“COMPARISON OF POSTOPERATIVE ANALGESIA USING INTRATHECAL FENTANYL WITH 0.75% ISOBARIC ROPIVACAINE
AND INTRATHECAL FENTANYL WITH 0.5% HYPERBARIC BUPIVACAINE FOR UROLOGICAL PROCEDURES”
Dissertation submitted to
THE TAMIL NADU Dr. M.G.R. MEDICAL UNIVERSITY in partial fulfillment for the award of the degree of
DOCTOR IN MEDICINE IN
ANAESTHESIOLOGY BRANCH-X
INSTITUTE OF ANAESTHESIOLOGY AND CRITICAL CARE MADRAS MEDICAL COLLEGE, CHENNAI-600 003.
MAY- 2020
CERTIFICATE
This is to certify that the dissertation entitled, “COMPARISON OF POSTOPERATIVE ANALGESIA USING INTRATHECAL FENTANYLWITH 0.75% ISOBARIC ROPIVACAINE AND INTRATHECAL FENTANYL WITH 0.5% HYPERBARIC BUPIVACAINE FOR UROLOGICAL SURGERIES”
submitted by Dr.G.KOPPERUNDEVI ,in partial fulfilment for the award of the degree of Doctor of Medicine in Anaesthesiology by The Tamil Nadu Dr.M.G.R.Medical University,Chennai.,is a bonafide record of the work done by her in the INSTITUTE OF ANAESTHESIOLOGY AND CRITICAL CARE, Madras Medical College and government hospital, during the academic year 2017-2020.
Prof.DR.ANURADHA SWAMINADHAN MD.DA, Prof. Dr. R.JAYANTHI, M. D.
F.R.C.P (Glasg)., Professor and Director, The Dean,
Institute of Anaesthesiology and Critical Care, Madras Medical College,
Madras Medical College, Rajiv Gandhi Got General Hospital, Rajiv Gandhi Govt General Hospital Chennai-600 003.
CHENNAI -600 003.
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled, “COMPARISON OF POSTOPERATIVE ANALGESIA USING INTRATHECAL FENTANYLWITH 0.75% ISOBARIC ROPIVACAINE AND INTRATHECAL FENTANYL WITH 0.5% HYPERBARIC BUPIVACAINE FOR UROLOGICAL SURGERIES”
submitted by Dr.G.KOPPERUNDEVI, in partial fulfilment for the award of the degree of Doctor of Medicine in Anaesthesiology by the Tamil Nadu Dr.M.G.R.Medical University,Chennai.,is a bonafide record of the work done by her in the INSTITUTE OF ANAESTHESIOLOGY AND CRITICAL CARE, Madras Medical College and government hospital, during the academic year 2017-2020.
PROF.DR.N.LATHA.M.D.D.A,
PROFESSOR OF ANAESTHESIOLOGY,
INSTITUTE OF ANAESTHESIOLOGY AND CRITICAL CARE, MADRAS MEDICAL COLLEGE
CHENNAI-600 003.
Date:
Place:
DECLARATION
I hereby, solemnly declare that this dissertation entitled, “COMPARISON OF POSTOPERATIVE ANALGESIA USING INTRATHECAL FENTANYL WITH 0.75% ISOBARIC ROPIVACAINE AND INTRATHECAL FENTANYL WITH 0.5
% HYPERBARIC BUPIVACAINE FOR UROLOGICAL SURGERIES” is a bonafide record of the work done by me in the Institute of Anaesthesiology and Critical Care ,Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, during the academic year 2017-2020 under the guidance of Dr.N.LATHA M.D.D.A, Professor of Anaesthesiology, Institute of Anaesthesiology and Critical Care, Madras Medical College,Chennai-03,and submitted to The Tamil Nadu Dr.M.G.R.Medical University,Guindy,Chennai-32,in partial fulfilment for the requirements for the award of the degree of M.D.Anaesthesiology(Branch X),examinations to be held on May 2020.
I have not submitted this dissertation previously to any university for the award of degree or diploma
DR.G.KOPPERUNDEVI.
Date:
Place:
ACKNOWLEDGEMENT
I am extremely thankful to DR.R.JAYANTHI M.D.,F.R.C.P(Glasg)., Dean, Madras Medical College& Rajiv Gandhi Govt.General Hospital, for her permission to carry out this study.
I am extremely grateful to Prof.DR.ANURADHA SWAMINADHAN, M.D.D.A, Director, Institute of Anaesthesiology and critical care,for her concern and support in conducting this study
I am extremely grateful and indebted to my guide Prof.DR.N.LATHA M.D.D.A, Professor of Anaesthesiology, Institute of Anaesthesiology and Critical Care,for her concern,inspiration,meticulous guidance,expert advice and constant encouragement in preparing this dissertation.
I am extremely thankful to my Assistant professors especially DR.D.ASHOK KUMAR, DR.A.GANESH, DR.N.RAMYA, DR.KATHIRAVAN for their guidance and expert advice in carrying out this study.
I am thankful to the Institute Ethical committee for their guidance and approval for this study.
My sincere thanks to the statistician, who played an important role during my study.
I am thankful to all colleagues,family, friends for their moral support, help and advice in carrying out this dissertation.
Last but not least, I thank all the patients for willingly submitting themselves for this study. Above all I pay my gratitude to the Lord Almighty for blessing me to complete this work
CONTENTS
S. No CHAPTER PAGE. NO
1 INTRODUCTION 1
2 AIM OF THE STUDY 3
3 SPINAL ANAESTHESIA 4
4 PHYSIOLOGICAL EFFECTS OF SUBARACHNOD
BLOCK 15
5 PHARMACOLOGY OF LOCAL ANAESTHETICS 20
6 PHARMACOLOGY OF OPIOIDS 38
7 MATERIALS AND METHODS 43
8 REVIEW OF LITERATURE 50
9 OBSERVATION AND RESULTS 56
10 DISCUSSION 79
11 CONCLUSION 82
12 BIBLIOGRAPHY 83
13 ANNEXURES 87
1
INTRODUCTION
Subarachnoid block is the most commonly used regional anaesthesia technique in contemporary anaesthesia practice. Motor block from subarachnoid block beyond the duration of surgery is undesirable as it prevents early ambulation and urinary retention. Selection of rapid, short acting local anaesthetic agents minimize the adverse effects of anaesthesia on the recovery process.
