared to females,
which is shown in the Table- V
97
3
SEX INCIDENCE
MALE
FEMALE
60
WEIGHT DISTRIBUTION:
TABLE – 6
Weight in Kgs No. Of Cases
31-40 3
41-50 27
51-60 32
61-70 32
71-80 6
GRAPH - 3
TABLE VI shows the weight distribution of patients.
Maximum weight was 85 Kgs
Minimum weight was 37 Kgs
Mean weight 57.65 Kgs with a standard deviation of 9.1
3
27
32 32
6
0
5
10
15
20
25
30
35
31-40 41-50 51-60 61-70 71-80
WEIGHT INCIDENCE
61
HEIGHT DISTRIBUTION:
TABLE - 7
Height in cms No. of Cases
141-150 5
151-160 30
161-170 36
171-180 29
GRAPH - 4
TABLE VII shows the Height distribution of patients.
Maximum Height 180 cms
Minimum Height 148 cms
Mean Height 165.16 cms with a standard deviation of 8.24.
0
5
10
15
20
25
30
35
40
141-150 151-160 161-170 171-180
Height
Height
62
TYPE OF HERNIA:
TABLE – 8
Type of Hernia No. Of Cases
Indirect 73
Direct 27
Total 100
GRAPH - 5
Incidence in type of hernia is shown in the Table- VIII
Direct hernia 27 cases
Indirect hernia 73 cases
73
27
TYPE OF HERNIA
INDIRECT
DIRECT
63
VOLUME OF BUPIVACAINE USED:
TABLE - 9
Volume of drug No. Of Cases
5ml 53
6ml 22
7ml 16
8ml 9
GRAPH - 6
Volume of Bupivacaine required, ranged from 5 ml to 8 ml. with a mean volume of
5.8 ml.
53
22
16
9
VOLUME OF DRUG
5 ml
6 ml
7 ml
8 ml
64
QUALITY OF ANALGESIA:
TABLE – 10
No. Of Cases
Excellent 53
Good 34
Fair 10
Poor 3
Cases excluded from study 2
Total 102
GRAPH - 7
53
34
0
10
20
30
40
50
60
EXCELLENT GOOD
64
QUALITY OF ANALGESIA:
TABLE – 10
No. Of Cases
Excellent 53
Good 34
Fair 10
Poor 3
Cases excluded from study 2
Total 102
GRAPH - 7
34
10 3 2
GOOD FAIR POOR CASESEXCLUDED
64
QUALITY OF ANALGESIA:
TABLE – 10
No. Of Cases
Excellent 53
Good 34
Fair 10
Poor 3
Cases excluded from study 2
Total 102
GRAPH - 7
CASESEXCLUDED
65
Table X shows the quality of analgesia and relaxation in patients.
53 patients had an excellent type of analgesia and relaxation. Patients were
comfortable no supplementation required during surgery.
In 34 patients analgesia and relaxation was adequate, minimal discomfort was present
during surgical procedure. Additional top-ups of local anaesthetic at an incremental
dose of 1 ml were given.
In 10 patients, discomfort was present even after additional top-up of epidural local
anaesthetic, this was alleviated by analgesic dose of Ing.Fentanyl 1 Mcg/kg IV.
3 patients had no analgesia at all, Patients were complaining of severe intolerable
pain during surgery without relaxation. These cases were converted to general
anaesthesia.
2 cases were withdrawn from the study as there was an inadvertent dural puncture.
66
DURATION OF ANALGESIA:
TABLE – 11
Time range in minute Number of patients
120-130 12
131-140 11
141-150 11
151-160 13
161-170 12
171-180 15
181-190 4
191-200 9
201-210 7
211-220 0
221-230 1
231-240 2
67
GRAPH - 8
TABLE XI shows the Duration of analgesia in minutes. The patients who received general
anaesthesia, had no analgesia.
Mean duration 167.42 min
Minimum duration 120 min
Maximum duration 240 min
In 3 patients who had poor quality of analgesia and converted to general anaesthesia,
duration of analgesia could not be recorded.
1211 11
1312
15
4
9
7
01
2
0
2
4
6
8
10
12
14
16
DURATION
68
LEVEL OF ANALGESIA PRE-OPERATIVELY:
TABLE – 12
LEVEL NO. OF CASES
T8 2
T9 16
T10 54
T11 22
T12 3
GRAPH - 9
TABLE XII shows the sensory level of analgesia pre operatively.
In majority of the patients (54) level of analgesia was up to T10
In 22 patients T11
In 16 patients T9
In 3 patients T12
In 2 patients T8
In 3 patients who had poor quality of analgesia and converted to general anaesthesia,
level of analgesia could not be appreciated.
2
16
54
22
30
10
20
30
40
50
60
T8 T9 T10 T11 T12
69
LEVEL OF ANALGESIA POST OPERATIVELY
TABLE – 13
LEVEL NO. OF CASES
T7 2
T8 33
T9 43
T10 17
T11 1
T12 1
GRAPH - 10
TABLE XIII Shows the sensory level post operatively
In majority of the patients (43) level of analgesia was up to T9
In 33 patients T8
In 17 patients T10
In 2 patients T7
In 2 patients T11 & T12
2
33
43
17
1 10
5
10
15
20
25
30
35
40
45
50
T7 T8 T9 T10 T11 T12
70
SIDE EFFECTS:
TABLE – 14
SIDE EFFECTS NO. OF CASES
Inadvertent dural puncture 2
Shivering 5
Sweating 9
Hypotension NIL
GRAPH - 11
TABLE XIV Shows the incidence of side effects.
Sweating is seen in 9 patients.
Shivering in 5 patients.
Inadvertent dural puncture in 2 patients.
No cases of Hypotension.
9
70
SIDE EFFECTS:
TABLE – 14
SIDE EFFECTS NO. OF CASES
Inadvertent dural puncture 2
Shivering 5
Sweating 9
Hypotension NIL
GRAPH - 11
TABLE XIV Shows the incidence of side effects.
Sweating is seen in 9 patients.
Shivering in 5 patients.
Inadvertent dural puncture in 2 patients.
No cases of Hypotension.
2
5
0
SIDE EFFECTS
IDP
SH
SW
HYPOTENSION
70
SIDE EFFECTS:
TABLE – 14
SIDE EFFECTS NO. OF CASES
Inadvertent dural puncture 2
Shivering 5
Sweating 9
Hypotension NIL
GRAPH - 11
TABLE XIV Shows the incidence of side effects.
Sweating is seen in 9 patients.
Shivering in 5 patients.
Inadvertent dural puncture in 2 patients.
No cases of Hypotension.
IDP
SH
SW
HYPOTENSION
71
ANALGESIA AND RELAXATION SUCCESS RATE
TABLE 15
QUALITY OF ANALGESIA NO. OF CASES
EXCELLENT 53
34
1097 %
GOOD
FAIR
POOR 3
GRAPH - 12
SUCCESS RATE 97%
97
3
NO.OFCASES
SUCCESS
FAILURE
72
MEAN HEART RATE CHANGES
TABLE- 16
MINUTES MEAN HEART RATE
PREOP 83.8
0 87.22
1 86.58
2 86.44
3 86.72
4 85.9
5 85.06
10 85.24
15 85
20 84.32
25 83.8
30 84.44
35 84.14
40 84.03
45 83.48
50 83.76
55 83.36
60 83.08
END 83.42
73
GRAPH- 13
81
82
83
84
85
86
87
88
HR
74
MEAN BLOOD PRESSURE CHANGES
TABLE- 17
MINUTES MEAN SYST.BP. MEAN DIAST.BP.
PREOP 130.26 80.44
0 132.84 82.6
1 132.3 82.18
2 130.56 81.56
3 130.56 80.9
4 129.62 81.12
5 126.55 80.66
10 127.76 79.98
15 127.87 79.88
20 127.7 79.46
25 127.82 79.5
30 128.26 79.66
35 128.92 79.48
40 128.42 78.82
45 128.3 79.66
50 128.58 79.9
55 128.36 79.48
60 129.08 80.06
END 130.48 81
75
GRAPH –14
0
20
40
60
80
100
120
140PR
EOP 0 1 2 3 4 5 10 15 20 25 30 35 40 45 50 55 60
END
SYSTOLIC
DIASTOLIC
76
TABLE – XVIII
SUMMARY OF RESULTS ( AGE GROUPS)
AGEGROUP(YEARS)
NO.CASES MEANAGE
(YEARS)
MEANWEIGHT
(Kg)
MEANHEIGHT
(cm)
MEANDRUGVOL
(ml)
MEANONSET
(Min)
MEANDURATION
(Min)
MEANBP
FALL
MEAN% BPFALL
18-30 21 26.19(STD DEV 3.31)
55.66(STD DEV 8.77)
164.90(STD DEV 8.08)
6.81(STD DEV 1.07)
8.11(STD DEV 1.24 )
171.42(STD DEV 30.21)
8.76 6.69
31-40 30 36-63(STD DEV2.95 )
56.23(STD DEV9.05 )
166.57(STD DEV 7.24)
5.60(STD DEV 0.85)
8.03(STD DEV 1.19)
162.03(STD DEV 26.24)
8.74 6.64
41-50 22 46.09(STD DEV 2.88)
60.50(STD DEV 9.63)
167.09(STD DEV 7.43)
5.59(STD DEV 0.73)
7.88(STD DEV 0.90)
166.67(STD DEV 24.56)
9.90 7.36
51-60 17 55.47(STD DEV 3.28)
59.47(STD DEV 8.90)
162.56(STD DEV 10.55)
5.53(STD DEV 0.79)
8.36(STD DEV 1.17)
174.11(STD DEV 34.65)
14 10.20
61-70 10 65.9(STD DEV 2.51)
56.17(STD DEV 9.10)
161.3(STD DEV 8.40)
5.3(STD DEV 0.94)
8.17(STD DEV 1.09)
163.89(STD DEV 28.26)
15.56 13.38
77
DISCUSSION
Inguinal hernia repair is one of the most commonly encountered surgical corrections
in men representing 12.5% of total surgical repair in Britain. In providing anaesthesia
for inguinal herniorraphy, the technique chosen must be cost effective with respect to
speed of recovery, patient comfort, and associated incremental costs.
Inguinal hernia repair is one of the common treatments performed. Which can be
performed under spinal, epidural, general and inguinal field block.
Epidural anaesthesia is suitable as a sole agent for lower abdominal surgery and on
lower limbs. It has some definite advantages over spinal anaesthesia like avoidance of
post spinal headache, minimal chances of meningitis, and minimal chances of nausea
and vomiting in post operative period.
Segmental epidural block, though introduced by Fidel Pages (1921) and Dogliotti
(1931), clinically its use has been advocated by Massey Dawkins (1971) for thoracic
epidural for upper abdominal surgery and Doughty (1969) and Steel (1972) in labour
analgesia for uterine and perineal pain and have recommended that this technique to
be a very safe and satisfactory procedure to all concerned.
These works have given a useful suggestion for extending the technique as
“Segmental Epidural Block” for Inguinal hernia repair as the nerve supply to this area
is very suitable for carrying out this procedure and also has some attractive
advantages over the conventional epidural block using larger doses.
78
The study of Segmental Epidural Analgesia for inguinal hernia repair was carried out
with an intension of administering limited quantity of drug required to make the
procedure precise and safe.
Segmental or conventional block can be performed at any region like cervical,
thoracic, lumber or caudal. However the volume used in the segmental block is very
small so that the block covers only the particular segments concern. Whereas in
conventional block, the volume used is large enough to spread widely giving rise to
complications like arterial hypotension, bradycardia etc.
Advantages claimed with segmental epidural analgesia are:
1. Small quantity of local anaesthetic drug enabling to use an effective dose or
higher concentration without the fear of complications like extensive muscular
paralysis and toxic effects.
2. Complications like hypotension and bradycardia are reduced.
3. Even in accidental subarachnoid block the cardio-respiratory involvement is
minimal, as these small doses used will act as subarachnoid block.
4. Economical.
In our study the following parameters were studied.
1. Volume of local anaesthetic used.
2. Level of sensory blockade achieved pre-operatively (using standard
dermatome map).
3. Level of sensory blockade achieved post operatively.
4. Effectiveness of block or quality of analgesia.
79
5. Onset and Duration of analgesia.
6. Complications encountered.
In our study site of puncture for epidural space is fixed (L1-L2) so as to block only
the segments involved in the field of surgery and keep the dose to minimum.
Along with the site of injection, posture of the patient was also important so as to get
a denser block on the operative side.13 Hence with the patient on the side of surgery
the slow injection of small volume of drug permits gravity to deposit all the solution
on the dependent side to block the nerves which supplies the region involved in the
surgical procedure thereby minimising the complications associated with large
volume.59
Volume of the drug used:
Sicard stated that spread of analgesia depends upon the volume of the drug injected.12
Cedric Prys-Roberts and Andrew M.S.Black stated that segmental epidural block with
local anaesthetic is far more satisfactory when placed at correct vertebral level and in
more than 90% patients undergoing lower abdominal surgeries where block required
is between T10-L2 the volume of local anaesthetic required is 5ml.52
Studies conducted by Dr.M.H.Rao, and Dr.Phani Thota, on Segmental dose
requirement of epidural lignocaine stated that dose required to block each segment in
males was about 22.3mg/segment and in females about 19.7 mg/segment.50
Based on these studies volume of the drug injected by us was 5 ml, so as to limit the
spread to only the segments involved in the field of surgery.
80
In this study, a majority of patients (53 patients) who received 5ml the analgesic
effect was found to be satisfactory. 22 patients received 6 ml, 16 patients 7 ml and 9
patients received 8ml. It is observed that the majority of patients who required the
additional topups upto 7 and 8 ml were younger age group. This can be explained by,
in younger age group the spread is minimal due to spillage of drug through the patent
intervertebral foraminae. But escape of fluid is reduced to minimum in the elderly
patients due to the stenosed intervertebral foraminae which can be observed by the
largest spread of volume as seen in two patient aged 70 and 65 years, where the
spread was upto T8 with 5ml of drug.
The mean volume of drug is 5.8 ml. The TABLE XVIII shows that, with the increase
in age the volume required decreases.
Level of sensory blockade achieved pre-operatively and post operatively:
While using the minimal quantity of local anaesthetic drug of 5 ml, the extent of
spread of analgesia was tested 5-10 minutes after the block was given and at the end
of surgery. The extent of analgesia was elicited with the help of pin prick.