Bupivacaine is being extensively used for subarachnoid block as it produces adequate sensory and motor blockade. However it has its own disadvantages such as prolonged motor blockade and cardiac toxicity.
But Ropivacaine has it's own advantages such as early motor recovery and hemodynamic stability.
Intrathecal opioids are synergistic action with local anaesthetics and intensify the sensory block without increasing the sympathetic blockade. One such opioid commonly used is Fentanyl which acts on mu receptors thereby intensifies sensory blockade.
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We designed this study to compare the postoperative analgesia using intrathecal 0.75% isobaric Ropivacaine with fentanyl and intrathecal 0.5%
hyperbaric Bupivacaine with fentanyl for urological procedures.
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AIM AND OBJECTIVES
“Comparison of postoperative analgesia using intrathecal 0.75% Isobaric Ropivacaine with Fentanyl and 0.5% Hyperbaric Bupivacaine with Fentanyl for urological procedures”
Primary Objective:
To assess analgesic efficacy ( duration of sensory blockade) of these drugs Secondary Objective:
To assess the severity of pain using numeric scoring system
To assess early motor recovery
To assess intraoperative and postoperative hemodynamics
To evaluate systemic toxicity
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SPINAL ANAESTHESIA
Spinal anaesthesia is the one among regional anaesthesia technique employed for all lower abdominal surgeries and lower limb surgeries.
Here, anaesthesia is achieved by blocking spinal nerve roots by administering local anaesthetic agents into subarachnoid space which causes temporary interruption of nerve transmission.
ANATOMY
The spine consists of 33 vertebra of which Cervical- 7; Thoracic - 12;
Lumbar- 5 ; 5 Sacral and 5 Coccyx. ThE vertebral canal contains spinal cord, cerebrospinal fluid, meninges, spinal nerves and epidural space.
Each vertebrae has a body anteriorly, two pedicles posteriorly projecting from the body and laminae which connects the two pedicles. The transverse process arise from the junction of pedicle and laminae and the spinous process projects posteriorly from the union of bilateral laminae.
The pedicles form the superior and inferior vertebral notches through which spinal nerves leaves the vertebral canal.
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The vertebrae are held in position by various ligaments. They are anterior and posterior longitudinal ligaments, supraspinous ligaments, interspinous ligaments, ligamentum flavum and intervertebral disc.
The vertebral canal extends from foramen magnum above to sacral hiatus below.
In first trimester, the spinal cord extends from foramen magnum as direct continuation of medulla oblongata to sacrum. The vertebral column grows more faster than spinal cord and therefore at birth, spinal cord usually terminates at the upper border of L3. In adults, the cord ends at the lower border of L1.
The spinal cord is surrounded by three membranes-the Piamater, the Arachnoid mater and the Duramater. The innermost piamater is highly vascular and closely adherent to the spinal cord. The middle arachnoid mater is a delicate nonvascular membrane and closely adherent to duramater. The outer duramater is a fibroelastic membrane which continues from cranial duramater proximally and extends distally upto S2 where it terminates as filum terminale.
Epidural space lies outside the dural sac and extends from foramen magnum to sacral hiatus. Between the piamater and arachnoid mater is the subarachnoid space. This space contains cerebrospinal fluid, spinal nerves, blood vessels supplying spinal cord and dentate ligaments.
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Cerebrospinal fluid:
It is a clear, colourless fluid present in the cerebral ventricle and the subarachnoid space. It is formed by ultrafiltration of the plasma through the choroid plexus of the lateral ventricles.
In adults, the total volume is about the 120-150 ml. Of this, 20-25ml present in the cerebral ventricles, 25-30 ml in the subarachnoid space of the spinal compartment and 30-90ml in cisterns reservoirs at the base of brain.
CSF is secreted at a rate of 0.3 to 0.4 ml/min or 25 ml/hr or 600 ml/ day.
Characteristics of Cerebrospinal fluid:
Volume : 120-150 ml
Pressure : 8-12 mmHg or 70-80 cmH20 Specific gravity : 1.003-1.009
pH : 7.4 - 7.6 Density : 1.003g/ ml Baricity : 1.000
Protein : 14-45 mg/ dl
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Glucose : 50-80 mg/dl Lymphocytes : 1-5 cells/ cu.mm Chloride : 115-130 mmol/L Sodium : 140-150 mEq/L Potassium : 2.6-3.0 mEq/L
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STEPS IN SPINAL ANAESTHESIA:
The steps in spinal anaesthesia includes preparation, position, projection and puncture.
Preparation:
- Strict aseptic precautions should be followed
- check Boyle‟s machine, oxygen cylinder, AMBU bag and kept ready with emergency drugs, resuscitation equipments and standard airway gadgets.
- Working suction apparatus should be kept ready.
- After shifting the patient to operation theatre, standard monitors like electrocardiogram, noninvasive blood pressure and pulse oximetry were connected and baseline value recorded.
- I. V line secured and preloaded with 20 ml/ kg crystalloid.
Position:
The three different positions in spinal anaesthesia are
Sitting position
Lateral decubitus
Prone position
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Sitting position:
Patient is asked to sit on the table with knees resting on the edge and feet supported on the stool. This position minimize the lumbar lordosis and maximize the spinous processes.
This is preferred when low sensory level of blockade is adequate for the surgical procedure planned or when obesity or spinal deformity makes difficult for the identification of the spine and when hip and joint problem exists.