Bromage in 1954 demonstrated that there are two mechanisms in the spread of
analgesia, one by the longitudinal spread and the other by neuraxial spread. Diffusion
gradient appears to be important in relation to solutions of small volume but of high
concentration. With these small volumes of concentrated solution longitudinal spread
in the epidural space is presumeably confined to a fewer segments but neuraxial
spread is extensive owing to the concentration gradient blocking more segments
which was seen at the end of surgery. The same has been corroborated in this study
81
after the block and before starting of the surgery the longitudinal ascent of analgesia
with the small volume was minimal, affecting only few segments. Whereas at the end
of surgery the spread was definitely wider than what it was in the beginning which
was probably due to the neuraxial spread owing to the diffusion gradient with higher
concentration solution of 0.5% Bupivacaine.
Bromage in 196215 has also drawn attention to the exaggerated spread of epidural
analgesia in atherosclerotic patients. 56 patients who were severely atherosclerotic
reacted to 2% ligocaine as if they had received the drug of higher concentration than
that. It is probable that the degenerative changes in the connective tissue associated
with atherosclerotic disease produces increased permeability of neural coverings.
Furthermore sclerosis of vasa nervosium hastens the neural degeneration of myelin
sheaths which occur with increasing age, thus bringing the solution more readily into
contact with the axons of the posterior nerve roots.
In our study, even with 5 ml of local anaesthetic when injected at L1-L2 in elderly
patients (60 years and above) it has been found that the spread has been usually high
(T8).
Effectiveness of block or quality of analgesia:
In the present study we graded 53 patients as excellent analgesia and relaxation, i.e.
patient comfortable, analgesia and surgical relaxation adequate no supplementation is
required during surgery.
82
34 patients had good analgesia and mild discomfort during surgical procedure, which
required Additional top-ups of local anaesthetic at an incremental dose of 1 ml.
10 patients had analgesia graded as fair where mild discomfort was present even after
additional top-up of epidural local anaesthetic; These patients were given an analgesic
dose of Inj.Fentanyl 1 μg/kg IV to alleviate the pain.
3 patients had severe intolerable pain during surgery, requiring conversion to general
anaesthesia.
It has been observed by various authors that at the time of traction on the sac, patients
often complain of discomfort.60 This finding was observed in 9 patients in our present
clinical study.
Onset and Duration of analgesia:
Many studies did not mention about duration of analgesia.
A study conducted by Hollman A et al. In 418 parturients, the onset of analgesia was
rapid that is 3-5 mins and the duration was on average 150 mins.41
In a study by Prys Roberts and Andrew Black, stated that in 90% of the patients
undergoing lower abdominal surgeries where block required is between T10-L2 the
volume of local anaesthetic required is 5 ml and the duration of block with
Bupivacaine 0.5% is limited to 3-4 hours.52
83
In the present study mean onset of analgesia was 8.09 minutes and mean duration of
analgesia was 167.42 minutes (120 min – 240min).
In the present study onset of analgesia was relatively late and duration of analgesia
correlates with studies done by Hollman A et al.
Complications encountered:
Hypotension: Criteria for hypotension was taken as a fall in systolic blood pressure
more than 20% of patient’s basal reading.
Odom (1936), Guiterrez (1939), Doglitotti (1939) and Dawkins (1954) claimed that
the hypotension in epidural block is less than that from spinal analgesia. But the
works of Bromage (1954) and Bonica et al (1957) found that the extent of fall in
blood pressure is similar in both the techniques, speed of onset is slow in epidural
analgesia.
Factors contributing to the hypotension in epidural block have been enumerated as the
advanced age of the patient, high volume of the drug and height of the block.
In our study as the volume of the drug used is minimal and height of the block is
limited, thereby the incidence of hypotension is nil.
Only 4 patients had a 15-17% fall in blood pressure, in 20 patients 10-15%, in 50
patients 5-10% and in 24 patients 1-5% fall in blood pressure. TABLE XVI Shows
that percentage of fall in blood pressure increases with the increase in age.
84
Inadvertent Dural Puncture: The incidence of dural puncture was claimed to be low
with thoracic epidurals than with lumbar epidurals. Dawkins and Steel (1971) claimed
to be as 1.6% in 282 cases of thoracic epidurals as against 2.6% in 397 cases of
lumbar epidurals. This is because of the obliquity of the anatomy of spinous
processes.
In this present study there were 2 cases of dural puncture. These cases were
withdrawn from the study as the epidural puncture site was fixed at L1-L2.
In 9 cases symptoms of sweating are seen, majority of these cases were under fair or
poor quality of analgesia groups. So poor quality of analgesia may be the reason for
sweating. The symptoms were decreased after the analgesic dose of Inj.Fentanyl IV.
5 patients complained of shivering, was relieved by sedation.
Other complications like massive subarachnoid block, massive extradural block, toxic
reaction to local analgesic drug, bradycardia, respiratory depression, nausea and
vomiting, retention of urine and any neurological complications were not encountered
in the present study.
85
CONCLUSION
It can be concluded that
Segmental epidural block with 5-6 ml of 0.5% Bupivacaine is found to be safe
and fulfils the surgical requirement.
Could be successfully employed for inguinal hernia repair with limited spread
of analgesia involving only few segments.
Fall in blood pressure and other complications were very minimal.
This technique can be safely used in elderly patients.
In respiratory and cardiac cripple, this segmental epidural analgesia is safest
mode of regional anaesthesia.
In fit patients ideal as a day care anaesthesia.
86
SUMMARY
A clinical study “SEGMENTAL EPIDURAL BLOCK FOR INGUINAL HERNIA
REPAIR” was undertaken at the Department of Anaesthesiology, M.V.J. Medical
College and Research Hospital, Bangalore during the period of September 2008 to
August 2010.
This study includes a brief outline of the historical events in the development of
Epidural analgesia, the physiological and pharmacological aspects including the site
of action of the drug and the factors affecting the spread of the epidural block.
The segmental epidural block denotes the use of a small volume enough to block only
the segments involved in the field of surgery. This was achieved by selecting the site
of puncture, position and speed of injection of the local anaesthetic drug.
The study population consisted of 100 patients undergoing Inguinal hernia repair of
ASA class I and II. All the patients were explained about the procedure and
anaesthetic technique and consent for the same obtained. Local anaesthetic test dose
was carried out on previous day. Patients were premedicated with oral Alprazolam 0.5
mg and Oral Ranitidine 150 mg on the night prior to surgery and 2 hours before the
surgery.
Each patients selected for the study was positioned laterally (on herniated side) on the
operation theatre table. With all aseptic precautions the epidural space was identified
at L1-L2 space , with 18G epidural needle 5ml of 0.5% Bupivacaine is injected very
87
slowly only to block the segments(T12-L2) involved in the field of surgery. Later
epidural catheter was inserted and secured and patient positioned back to supine
position.
Level of analgesia was checked by needle prick. After conforming the adequacy and
level of analgesia, the surgery was commenced. If the patient complains of pain
during needle prick, then injected local anaesthetic (0.5% Bupivacaine) with an
incremental dosage of 1ml at a time, till the complete onset of analgesia.
Irrespective of discomfort during hernia repair, Inj. Medazolam 1mg was given as a
sedative. Pulse Rate and Blood Pressure were recorded at an interval of 1 minute for
first 5 minutes and then every 5 minutes till the end of the surgery. Oxygen saturation
and ECG monitoring was done continuously.
Onset of analgesia, Level of analgesia (pre & post operatively), Duration of analgesia,
Total dosage of local anaesthetic used were recorded.
If the patient complained of discomfort even after additional top-up of epidural local
anaesthetic, an analgesic dose of Ing. Fentanyl 1 Mcg/kg IV was given.
The following observations were made from the present study:
Total study population 100 patients
Mean Age 42.65 years (18-70 years)
Sex M/F 97/3
Mean weight 57.65 Kgs (37-85 Kgs)
88
Mean height 165.16 cms (148-180 cms)
ASA Physical status I and II
Type of Hernia Direct / Indirect 27 / 73
Volume of Drug 5.8 ml (6-8 ml)
Duration of Analgesia 167.42 minutes
Quality of Analgesia
1) Excellent 53
2) Good 34
3) Fair 10
4) Poor 3
53% of patients had excellent quality of analgesia and relaxation. 34% patients had
good quality analgesia and relaxation, mild discomfort while handling sac. 10% of
patients had fair quality of analgesia and relaxation only. In 3% patients the epidural
block failed, in whom general anaesthesia was given. Overall success rate was 97%.
Complications
Intraoperative and post operative complications were very minimal. No cases of
hypotension, bradycardia, nausea vomiting, total spinal block and respiratory
depression were seen.
2 cases of inadvertent dural puncture, which were excluded from the study.
89
9 patients complained of sweating and 5 patients complained of shivering, which may
be due to inadequate analgesia or anxiety and successfully treated with Inj.Fentanyl 1
mcg/Kg IV.
From the present study it can be inferred that 0.5% Bupivacaine 5-6 ml is effective for
segmental epidural block for inguinal hernia repair. Segmental epidural block is safe
anaesthesia with minimal physiological alterations.
90
BIBLIOGRAPHY
1) Kingsnorth, Bennett DH. Hernias, Umbillilus, Abdominal Wall. In: Short
practice of surgery Bailey and Love. 23rd ed. 2000.p.1143.
2) Dexter F, Macario A, Penning DH, Chung P. Development of an appropriate list
of surgical procedures of a specified maximum anaesthetic complexity to be
performed at a new ambulatory surgery facility. Anesth Analg 2002;95:78-82.
3) Song D, Greilich NB, White PF, Watcha MF, Tongier WK. Recovery profiles
and costs of anaesthesia for outpatient unilateral inguinal herniorrhaphy. Anesth
Analg 2000;91:876-81.
4) Cheng P.A. The anatomical and clinical aspects of epidural analgesia, part I and
II. Anesth Analg 1963;42:398-407.
5) Cousins MJ, Bromage PR. Epidural neural blockade, neural blockade in clinical
anesthesia and management of pain. Cousins MJ,Bridenbaugh PO (eds): Neural
Blockade. Philadelphia: JB Lippincott; 1988. p.253–260.
6) P.Prithviraj. Textbook of regional anaesthesia. Vol (1). Elsevier (USA):
Churchill Livingstone;2003.p.568.
7) Reynolds FJM. Spinal and Epidural block. In: Wylie and Churchill D.
A Practice of Anaesthesia 5th ed. New Delhi: PG Publishers; 1984.p.856-888.
8) Christoper MB. Epidural and Spinal Anaesthesia. In: Paul BG, Bruce CF,
Robert SK. Clinical Anaesthesia 4th ed. Pheladelphia: Lippincott Williams and
Wilkins;1992.p.689-714.
91
9) Blomberg R. The dorsomedian connective tissue band in the lumbar epidural
space of humans – an anatomic study using epiduroscopy in autopsy cases.
Anesth Analg1986;65:747.
10) Brown LD. Spinal, Epidural, Caudal Anesthesia. In: Miller RD. Miller’s
Anesthesia. 6thed. Philadelphia : Churchill Livingstone; 2005.p.1653-84.
11) Collins VJ. Epidural Anaesthesia. In: Principles of Anesthesiology. 3rd ed.
Philadelphia: Lee and Febiger; 1993.p.1571-1610.
12) Sicard M. “Les injections medicamenteuses extradurales par voie sacro-
coccygienne” C R Soc Dev Biol 1901;53:396-398.
13) Burn, J.M.Guyer, B.P.Langdon L. Spread of solution injected in the epidural
space. Br J Anaesth 1973;45:338.
14) Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to
spread of anaesthetic solution in epidural space. Anesth Analg Curr Reser
1967;46:440.
15) Bromage P.R. Exaggerated spread of epidural analgesia in atherosclerotic
patients. Dose in relation to biological and chronological ageing. BMJ
1962;2:1634.
16) Kingsnorth, Bennett DH. Hernias, Umbillilus, Abdominal Wall. In: Short
practice of surgery Bailey and Love. 23rd ed. 2000.p.1143.
17) Atkinson RS, Rushman GB, Lee JA. Regional techniques. Lees synopsis of
anaesthesia. 11th ed. 1993.p.666.
18) Singh I. The abdomin and pelvis. In: Text book of anatomy with colour atlas.
Vol. 2. 2nd ed. 1999.p. 597-602.
19) Snell RS. The abdomen. Part I. The abdominal wall. In: Clinical anatomy. 4th
ed. 2004. p.172-174.
92
20) Healy CJ, Borley NR. Posterior abdominal wall and retroperitoneum, Section 7,
Abdomen and pelvis. In: The anatomical basis of clinical practise, Grays
Anatomy. 39th ed. 2005.p.1124-1126.
21) Prys Roberts C, Brown BR. Local Anaesthetic Pharmacology. In: International
Practice of Anaesthesia, 1st ed. Vol. 2 Oxford: Butterworth, Heinemann; 1996.
22) Hardman JG, Limbird LE, Goodman Gillman A. Local Anaesthetics in: The
Pharmacological Basis of Therapeutics. 10th ed. United States of America:
McGraw Hill: 2001.
23) Dollery C. Bupivacaine Hydrochloride in: Therapeutic Drugs. 2nd ed.
Edinburgh: Churchill Livingstone; 1999.
24) Miller Ronald D. Local Anaesthetics in: Anesthesia. 6th ed. Vol. 1 Philadelphia:
Churchill Livingstone; 2005.
25) Stoelting RK. Local Anaesthetics in: Pharmacology & Physiology. In:
Anaesthetic Practice. 3rd ed. Philadelphia (New York): Lippincott Raven;1999.
26) Bromage PR. Epidural analgesia. Philadelphia: WB Saunders; 1979.p.118.
27) Miller Ronald D. Anesthesia. 6th ed. Vol. 1 Philadelphia: Churchill Livingstone;
2005.p. 27.
28) Lund, PC Charles, C Thomas. Peridural analgesia and anaesthesia; 1966.p.4.
29) P.Andrade. A new interpretation of the origin of extradural space negative
pressure. Br J Anaesth 1983;55: 857.
30) Bromage P. The “Hanging Drop” sigh. Anaesthesia 1953;8:237-241.
31) Odom.C. Epidural anesthesia .Am J Surg 1936;34:547-558.
32) Lemmon.W. A method of continuous spinal anaesthesia: A preliminary report.
Ann surg 1940;111:141-144.
93
33) Touhy E. Continuous spinal anaesthesia: its usefulness and technique involved.
Anesthesiology 1944; 5:142-148.
34) Cubelo MM. Continuous peridural segmental anesthesia by means of a ureteral
catheter. Anesth Analg 1949; 28:13-23.
35) Bromage P. Epidural analgesia. Philadelphia: WB Saunders; 1979.
36) Bonica J. Regional anaesthesia recent advances and current status. Philadelphia:
Davis; 1969.
37) Ekboln L, Widman. A comparison of the properties of LAC43, prilocaine and
bupivacaine in extradural anaesthesia. Acta Anaesthesiol Scand 1966; 21:33.