Lateral decubitus position:
In this, the patient back should be parallel to edge of the table with hips and knee flexed, neck and shoulder flexed towards knees so as to open up the vertebral spaces.
This is the most commonly used position for spinal anaesthesia.
Prone position (jack-knife position)
Patient should be placed in prone position with OT table flexed under his/
her flanks just above the iliac crest. This is rarely used position for rectal and perineal surgeries.
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Projection and Puncture:
The spinal anaesthesia is performed either in the midline or paramedian approach usually at L2-L3, L3-L4 interspaces. After positioning, the patient back should be painted with povidone iodide solutions and sterile drape applied.
Tuffier's line is a line that is drawn between the highest point on the iliac crest which passes through either the L4 spinous process or L4-L5 interspace . In our study we use midline approach with patient in sitting position is used.
Place a skin wheal of local anaesthetic at the desired spinous interspace.
Cutting spinal needles should be inserted in the midline at a cephalad angle of 10- 15 degrees through the skin with the bevel parallel to the longitudinal fibres of the dura. This helps to reduce cutting fibres and enhances tactile sensation as anatomical structures are crossed.
Anatomical structures that will be traversed include
Skin
Subcutaneous tissue
Supraspinous ligament
Interspinous ligament
Ligamentum Flavum and
Duramater
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Once passing the dura, there is a slight click or pop off sensation felt. The stylet is removed at this point to check for CSF at the needle hub.
Using the non dominant hand, the hub of the needle is firmly held between the thumb and the index finger and the dorsum of the same hand steadies the patient‟s back. The syringe containing anaesthetic drug is firmly attached to the needle, CSF is aspirated freely and drug is injected at a rate of 0.2ml/sec.
The patient is then positioned supine and vitals monitored. Sensory block is assessed by loss of sensation to pinprick and the motor blockade by modified Bromage score.
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Onset of blockade is related to pKa of the local anaesthetics. ( lower pKa – faster acting). Sensitivity of nerve fibres to local anaesthetics varies with axonal diameter and myelination. Smaller and myelinated fibres are blocked more easily.
Larger and unmyelinated fibres are less sensitive. This results in differential blockade.
In general, Sympathetic blockade after spinal anaesthesia is 2 to 6 dermatome segments higher than sensory and sensory blockade is generally two segments higher than motor.
Adjuvants used are Opioids:
Addition of opioids improves analgesic quality, prolongs sensory block, reduces local anaesthetic requirements, reduces duration of motor blockade and improves hemodynamic stability
Fentanyl – 12.5 mcg Sufentanyl - 2.5- 5 mcg Morphine - 0.1 to 0.2 mg
Epinephrine ( dose-0. 2 mg): decreases the blood flow
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Clonidine ( dose-15 to 45mcg): prolongs sensory aanalgesia
Neostigmine( dose-5 to 100 mcg): inhibits break down of acetylcholine.
Factors influencing block height:
Most important factor is baricity of anaesthetic solution. Baricity is ratio of density of local anaesthetic solution at specific temperature to the density of the CSF at the same temperature.
Solutions with specific gravity 1.007 are called isobaric. Solution with specific gravity less than 1.007 or baricity less than 1.000 are called hypobaric. A solution is hyperbaric when it‟s specific gravity is more than 1.007 or baricity is more than 1.000.
Hypo or hyperbaric solutions are prepared by adding various amounts of distilled water or dextrose to isobaric solutions. As hyperbaric solutions are heavier than CSF it tends to settle down to the most dependent part which is determined by the position of the patient. Isobaric solutions do not spread with position changes and the level of anaesthesia is independent of positioning and remain at the site of injection. But several studies have shown that isobaric solutions behave more likely a hyperbaric solution.
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Other factors include:
Patient factors- Age, Height, Weight, Gender, Pregnancy, Position.
Characteristics of anaesthetic solutions- Density, amount, concentration, temperature, volume, vasoconstrictors.
Characteristics of spinal fluid- volume, density, pressure Drug Elimination:
The rate of elimination of local anaesthetic depends upon the rate of diffusion of the drug which is proportional to the concentration gradient, distribution of local anaesthetics and lipid solubility of the drug.
Regression of neuraxial blockade occurs with decrease in CSF concentration of the drug which in turn occurs by neuronal uptake of the drug, primarily through vascular absorption. Before entering into the systemic circulation, the drug is being absorbed into the vessels in the piamater or the epidural vessels through back diffusion. No hydrolysis or degradation takes place in the subarachnoid space or in the CSF. Larger the spread of the drug, greater the exposure of drug for vascular absorption and has shorter duration of action. Lipid soluble drugs binds to epidural fat which slows down its vascular absorption.
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PHYSIOLOGICAL EFFECTS OF SPINAL ANAESTHESIA
Cardiovascular system:
Neuraxial blockade produces hypotension due to various reasons:
Sympathetic denervation
Loss of vasomotor tone
Arterial and venous dilation
Decreased peripheral vascular resistance and peripheral pooling of blood
Decreased venous return to heart.
In addition to that, there may be blockade of cardio accelerator fibres T1 to T4 thus produce bradycardia and hypotension.
Respiratory system:
There is a little effect on pulmonary functioning in patient's without pre- existing lung disease. Patient with chronic lung disease mainly rely on intercostal and abdominal muscles for respiration. Neuraxial blockade causes relaxation of these muscles and thus causes decrease in expiration and also decreased in the clearance of tracheo- bronchial secretions.
Affective dyspnoea is the one in which patient may complain of difficulty in breathing. It is due to blockade of sensory input which causes an inappropriate
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response to the given muscular effort. This is managed by asking the patients to take deep breaths, providing supplemental oxygen.
Infact, apnoea associated with high spinal is thought to be due to brainstem hypoperfusion.