38) Philip R. Bromage. Unblocked segments ESI epidural analgesia for relief of
pain in labour; Br J Anaesth 1972; 44(7):676-679.
39) Bromage P R. Lower limb reflex changes in segmental epidural analgesia. Br J
Anaesth 1974; 46(7): 504-508.
40) Maltau JM. The frequency of fetal bradycardia during selective epidural
anaesthesia. Acta Obstet Gynecol Scand 1975;54(4):357-61.
41) Hollman A, Jouppila R, Pihlajaniemi R, Karvonen P, SjostedtE. Selective
lumbar epidural block in labour. A clinical analysis. Acta Anaesthesiol Scand
1977; 21 (3):174-81.
42) Jouppila R, Pihlajaniemi R, Hollman A, Jouppila P. Segmental epidural
analgesia and postpartum sequelae. Ann Chir Gynaecol 1978; 67(2):85-8.
43) Jouppila R, Jouppila P, Karinen JM, Hollman A. Segmental epidural analgesia
in labour: related to the progress of labour, fetal malposition and instrumental
delivery. Acta Obstet Gynecol Scand 1979; 58(2):135-9.
94
44)Willdeck-Lund G, Lindmark G, Nilsson BA. Effect of segmental epidural block
on the course of labour and the condition of the infant during the neonatal
period. Acta Anaesthesiol Scand 1979; 23(4):301-11.
45)Gal D, Choudhry R, Ung KA, Abadir A, Tancer ML. Segmental epidural
analgesia for labor and delivery. Acta Obstet Gynecol Scand 1979; 58(5):429-
31.
46)Pentti Jouppila, RiittaJouppila, Arno Hollman, Antero Koivula. Lumbar
Epidural Analgesia to Improve Intervillous Blood Flow During Labor in Severe
Preeclampsia. Obstet gynaecol 1982;59:158- 161.
47) Kanto J, Erkkola R, Mansikka M, Aärimaa L. Segmental epidural analgesia - a
modern method for safe and effective management of labor pains. Biol Res
Pregnancy Perinatol 1983;4(4):172-6.
48) Anthony C. Webster, J. D. McKishnie, J. T. Watson, W. Donald Reid. Lumbar
epidural anaesthesia for inguinal hernia repair in low birth weight infants. Can J
Anaesth 1993;40(7): 670-675.
49) Peutrell JM, Hughes DG. Epidural anaesthesia through caudal catheters for
inguinal herniotomies in awake ex-premature babies. Anaesthesia 1993;
48(2):128-31.
50) M.H.Rao, Phani Thota. Segmental dose requirement of epidural lignocaine. J
Anaesth Clin Pharmacol 1995; 11: 99-102.
51) William M. Splinter, Juan Bass, Lydia Komocar. Regional anaesthesia for
hernia repair in children: local vs caudal anaesthesia. Can J Anaesth 1995;42:3.
52) Cedric Prys-Roberts and Burnell R.Brown. International practice of anaesthesia.
1st ed. Vol. 2. Oxford: Butterworth, Heinemann; 1996.p.140/9.
95
53) Della RoccaG, Giampalmo M, Giorni C, Di Marco PA, Monaco S, Romboli
D, Gossetti F, et al., Anesthesia for inguinal hernioplasty: a comparison of
techniques. Chir Ital 2000; 52(6):687-93.
54) Gunal O, Arikan Y, Celikel N. Clinical assessment of spinal and epidural
anaesthesia in inguinal hernia repair. J Anesth 2002; 16(2):119-22.
55) Todorovic Dragana, Konstatinovic Slavko, Jankovic Radmilo. Administration of
epidural anaesthesia in operations of inguinal hernia: Comparison of different
anaesthetic concentrations. Acta Medica Mediane 2005; 44(4):25-29.
56) Srivastava U, Kumar A, Saxena S, Neeraj, Sehgal . Comparison of local spinal
and general anaesthesia for inguinal hernia repair. Journal of Anaesthesiology
2007; 23(2): 151-4.
57) A. A. J. Van zundert, G. Stultiens, J. J. Jakimowicz, D. Peek, W. G. J. M. Van
der ham, H. H. M. Korsten et al., Laparoscopic cholecystectomy under
segmental thoracic spinal anaesthesia: A feasibility study. Br J
Anaesth 2007; 98 (5):682-686.
58) Yang B, Liang MJ, Zhang YC. Use of local or epidural anaesthesia in inguinal
hernia repair: a randomized trial. Zhonghua Wai Ke Za Zhi 2008; 46(16):1234-
6.
59) Swerdlow M, Sayle Creer W. A study of extradural medication in the relief of
lumbosciatic syndrome. Anaesthesia 1970; 25:341-345.
60) Tverjkoy M, Cozacovc, Ayache M, Bradley EL, Kissin I. Post operative pain
after inguinal herniuorrhaphy with different type of anaesthesia. Anesth Analg
1990;70:29-35.
96
ANNEXURE – I
“SEGMENTAL EPIDURAL ANALGESIA FOR INGUINAL HERNIA
REPAIR” – A CLINICAL STUDY
PROFORMA
Name: I.P.No: Age/Sex: Wt:
Kg Ht: cms
Diagnosis: Surgery: Date of
Operation:
Pre Anaesthetic Evaluation:
Cardiovascular system: PR: BP: Heart:
Respiratory system: RR: Lungs: Airway:
MP: MO: cm
Central nervous system:
Investigations:
BLOOD: Hb: TC: DC: CT: BT:
Bl.Urea: Sr.Creatinine: FBS/RBS:
HIV: HbSAg:
URINE: Albumin: Sugar: Microscopy:
OTHERS : ECG: CXR:
97
INTRA OP VITAL SIGNS:
Drug used:
Dosage:
Time of injection:
Level of injection:
Observations
mins
0 1 2 3 4 5 1
0
1
5
2
0
2
5
3
0
3
5
4
0
4
5
5
0
5
5
6
0
END of
surg
Heart rate
B.P.
Systolic
diastolic
Respiratory rate
SpO2
MONITORING SENSORY BLOCK
Onset of Analgesia:
Height of Analgesia pre op: Height post op :
Duration of Analgesia : Quality of Analgesia: E / G / F / P
SEDATION GIVEN:
SIDE EFFECTS DURING SURGERY:
1. Bradycardia
2. Hypotension: Fall in systolic: diastolic:
3. Respiratory Depression 4. Shivering 5. Nausea & vomiting 6.
Sweating
7. Inadvertent dural puncture
98
ANNEXURE – II
CONSENT FORM FOR ANAESTHESIA/OPERATION
I ……………….. Hosp. No……………..in my full senses hereby give my complete
consent for ………………..or any other procedure deemed fit which is a / and
diagnostic procedure / biopsy / transfusion / operation to a be performed on me / my
son / my daughter / my ward ………………age ………under any anaesthesia deemed
fit. The nature and risk involved in the procedures have been explained to me to my
satisfaction. For academic and scientific purpose the operation / procedure may be
televised or photographed.
Date:
Signature / Thumb Impression of
the Patient / Guardian
Name:
Place:
Guardian
Relationship
Full Address
103
KEY TO MASTER CHART
A Serial number
A1I.P. No.
A3Name
A4Sex
A5Weight in kilograms
A6Height in centimetres
A7ASA grade
A8Type of hernia : Direct- D : Indirect- IN
A9Volume of bupivacaine in millilitres
A10Injection level
A11Onset of analgesia in minutes
A12Preoperative sensory level
A13Postoperative sensory level
A14Duration of analgesia in minutes
A15Quality of block (Analgesia)
E-Excellent; G-Good; F-Fair; P-Poor
HEART RATE
A16Preoperatively
A17At 0 minute (immediately after block)
A18At 1 minute
104
A19At 2 minutes
A20At 3 minutes
A21At 4 minutes
A22At 5 minutes
A23At 10 minutes
A24At 15 minutes
A25At 20 minutes
A26At 25 minutes
A27At 30 minutes
A28At 35 minutes
A29At 40 minutes
A30At 45 minutes
A31At 50 minutes
A32At 55 minutes
A33At 60 minutes
A34At the End
BLOOD PRESSURE
A35Preoperatively
A36At 0 minutes
A37At 1 minutes
A38At 2 minutes
A39At 3 minutes
105
A40At 4 minutes
A41At 5 minutes
A42At 10 minutes
A43At 15 minutes
A44At 20 minutes
A45At 25 minutes
A46At 30 minutes
A47At 35 minutes
A48At 40 minutes
A49At 45 minutes
A50At 50 minutes
A51At 55 minutes
A52At 60 minutes
A53At the End
A54Fall in Systolic Blood Pressure
A55Percentage of fall in Blood Pressure
A56Side effects
A57Remarks
A A1 A2 A3 A4 A5 A6 A7 A8 A9 A10 A11 A12 A13 A14 A15 A16 A17 A18 A19 A20 A21 A22 A23 A24 A25 A26 A27 A28 A29 A30 A31 A32 A33 A34
SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST
1 63449 Munishammappa 65 M 60 167 1 IN 5 L1-L2 8 T8 T8 190 E 64 56 56 58 56 54 52 58 58 60 62 66 64 68 60 60 64 62 58 126 82 130 80 126 80 122 80 122 82 124 80
2 64077 Shanthamma 63 F 41 156 2 D 5 L1-L2 8 T12 T11 200 E 84 82 84 88 86 84 86 82 88 96 76 98 96 80 88 86 80 76 74 130 80 126 80 124 80 122 78 126 78 128 78
3 64737 Lakshmana 18 M 46 152 1 IN 8 L1-L2 6 T11 T10 240 G 78 86 82 82 84 86 80 80 78 72 76 68 80 78 76 82 80 74 74 124 80 128 84 130 80 124 80 128 74 126 82
4 64455 Fayaz Khan 48 M 64 168 1 D 5 L1-L2 7 T11 T9 180 E 70 80 78 76 78 80 82 88 88 90 86 88 86 86 84 84 88 86 84 110 72 120 80 122 82 116 80 118 80 116 80
5 64557 Salmath Khan 52 M 65 164 1 D 5 L1-L2 7 T10 T8 210 E 88 90 88 88 90 90 88 92 90 88 86 88 84 82 80 78 80 86 82 128 72 132 78 132 78 134 76 130 78 124 70
6 64522 Venkatesh 38 M 40 158 1 IN 8 L1-L2 0 0 0 P 70 84 86 86 88 90 86 88 88 90 98 96 106 110 98 78 72 76 78 110 70 138 80 136 78 138 78 142 78 148 78
7 64800 Govindappa 52 M 58 156 1 D 5 L1-L2 7.3 T10 T9 150 E 82 88 90 90 92 90 86 88 88 88 86 86 84 82 80 88 82 86 86 128 80 138 90 136 88 124 82 128 80 126 84
8 64300 Shivappa 37 M 57 160 1 IN 7 L1-L2 8.3 T10 T9 170 G 86 82 82 82 82 86 84 86 86 88 88 84 82 84 78 82 80 80 80 124 84 130 86 128 84 128 86 126 82 134 88
9 66429 Venkataravanappa 41 M 73 169 1 IN 6 L1-L2 7 T11 T10 180 G 84 110 112 116 112 112 110 108 110 98 104 98 102 100 98 94 98 92 96 136 90 122 74 120 72 118 72 120 70 116 70
10 65837 Manjunath 26 M 49 158 1 IN 8 L1-L2 9 T12 T10 200 F 86 88 86 86 84 82 80 82 80 82 86 88 88 78 80 82 84 84 82 110 70 124 78 128 76 120 76 126 78 128 80
11 65444 A.Nagaraj 25 M 60 168 1 IN 5 L1-L2 7 T11 T10 180 E 86 86 82 82 84 86 80 80 86 72 76 62 70 62 64 66 60 62 70 126 80 128 84 128 82 128 82 126 80 122 80
12 66411 Venkataswamy 25 M 58 166 1 IN 7 L1-L2 9 T11 T10 210 F 92 98 96 96 92 94 94 92 94 92 92 88 90 94 86 92 88 92 96 128 90 138 88 140 94 136 96 128 90 130 92
13 66620 Nagarj 38 M 75 166 1 D 5 L1-L2 12 T9 T7-8 180 E 88 86 88 84 84 82 82 86 88 88 86 88 88 82 86 88 86 86 88 120 86 122 90 124 88 126 86 124 88 124 84
14 66885 Chikkanna 48 M 58 154 1 IN 5 L1-L2 8 T12 T10 180 E 86 90 92 90 88 86 88 86 84 84 86 78 76 84 78 76 78 78 76 120 82 122 80 120 80 122 80 124 86 120 80
15 66890 Anjanappa 49 M 62 160 1 IN 5 L1-L2 7 T10 T8 140 E 86 88 88 90 86 92 88 94 90 92 88 92 90 88 86 86 88 84 82 128 90 132 94 128 92 130 94 126 92 128 90
16 67763 Nagappa 55 M 49 158 1 IN 5 L1-L2 9 T11 T10 150 E 84 78 78 80 78 76 76 78 74 82 78 80 82 78 80 80 78 74 72 100 70 118 76 116 76 116 74 114 72 116 72
17 68226 Rudrappa 51 M 57 156 1 IN 6 L1-L2 8 T10 T8 210 G 86 90 88 92 94 92 90 90 90 82 88 86 82 88 88 88 86 86 88 150 86 148 92 148 90 148 90 148 90 140 90
18 68261 Prabhakar 46 M 46 164 2 D 5 L1-L2 9 T11 T10 190 E 86 82 82 82 84 84 84 86 86 82 84 84 80 84 92 82 90 80 78 124 82 132 80 134 80 132 78 130 80 128 80
19 69641 Bhavani 27 F 46 150 1 IN 7 L1-L2 7 T11 T10 200 F 88 90 88 92 94 90 86 82 86 88 86 80 84 90 88 86 84 84 92 136 82 136 84 138 86 136 84 136 84 134 84
20 69951 Sudharani 22 F 37 158 1 D 5 L1-L2 6.3 T10 T8 130 E 74 88 86 88 90 92 90 94 90 86 88 86 82 88 80 86 84 86 92 128 72 134 78 134 78 132 78 130 72 132 72
21 68640 Kiran 29 M 68 172 1 IN 6 L1-L2 8 T10 T9 180 G 86 86 88 88 88 88 90 86 88 84 82 88 86 88 86 90 84 94 92 130 82 136 84 136 84 130 82 128 78 128 78
22 69680 Venkateshmurthy 32 M 64 164 1 IN 5 L1-L2 7 T10 T8 130 E 96 106 100 100 98 96 92 106 98 100 98 98 98 94 96 98 94 98 96 126 84 130 90 128 92 130 90 138 94 138 90