Thoracic and abdominal surgical procedures are associated with decreased phrenic nerve activity resulting in decreased diaphragmatic function and functional residual capacity. This can lead to atelectasis and hypoxia due to ventilation- perfusion mismatching.
Gastrointestinal system:
Nausea is the most common complication experienced by the patient during spinal anaesthesia.
Renal system:
Neuraxial blockade has a little effect on the blood flow to the renal system. It effectively blocks the sympathetic and parasympathetic control of bladder at the lumbar and sacral levels. Urinary retention can occur due to the loss of autonomic bladder control. Normal function doesnot return until sensory function returns to S3.
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Autonomic nervous system:
Shivering is common during spinal anaesthesia due to decrease in core temperature which leads to hypothermia.
Complications:
During intraoperative period:
Hypotension
Respiratory impairment
Nausea and vomiting
Total spinal
During postoperative period:
Postdural puncture headache.
Infections
Treatment of hypotension:
All hypotensive patients should be given oxygen by mask until the blood pressure returns to normal.
Increase the rate of intravenous fluid infusion to a maximum until the blood pressure restores to normal.
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Ephedrine 2.5 to 6 mg titrated according to blood pressure. Its effect generally lasts for 10 minutes.
Phenylephrine.
Vasopressors like dopamine, noradrenaline, adrenaline.
Treatment of Total spinal :
Numbness and weakness of the arms and hands indicates that the block has reached the cervico- thoracic junction
Ask for help
Intubate and ventilate the patient with 100% oxygen.
Postdural puncture headache and management:
It begins within 24 to 72 hrs following spinal anaesthesia and may last for a week. It is due to continuous loss of CSF through the hole made in the dura by the spinal needle.
It is postural headache being more severe in standing or even raising the head and relieved by lying down. Nausea, vomiting, photophobia, dizziness often accompanies it.
The incidence of headache is directly related to the size of the spinal needle used. A 16 gauge spinal needle produce headache in about 75℅ individuals when
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compared with 20 or 25 gauge needle. If the needle bevel is parallel to fibers of the dura, it will separate rather than cut them and therefore leave a hole in the dura.
Treatment of posdtural puncture headache:
Reassurance to the patient.
Adequate hydration
Head down position is advisable.
Analgesics and antiemetics – aspirin, paracetamol, ondansetron.
Abdominal binders- raises the pressure in the peridural venous plexus thereby increases CSF pressure.
Oxygen administration.
Prolonged severe headache may be treated with epidural blood patch.
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LOCAL ANAESTHETICS
Local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of conduction process in peripheral nerves.
Local anaesthetics are drugs which causes reversible loss of sensory perception especially of pain in a localised area of the body.
CLASSIFICATION
BASED ON CHEMICAL STRUCTURE Esters of Benzoic Acid
Butacaine
Cocaine
Benzocaine
Tetracaine
Esters of Para-Aminobenzoic Acid
Chlorprocaine
Procaine
Propoxycaine
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- Amides
a) Atricaine e) Mepivacaine b) Bupivacaine f) Prilocaine c) Dibucaine g) Ropivacaine d) Etidocaine h) Centribucridine i) Lidocaine BASED ON DURATION
Ultra Short Acting (<30 mins)
Procaine ,Chlorprocaine Short Acting (45-75 mins)
Lidocaine, Prilocaine Medium Acting (90-150 mins)
Mepivacaine, Atricaine Long Acting (180 mins and more) Bupivacaine , Etidocaine
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MECHANISM OF ACTION
Local Anaesthetics prevent the transmission of nerve impulses by inhibiting the entry of sodium ions through ion selective sodium channels in nerve membranes. Local anaesthetics do not alter resting membrane potential or threshold potential.
Sodium channels exist in activated-open, inactivated-closed and rested-closed states during various phases of action potential.
By selectively binding to sodium channels in inactivated-closed states, local anaethetic molecules stabilise these channels in this configuration and prevent their change to rested-closed and activated-open states in response to nerve impulses.
Sodium channels in the inactivated-closed state are not permeable to sodium and thus conduction of nerve impulse in the form of propagated action potentials cannot occur.
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LOCAL ANAESTHETICS ORDER OF ACTION
Local Anaesthetic drugs are deposited near the nerve .
Penetration of nerve sheath by the remaining free drug molecules local anaesthetic molecules then permeate the nerve's axon membranes and accumulate within the axoplasm.
Binding of local anaesthetic to voltage gated Na+ Channels prevents opening of the channels by inhibiting the conformational changes that underlie channel activation (Tonic inhibition).
During onset and recovery from local anaesthesia, impulse blockade is incomplete and partially blocked fibers are further inhibited by repetitive stimulation which produces an additional, use dependant binding to Na+
channels(Phasic inhibition)
The recovery from blockade is by relatively slow diffusion of local anaesthetic molecules into and out of the whole nerve,not by their much faster binding and dissociation from ion channels.
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Sequence of blockade:
Sympathetic nervous system fibres ( B fibres: vasodilation, rise in skin temperature)
Temperature and pain conduction (A delta and C fibres)
Proprioception and touch( A gamma and A beta fibres)
Motor
FACTORS AFFECTING LOCAL ANASTHETIC ACTION Lipid solubility
All local anaesthetics are weak bases. Increasing their lipid solubility leads to faster nerve penetration and speeds the onset of action.
The more tightly local anaesthetics bind to the protein, the longer the duration of action.
The non ionised form of local anaesthetics cross the nerve membranes and produce faster conduction blockade.
Use of Vasoconstrictors
The duration of action of a local anaesthetic is proportional to the time the drug is in contact with nerve fibres
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Epinephrine(1:200000 or 5mcg/ml) may be added to local anaesthetic solutions to produce vasoconstriction, which limits systemic absorption and maintains the drug concentration in the vicinity of the fibres to be anaesthetised.
Benefits:
Additional analgesic effect( alpha 2 agonism)
Decreased possibility of systemic toxicity Side effects:
Systemic hypertension in susceptible individuals.
Increased chances of cardiac irritability in presence of inhalational agents.
3. Dosage
Increasing the concentration of drugs- rapid onset and longer duration of action
Increasing the volume of drugs speeds the spread of anaesthesia 4. Site of Injection
The differences in onset and duration of anaesthesia and analgesia are due to the particular anatomy of the area of injection, which will influence the rate of
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diffusion and vascular absorption and in turn, affect the amount of local anaesthetic used for various types of regional anaesthesia.
5. pH Adjustment:
The addition of sodium bicarbonate to a local anaesthetic solution accelerates the onset and decreases the minimum concentration needed or conduction blockade.
6. Pregnancy:
The effects of pregnancy on local anaesthetic potency may reflect a combined effect of mechanical factors associated with pregnancy (i,e.,dilated epidural veins) and direct effects of hormones such as progesterone on the susceptability of nerves to conduction blockade by local anaesthetics.
The dosage of local anaesthetics should be decreased in patients in all stages of pregnancy.
PHARMACOKINETICS OF LOCAL ANAESTHETICS 1.Absorption:
It depends upon the speed of administration and volume of drugs.
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RATES AT WHICH LOCAL ANAESTHETICS ARE ABSORBED AND REACH THEIR PEAK BLOOD LEVEL
Route Time to peak level(min)
Intravenous 1
Topical 5
Intramuscular 5-10
Subcutaneous 30-90
2. Distribution
Once absorbed in the blood stream local anaesthetics are distributed throughout the body to all tissues.
Highly perfused organs such as brain, liver, kidney, lungs have higher blood concentration of drugs than do less perfused organs (muscle, fat)
All local anaesthetic agents readily cross the blood-brain barrier and placenta.
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Metabolism and Excretion:
Esters(except cocaine) are broken down rapidly by plasma esterases to inactive compounds and excreted through kidneys. Cocaine is hydrolysed in the liver.
Amides are metabolised in liver by amidases.
Adverse Effects:
CNS: excitation followed by depression (drowsiness to unconsciousness and death due to respiratory depression)
CVS: Bradycardia, heart block, hypotension
Allergic reactions: rare but occur more often with ester group drugs.
Local Anaesthetic Systemic Toxicity (LAST):
LAST is due to an excess plasma concentration of the drug. The most common cause is accidental intravascular injection of local anaesthetics.
Effects of Local anaesthetic Toxicity:
CNS : Low plasma concentration of local anaesthetics produce initial numbness of tongue.
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As the plasma concentration of drug continues to increase , inhibitory pathways are blocked and produce seizures which is accompanied by hypotension and apnoea.
CVS : Local anaesthetics depress myocardial contractility by affecting calcium influx as well as by inhibiting cardiac sarcolemmal ca2+ and Na+
channels.
Management:
1. Stop injecting local anaesthetics.
2. Call for help. Consider lipid emulsion therapy at the first sign of serious LAST event
3. Airway management- Ventilate with 100% oxygen. Consider advanced airway if necessary.
PHARMACOLOGY OF BUPIVACAINE
Bupivacaine is a long acting amide local anaesthetics and has a butyl group in piperdine nitrogen atom. It belongs to pipecoleoxylidides.
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Preparation :
It is a clear, colourless solution in a racemic mixture with equal proportions of S and R enantiomers.
It is chemically related to lidocaine and a homologue of mepivacaine. All these three drugs contain an amide linkage between the aromatic nucleus and the amino or piperdine group.
Chemically it is 1-butyl-N-(2, 6 dimethylphenyl) piperdine-2- carboxamide It is available as hydrochloride salt.
Physiochemical properties:
Molecular weight : 288 pKa : 8.1 Plasma protein binding : 95%
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Mechanism of action:
Bupivacaine prevents the transmission of nerve impulses by inhibiting the entry of sodium ions through ion selective sodium channels thereby blocks the nerve conduction. It also prevents the permeability of the resting nerve membrane to potassium
Pharmacodynamics:
Bupivacaine has slow onset of action in peripheral nerve blockade, moderate in epidural, faster in neuraxial blockade. It provides longer duration of blockade and hence more potent than lignocaine. Sensory block is more pronounced than motor blockade.
Duration of action
Spinal – 1 to 6 hours Epidural – 2 to 5 hours Peripheral nerve blockade- 4 to 13 hours
It‟s over dosage can produce restlessness, tremors and seizures.
R enantiomers decrease the automaticity of heart whereas S enantiomers (Levobupivacaine) produces less cardiotoxicity.
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Pharmacokinetics:
Absorption is rapid and plasma concentration depends upon the route of administration. Peak systemic concentration occurs after 5 to 30 minutes of administration. Vasoconstrictors like epinephrine if added, delays the absorption and results in lower plasma concentration.
Half life (t ½) : 2.7 minutes Volume of distribution : 72 liters Clearance : 0.47 L/ min
Bupivacaine is degraded in the liver. It undergoes aromatic hydroxylation, N- dealkylation, amide hydrolysis and conjugation. After epidural and spinal anaesthesia, N- desmethyl bupivacaine has been measured in the blood and urine.
Only less than 10% of the drug is excreted unchanged in the urine.
Uses of Bupivacaine:
It's unique property of sensory and motor dissociation can provide sensory analgesia with minimal motor block. And hence, it has been popular drug for analgesia during labour. It is used for infiltration, spinal, epidural and nerve block.
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PHARMACOLOGY OF ROPIVACAINE:
Ropivacaine is a long acting amide and has a propyl group in piperidine nitrogen atom. It belongs to pipecoleoxylidides and first produced as a pure S enantiomer from the parent chiral molecule, propivacaine
It is a clear, colourless solution free from preservatives .It is available as hydrochloride salt. S enantiomer of ropivacaine produces less neurotoxicity and cardiotoxicity than R enantiomers.