23 71056 Machaiah 46 M 53 168 2 D 5 L1-L2 7.3 T10 T8 120 E 90 92 90 90 94 90 86 88 84 94 88 90 92 88 86 84 84 86 90 138 80 140 86 138 86 138 86 140 88 136 86
24 71203 Kodappa 65 M 56 164 2 IN 8 L1-L2 0 0 0 P 86 86 84 84 82 84 84 90 98 106 108 100 102 98 90 88 88 86 88 150 86 146 86 138 84 140 88 142 88 146 90
25 71416 Kodandaram 40 M 64 174 1 IN 5 L1-L2 7 T10 T9 140 E 88 82 78 76 76 76 78 74 74 74 72 76 78 76 78 76 76 78 82 126 82 130 72 128 64 122 60 118 60 122 64
26 71641 Narayanappa 40 M 63 178 1 D 6 L1-L2 8 T10 T9 200 F 98 100 100 94 98 98 100 92 90 92 90 92 92 92 94 94 88 96 96 120 78 128 80 126 80 120 74 118 72 120 78
27 67183 Lakshmanna 50 M 55 156 1 D 5 L1-L2 7.3 T10 T8 170 E 76 90 92 92 100 88 92 90 94 86 88 88 86 80 84 88 90 86 88 132 84 138 88 138 90 130 82 130 80 128 80
28 71553 Subramani 36 M 50 164 1 D 5 L1-L2 8 T9 T8 160 E 70 80 78 82 84 82 80 86 86 90 88 88 86 82 80 82 80 88 84 110 72 120 80 122 80 116 80 118 80 116 80
29 71890 Sudhakar 35 M 50 160 1 IN 6 L1-L2 8.3 T9 T8 200 G 82 88 86 88 82 84 82 84 84 80 82 80 78 82 80 86 80 88 84 136 80 140 80 138 80 136 82 138 82 136 84
30 72352 Rajanna 43 M 63 172 1 IN 5 L1-L2 7 T10 T8 170 E 78 88 88 82 84 82 80 80 84 86 84 84 82 86 88 84 86 86 88 132 80 138 80 138 78 138 82 136 80 136 82
31 72363 Nagesh 38 M 49 164 1 IN 5 L1-L2 7.3 T10 T9 180 E 78 86 88 86 84 86 84 86 88 82 80 82 82 86 84 84 88 80 84 130 80 134 82 132 82 130 80 130 80 130 80
32 72444 Murthy 45 M 58 171 2 IN 5 L1-L2 7.3 T11 T9 180 E 78 86 90 84 82 80 80 84 84 90 86 88 88 88 90 82 86 82 86 128 74 130 76 132 74 124 74 132 78 130 76
33 72593 ChanneGowda 47 M 68 178 1 IN 7 L1-L2 8 T10 T9 210 F 70 88 86 84 82 84 82 86 88 86 86 84 82 84 80 82 80 78 80 118 76 126 84 124 82 128 80 130 74 128 72
34 73002 Nandan 32 M 54 172 1 D 5 L1-L2 8.3 T10 T8 140 E 86 88 90 86 82 80 78 76 70 70 72 82 80 82 88 82 80 80 86 126 80 132 80 132 78 130 78 130 78 130 78
35 73130 Abhishek 29 M 51 161 1 IN 5 L1-L2 7.3 T10 T9 150 E 90 100 98 100 102 100 98 98 100 82 90 86 92 86 90 90 96 90 88 126 80 124 70 122 74 124 72 128 74 126 76
36 73174 Yuvraj 36 M 53 174 1 IN 6 L1-L2 7.3 T10 T8 180 G 86 88 86 88 88 86 80 80 76 84 78 82 80 82 86 88 86 88 86 128 80 132 90 130 90 130 90 132 88 132 86
37 73343 Nagendra 39 M 39 168 1 IN 5 L1-L2 6.3 T9 T8 130 E 86 90 88 86 84 82 82 82 80 84 80 88 88 84 82 88 86 88 88 136 78 132 80 132 84 132 80 130 80 130 78
38 73555 Ramaiah 55 M 50 160 2 D 5 L1-L2 6 T10 T9 120 E 96 110 116 112 114 112 110 126 124 136 120 130 128 116 118 108 112 104 100 150 90 150 90 148 90 146 90 148 88 138 98
39 73861 Mallikarjun 46 M 50 164 1 IN 7 L1-L2 9 T10 T8 180 G 86 90 88 90 92 86 84 86 84 86 82 88 84 84 86 88 88 86 84 136 82 140 82 140 84 138 82 136 80 132 78
40 74178 Muniraj 53 M 64 170 1 D 8 L1-L2 7.3 T11 T10 170 G 86 90 90 88 90 88 88 86 88 84 86 84 86 84 82 90 90 88 86 128 76 130 78 132 78 128 76 128 78 132 80
42 73901 Narayanappa 70 M 68 158 1 D 5 L1-L2 6.3 T10 T9 140 E 68 88 80 80 86 82 86 84 82 80 76 76 78 82 80 80 78 82 80 144 88 140 88 140 86 138 86 132 80 136 82
43 75395 Ravikumar 42 M 65 172 1 IN 6 L1-L2 7 T11 T10 150 G 92 90 92 92 96 90 90 84 86 88 86 82 88 88 86 84 82 84 86 134 80 136 88 138 88 132 86 136 84 138 88
44 75750 Rajesh 43 M 72 176 1 IN 5 L1-L2 7.3 T10 T10 130 E 78 80 78 84 82 80 82 84 80 76 78 82 80 80 76 80 78 78 84 136 80 136 80 136 78 132 76 134 78 130 76
45 75967 Varun 38 M 49 158 1 IN 6 L1-L2 9 T10 T9 135 G 86 90 88 82 86 84 80 82 78 82 80 88 82 88 78 86 78 86 88 128 80 130 80 132 80 134 80 132 78 130 76
46 75958 Shammi 37 M 49 168 1 IN 7 L1-L2 7.3 T9 T9 140 G 94 94 92 94 96 96 98 92 94 92 90 92 88 92 92 90 90 90 88 136 84 136 84 138 84 140 88 134 80 136 82
47 75383 Ravindraraj 55 M 64 178 2 IN 6 L1-L2 8 T10 T9 150 G 74 72 74 78 68 72 76 76 78 68 74 60 64 70 70 72 78 76 70 128 80 136 86 132 82 134 84 130 80 128 80
48 76846 Ravichari 40 M 58 164 1 IN 5 L1-L2 7.3 T10 T9 160 E 94 90 96 94 96 94 92 92 90 92 88 92 90 88 96 90 90 86 84 128 70 136 78 134 76 136 78 138 82 136 84
49 76831 Girish 30 M 62 168 1 IN 7 L1-L2 7.3 T10 T9 150 G 86 88 86 88 82 84 82 80 78 78 76 82 80 84 88 86 88 84 90 128 80 132 80 132 82 132 82 136 82 130 80
50 77114 Gangaraj 32 M 60 172 1 IN 6 L1-L2 8 T10 T8 140 G 92 92 90 90 88 84 80 92 90 92 88 86 86 82 80 84 84 88 86 134 86 130 78 128 80 120 86 142 100 140 94
A35 A36 A37 A38 A39 A40
99
A54 A55 A56 A57
SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST SYST DIAST
122 80 120 80 120 78 120 76 118 76 122 76 118 72 118 68 118 70 112 72 110 68 110 68 116 74 20 15.38 NIL
126 76 120 78 124 80 128 80 128 80 126 80 128 82 128 80 130 82 130 84 130 84 130 86 130 84 6 4.76 NIL
124 86 128 80 132 88 136 82 130 80 132 78 128 84 126 82 136 80 130 78 128 78 134 76 132 82 4 3.13 NIL