Ropivacaine has a differential blocking effect on nerve fibers and, at the lowest concentration used, there is good differentiation between sensory and motor block. Ropivacaine provides early motor recovery in contrast to Bupivacaine
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Mechanism of action:
Ropivacaine causes reversible blockade of impulse propagation along the nerve fibers by preventing the inward movement of sodium ions through the cell membrane.
Ropivacaine is 2 to 3 times less lipid soluble. Therefore, at high concentration, it act as a good sensory and motor blockade whereas at low concentration, it produces analgesia with minimal motor blockade.
Pharmacodynamics :
It is highly bound to alpha 1 acid glycoprotein of about 95%. It is metabolized by CYP450 hepatic enzymes in the liver mainly by aromatic hydroxylation to 2,6 pipecoleoxylidides and 3- hydroxyropivacaine. It has shorter elimination half life. It is excreted through kidneys.
Duration of action
Spinal : 1 – 4 hours Epidural : 2- 5 hours Peripheral nerve block : 5 – 8 hours Indications:
It is used for spinal, epidural, infiltration and peripheral nerve block. It has no topical action.
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OPIOIDS
Opioid is defined as any naturally occurring, semi synthetic or synthetic compounds that binds specifically to opioid receptors and share the properties of naturally occurring endogenous opioids.
Opioid receptors:
In general opioids act on mu, kappa, delta receptors on CNS neurons producing
Analgesia via decreased neuronal transmitter release and decreased nociceptive impulse propagation.
By raising pain threshold, it decreases the brain‟s awareness of pain.
Receptor type Location Effects Agonists
Mu Mu 1- spinal
Mu 2 - supraspinal
Analgesia, respiratory
depression, sedation, euphoria, Miosis, physical dependence
Morphine, codeine, fentanyl
Kappa k1 – spinal k2- supraspinal
Analgesia,
dysphoria, sedation, psychomimetic, physical dependence
Pentazocaine
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Receptor type Location Effects Agonists
Delta delta1- Spinal
delta2- Supraspinal
Analgesia, affective behaviour, respiratory depression, reduced GI motility
Opioid classification:
Based on the origin:
Naturally occurring
Morphine
Codeine
Papaverine
Thebine Semisynthetic
Diamorphine
Dihydrocodeine
Buprenorphine Synthetic
Phenylpiperdines: Pethidine, Fentanyl, Alfentanil, Sufentanil
Diphenylpropylamines: Methadone, Dextropropoxyphene
Benzomorphans: Pentazocaine
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Based on the function
Pure agonists
Morphine
Fentanyl
Sufentanil
Remifentanil
Alfentanil Partial agonist
Buprenorphine Agonists-Antagonists
Pentazocaine
Nalbuphine
Nalorphine Pure Antagonists
Naloxone
Naltrexone
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PHARMACOLOGICAL ACTIONS OF OPIOIDS:
Central nervous system:
Analgesia
Most effective in relieving dull, continuous and poorly localised pain arising from deeper structures. Less effective against superficial and sharp pain. It is resistant to neuropathic pain
Sedation
Drowsiness, feeling of heaviness and difficulty in concentration are common Sleep may occur with the relief of pain but they are not true hypnotics
Euphoria and dysphoria
Hallucination: These are more common with Kappa agonists Tolerance and Dependence
Cardiovascular system:
Mild bradycardia – It is due to decreased sympathetic drive and a direct effect on SA node.
Peripheral vasodilation – It is due to histamine release and reduced sympathetic drive.
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Respiratory system
a) Respiratory depression:
It is mediated via mu receptors at the respiratory centers in the brainstem.
The sensitivity of the brainstem to carbondioxide is reduced whereas its response to hypoxia is less affected but if hypoxia stimulus is removed by supplemental oxygen then respiratory depression may be augmented.
Concurrent use of other CNS depressants may cause marked respiratory depression.
b) Cough suppression:
Codeine suppresses cough but has lesser analgesic activity.
Morphine and diamorphine are used in paroxysmal nocturnal dyspnoea as they produce sedation, reduce preloaded and depress abnormal respiratory drive.
Gastrointestinal system:
a) Stimulation of chemoreceptor trigger zone causes nausea and vomiting.
b) Smooth muscle tone is increased but motility is decreased resulting in delayed absorption, increased pressure in the biliary system (spasm of sphincter of oddi) and constipation.
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Endocrine system:
The secretion of ADH is increased whereas it inhibits the release of ACTH, prolactin and gonadotrophic hormone.
Ocular effects
Opioids act on mu and Kappa receptors in Edinger-Westphal nucleus resulting in constriction of pupil (Miosis).
Muscle rigidity
Large doses of opioids may occasionally produce generalised muscle rigidity especially of thoracic wall and impair ventilation.
Others
Some opioids cause histamine release from master cells resulting in urticaria, itching, bronchospasm, hypotension.
All opioids cross the placenta and if given during labour can lead to neonatal respiratory depression. But there are no known teratogenic effects.
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PHARMACOLOGY OF FENTANYL:
It is a synthetic phenylpiperdine derivative and is 100 times more potent than morphine.
Dose
Fentanyl is available as a colourless solution in either 2 ml or 10 ml ampoule containing 50 mcg per ml.
When given in small doses (1 to 2 mcg/ kg) , it has rapid onset and short duration of action of about 30 minutes. In small doses it has little sedative effect.
Higher doses are used to blunt the sympathetic response to laryngoscopy and intubation.
Fentanyl has been used as an adjuvant in spinal and epidural analgesia to augment the local anaesthetic effects at 10 to 25 mcg and 25 to 100 mcg doses respectively.
Fentanyl is also available as a transdermal patch used for chronic pain condition and as a lollipop to premedicate the children.
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Pharmacokinetics:
Fentanyl is 500 times more lipid soluble than Morphine and hence it is rapidly and extensively distributed in the body. At small doses (1 to 2 mcg/ kg) plasma and CNS concentration may decrease quickly to below an effective level during the rapid distribution phase.
However, following prolonged administration or with high doses, it‟s duration of action is significantly prolonged. In these situations, the distribution phase is complete while the plasma concentration is still high. Recovery from the effect of the drug depends on its slow elimination from the body.
Fentanyl is metabolized in the liver to norfentanyl, the inactive metabolite which is excreted in the urine.
Effects
It acts on mu receptors and produce sedation, euphoria and hallucination. It is a potent analgesic. It produces respiratory depression in a dose-dependent manner.
Large doses have been used to blunt the metabolic stress response for cardiac surgery. At high doses, sedation is profound and unconsciousness may occur. In addition, Fentanyl produce muscle rigidity of chest wall which impairs the ventilation.
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MATERIALS AND METHODS
This study was conducted in 40 patients of ASA physical status 1 and 2 undergoing urological procedures at Rajiv Gandhi Government General Hospital, Madras medical college, Chennai-600 003 after getting approval from Government General Hospital ethical committee and written informed consent from all the patients included in the study.
STUDY DESIGN:
This study was done in a prospective randomized controlled method.
Patients were randomly allocated into two groups.
Each group consists of 20 patients.
Group B
Patients in this group received spinal anaesthesia with 0.5% hyperbaric Bupivacaine 2 ml (10 mg)with Fentanyl 20mcg.
Group R
Patients in this group received spinal anaesthesia with 0.75% isobaric Ropivacaine 2 ml (15 mg) with 20mcg Fentanyl.
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CASE SELECTION Inclusion Criteria:
Age : 30 – 65 years
ASAPS : I and II.
Surgery : Elective
Who have given valid informed consent Exclusion Criteria:
Those not satisfying inclusion criteria
Patients posted for emergency surgery
Patients with difficult airway
Lack of written consent
Bleeding disorders
History of seizures and any neurological deficit
Allergy to Local anaesthetic drugs
Patient refusal
Patients with severe cardiovascular, respiratory, renal and hepatic diseases
Local infection at injection site Preanaesthetic evaluation:
Patients included into the study should gone through preoperative evaluation including thorough history, physical examination and investigations.
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History
History of comorbid illness, previous surgery and anaesthesia, any drug allergy in the past were recorded.
Physical examination
General examination
Vital signs
Height, weight
Airway assessment
Cardiovascular system, respiratory system, central nervous system and vertebral column.
Investigations
Complete hemogram
Blood sugar
Blood urea
Serum creatinine
Bleeding time, clotting time
Urine analysis
Chest X- ray
Electrocardiogram
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Patients who satisfied the inclusion criteria were explained about the nature of the study and the anaesthetic procedure and written informed valid consent was obtained from the patients.
All the patients who were included in the study were reviewed one day prior to study. Patients were kept nil by mouth for 6 hours prior to the procedure.
Premedication
Prior to surgery in the premedication room, vital signs of the patient were recorded. An 18 G intravenous cannula secured in the nondominant hand and preloaded with Ringer Lactate solution 15 ml/ kg body weight 15 minutes before subarachnoid block.
Technique
In the operation room all equipments including appropriate equipment for airway management and emergency drugs were kept ready. Then the patient was shifted into the operating room and made lie on the operating table after confirming the horizontal position of the table. Standard monitors like Electrocardiogram, noninvasive blood pressure and pulse oximeter were connected to the patient. Preoperative baseline blood pressure, pulse rate, respiratory rate and oxygen saturation were recorded. Then the subarachnoid block was performed by an anaesthesiologist who was unaware of the drug and made observations in all
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patients. The patients were asked to sit straight and under aseptic precautions, a midline lumbar puncture was done in the L3-L4 space using 25 G Quincke needle and after confirming CSF flow by aspiration, drug was injected into the subarachnoid space. Patient is then placed in supine position. The time at which intrathecal injection given was taken as zero time and the following parameters were recorded every 3mins for 15 mins; thereafter every 5 minutes upto 90 minutes.
Sensory Block:
In our study, sensory block was assessed by loss of sensation to pinprick. The sensory block was assessed immediately after intrathecal injection and thereafter every 3 minutes till loss of sensation at T10.The time taken for peak block height was assessed. The time for two segment regression and the level of sensory block at the end of surgery was also noted. The regression of sensory block to L1 and the complete regression of block to S2 were also noted.
Motor Block
Motor block was assessed using modified Bromage scale.
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Modified Bromage scale
0 - No block; able to raise an extended leg against gravity 1 – Unable to raise an extended leg but able to flex knees 2 – Unable to flex knee but able to flex ankle
3 – Total block; inability to flex ankle/move leg
Motor block was assessed immediately after intrathecal administration of the drug and at an interval of 3 minutes for 15 minutes and after that every 5 minutes upto 90 minutes. The time to attain Bromage score of 3 was noted. The Bromage score at the end of the surgery was also noted. Regression of motor block to 0 was noted and is taken as the duration of motor block.
Vital signs
The pulse rate, noninvasive blood pressure were recorded every 3 minutes upto 15 minutes and every 5 minutes for 90 minutes. The fall in systolic blood pressure > 30% from baseline was considered as hypotension. Bradycardia was taken as heart rate < 60 per minute. Oxygen saturation < 90% was considered as respiratory depression.
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Assessment in recovery ward
After completion of surgery patient were shifted to the recovery room where the vital signs were recorded for 6 hours. After complete resolution of motor blockade, patients shifted to postoperative ward.
Assessment of Pain
At the end of surgery the degree of pain was assessed using numeric scoring system. Pain assessment was done every hourly for 6 hours. Rescue analgesia with Inj.Diclofenac sodium 2 mg / kg i.m. was given when the patient complaints of pain or numeric scoring was 4 or more.
Patients were monitored in the postoperative period for the side effects like headache, paraesthesia in the lower limbs, low back pain, nausea, vomiting and shivering.