112 78 110 82 110 76 118 74 112 72 114 72 114 74 120 82 122 78 118 78 118 76 116 74 118 76 10 8.33 NIL
126 72 124 74 122 78 124 76 126 72 128 72 126 76 124 70 120 70 122 72 126 74 124 74 126 74 12 9.09 NIL
129 80 126 78 145 88 146 90 136 80 130 78 128 78 128 80 126 88 130 88 132 80 132 82 128 82 SW INADEQUATE BLOCK-CONVERTED TO GA
130 86 132 88 138 94 136 92 136 90 136 88 136 88 134 88 136 90 138 92 130 84 132 88 136 88 14 10.14 SH
130 88 128 86 132 88 124 82 120 80 124 82 120 80 120 80 122 80 118 80 120 80 120 82 122 86 12 9.23 NIL
118 70 116 68 118 68 118 70 118 72 122 72 120 76 124 78 128 82 132 78 130 86 130 84 132 88 6 4.92 NIL
130 80 130 80 128 80 126 76 130 78 132 76 136 76 140 74 132 78 128 80 128 76 128 80 136 76 4 3.23 SW
124 82 122 77 124 74 118 72 118 70 120 68 120 68 124 66 118 68 118 70 124 68 124 70 124 74 10 7.81 NIL
138 92 136 84 136 88 134 86 136 86 130 86 130 84 128 84 130 86 130 86 130 84 132 88 132 86 10 7.25 SW
122 88 116 86 112 90 112 82 116 86 118 84 116 84 118 82 118 84 120 86 122 82 120 80 120 86 12 9.84 NIL
118 76 116 76 116 76 118 78 114 76 114 76 114 70 110 70 112 72 112 72 112 76 112 74 110 78 10 8.2 NIL
126 88 128 86 128 88 122 86 124 88 126 86 124 88 126 86 130 90 130 92 128 90 132 88 128 90 10 7.58 NIL
118 78 116 78 110 78 110 70 112 70 112 74 112 72 114 72 120 78 118 76 118 76 114 78 112 76 8 6.78 NIL
138 86 140 92 142 90 144 92 142 94 136 82 142 88 146 86 144 84 136 82 138 82 140 88 142 90 14 9.46 NIL
130 80 126 76 126 82 128 74 126 70 120 68 128 72 128 76 130 70 128 76 128 76 126 70 120 68 4 3.03 NIL
136 82 132 78 126 80 126 80 132 82 130 82 132 82 130 84 132 82 130 80 128 80 136 82 138 84 10 7.35 SW
132 72 138 74 140 78 130 80 132 78 132 78 128 70 126 70 126 72 128 74 128 72 130 74 130 78 8 5.97 NIL
130 78 130 84 132 84 126 82 128 80 136 82 130 82 132 82 134 84 130 80 126 78 128 82 126 80 10 7.35 NIL
140 96 136 92 138 88 134 90 138 94 136 92 136 88 134 88 136 90 138 92 130 86 132 88 136 88 2 1.54 NIL
136 86 146 82 138 82 138 82 154 82 150 78 148 78 150 82 134 82 136 84 136 84 136 86 136 90 12 8.57 NIL
134 84 130 88 138 82 128 80 130 86 136 88 142 90 128 84 132 86 136 84 132 82 138 90 142 86 18 12.32 SW INADEQUATE BLOCK-CONVERTED TO GA
120 62 120 64 126 64 130 66 136 66 142 74 142 74 142 76 144 76 150 76 146 74 146 76 148 72 12 9.23 NIL
122 76 124 76 124 76 124 74 124 74 122 70 122 70 116 68 116 68 116 70 116 70 128 76 126 76 12 9.38 SW
130 80 132 82 130 84 130 80 122 78 124 80 132 80 128 82 126 80 128 82 130 80 128 80 126 82 16 11.59 NIL
112 78 110 82 110 76 118 74 112 72 114 72 114 74 120 82 120 82 118 78 122 78 116 74 118 76 10 8.33 NIL
134 88 132 78 134 74 126 72 132 72 128 70 134 72 132 74 130 72 134 74 132 76 136 74 138 76 14 10 NIL
130 84 128 82 128 80 124 72 128 80 128 80 130 82 132 82 128 80 126 80 126 78 126 74 128 78 12 8.7 NIL
128 80 120 78 120 72 122 72 120 70 124 72 128 74 126 76 130 76 132 78 128 80 126 78 134 86 14 10.37 NIL
126 74 128 76 124 72 126 76 126 76 126 76 124 72 124 72 128 76 128 76 128 74 128 74 126 72 6 4.62 NIL
128 70 128 80 128 82 126 84 128 82 126 80 128 82 126 84 124 82 122 80 120 78 124 80 122 82 6 4.76 SH
124 76 118 68 120 80 128 82 132 86 126 74 124 80 126 90 124 86 122 84 124 86 128 82 132 74 14 10.61 NIL
130 74 132 72 128 74 124 76 126 72 124 74 126 72 122 70 124 72 126 78 128 78 126 76 132 74 2 1.61 NIL
132 88 130 82 128 80 124 80 122 78 124 76 120 84 118 82 122 80 120 78 120 80 122 78 128 84 12 9.09 NIL
128 76 126 76 128 78 122 72 124 72 128 72 124 74 122 74 122 70 128 72 122 72 124 74 128 74 10 7.58 NIL
142 88 140 86 140 88 128 86 132 88 132 94 138 94 138 92 138 92 138 90 130 90 138 92 146 92 20 13.33 NIL
132 76 134 80 136 84 132 76 136 78 136 74 136 74 138 76 138 76 132 78 134 80 136 82 134 78 8 5.71 NIL
130 80 132 82 132 80 130 80 124 78 122 76 126 74 124 72 128 78 134 84 128 80 132 86 130 84 8 6.15 NIL
128 84 120 80 118 76 124 80 138 86 138 88 138 86 136 84 136 84 138 88 140 88 136 86 138 88 22 15.71 SH
136 88 132 82 132 82 130 80 130 80 132 82 132 82 126 74 126 74 134 82 134 82 130 80 136 80 10 7.35 NIL
134 78 132 76 132 76 132 72 132 72 130 72 130 70 134 74 134 74 138 76 138 76 140 80 136 78 6 4.41 NIL
130 76 130 74 130 76 134 80 132 82 134 80 132 76 134 78 132 76 136 78 130 72 132 74 136 78 0 0 NIL
132 82 134 84 132 82 134 80 134 82 134 86 132 82 136 86 132 80 132 80 130 82 134 84 132 80 6 4.41 NIL
120 72 124 76 120 72 122 74 124 72 122 72 124 74 120 70 122 74 128 76 136 86 128 82 134 88 16 11.76 NIL
134 80 132 70 132 70 134 72 124 74 126 72 124 74 122 72 122 70 126 68 126 70 128 72 130 70 6 4.41 NIL
128 82 120 84 122 82 126 82 128 84 132 86 128 82 130 84 132 82 130 80 128 88 120 78 132 78 12 9.09 NIL
128 92 158 106 148 106 156 110 158 106 148 116 156 110 128 80 148 116 132 88 128 80 140 98 142 96 10 7.69 NIL
A44 A45 A46A41 A42 A43 A53A47 A48 A49 A50 A51 A52
99