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REVIEW OF LITERATURE
1. Dr Bhupendra Tiwari , Dr Shriphal Meena Volume 6 Issue 4, April 2017 conducted a randomized controlled study and compared the hemodynamic changes with the use of 0.5% hyperbaric Bupivacaine 2ml and Isobaric Ropivacaine 2ml with Fentanyl 20 mcg in geriatric patients posted for lower limb surgeries. First group (Group R) n= 3 received isobaric Ropivacaine 0.75% 2 ml with Fentanyl 20 mcg and second group (Group B) n= 30 received 0.5%
hyperbaric Bupivacaine 2ml(10 mg) with Fentanyl 20 mcg. They noted that incidence of hypotension was more pronounced in Bupivacaine group than Ropivacaine group (p value<0.05). Duration of sensory and motor blockade was less in Ropivacaine group than Bupivacaine group ( p value <0.05). Low dose of Ropivacaine and Fentanyl provides better hemodynamic stability and shorter duration of motor blockade so it is a better choice of anaesthesia in surgeries requiring early ambulation in geriatric patients.
2. Sheetal Jagatap, Dawoodi S, Jain A 2014;58:442-6 et al conducted a randomised double blind study to compare the analgesic efficacy with the usage of intrathecal Ropivacaine-Fentanyl(RF) with Bupivacaine-Fentanyl for orthopedic surgeries. One group received intrathecal 15 mg of 0.5% Ropivacaine with 25 mcg fentanyl (Group RF) or 15 mg 0.5% Bupivacaine with 25 mcg Fentanyl (Group
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BF).They found that both groups achieved higher sensory level of T6. There is no need to use supplemental analgesia intraoperatively. They observed that Group RF provides shorter sensory and motor blockade. The patients in Group RF were hemodynamically more stable than Group BF.
3. Lee YY, Muchhal K et al 2005 Nov; 49(10):1477-82 did a prospective study to compare the Ropivacaine 2 ml with Fentanyl 15 MCG and plain Bupivacaine 2 ml with Fentanyl 15 mcg for spinal anaesthesia in urological surgery. 34 ASAPS I to III patients were randomly assigned to receive intrathecal injection of either plain Ropivacaine 10 mg with Fentanyl 15 mcg ( Ropivacaine group) or plain Bupivacaine 1 mg with Fentanyl 15 mcg (Bupivacaine group) using a combined spinal-epidural technique. The primary outcome, the duration of motor block was shorter in Ropivacaine group (median of 126mins) compared with Bupivacaine group ( median of 189 mins). Ropivacaine provides shorter duration of motor blockade. There was no significant difference in onset of sensory and motor blockade as well as hemodynamic changes between two groups.
4. Layek A, Maitra S, Gozi NK 2015 Oct-Dec;31(4):542-6 et al has done a randomised controlled study and compared the analgesic efficacy in two groups using intrathecal isobaric Ropivacaine -Fentanyl and Bupivacaine-Fentanyl in orthopedic surgeries. They have selected 74 patients of which 32 individuals had
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received 3 ml 0.5% isobaric Ropivacaine with 25 mcg Fentanyl (Group R) and another 32 persons had received 3 ml 0.5% isobaric Bupivacaine and 25 mcg Fentanyl( Group B). They observed that there was no statistically significant difference regarding hemodynamic profiles between two groups. The time to reach peak block height was similar between two groups. There was statistical difference noted between two groups in two dermatome regression and mean total duration of sensory and motor block. They concluded that Intrathecal Ropivacaine provides adequate sensory blockade with early motor recovery and so useful in ambulatory surgery.
5. Shilpasri AM, Keerthana DS. 2019.08.555736 et al did a prospective randomised study and compared the analgesic efficacy by using intrathecal Ropivacaine-Fentanyl with Bupivacaine-Fentanyl in lower limb surgeries.They observed that there is no significant difference between two groups in onset of sensory and motor block. They noted that both groups attained similar level of sensory block. Ropivacaine provides adequate sensory blockade with stable hemodynamics. Hence, they concluded that Ropivacaine was useful in ambulatory surgery.
6.S Suresh kumar, Vandana Talwar et al did a randomised controlled trial to compare the efficacy of intrathecal isobaric Ropivacaine with Bupivacaine
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for patients undergoing arthroscopic knee surgery. A total of 90 patients were randomised into two groups to receive 2 ml plain solution of either 0.5% isobaric Bupivacaine (Group B) or 0.75% isobaric Ropivacaine(Group R). They found that Isobaric Ropivacaine provides good analgesia with early motor recovery.
7. Ritual Ruparel, Vaishali Gautham, Pushkar Desai 2001;1(3):175-82 et al did a randomised controlled study to compare the efficacy of 22.5 mg of 0.75%
isobaric Ropivacaine with a control group using 15 mg of 0.5% hyperbaric Bupivacaine in lower abdominal and lower limb surgeries. One hundred patients were randomly assigned to two groups. One group received 0.75% isobaric Ropivacaine (n=50) 3 ml intrathecal and other group received 0.5% hyperbaric Bupivacaine 3 ml intrathecal. They observed that the onset of sensory block in Ropivacaine is significantly delayed than Bupivacaine group (p value < 0.05).
And also onset of motor blockade in ropivacaine group is significantly delayed than Bupivacaine group (p value < 0.01). Duration of motor blockade is significantly shorter in Ropivacaine group than Bupivacaine group (p value<0.01).
There is significant difference in the postoperative analgesia between the two groups, longer duration of postoperative analgesia is seen in Bupivacaine group as p value <0.001.They finally informed that Ropivacaine provides good analgesia with early motor recovery and also maintain hemodynamic stability. So it can be used safely in day care surgery.
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8. C Radhika Rani, N S V Ramakrishna Volunteers 3;Issue 11; March 2017 et al conducted a randomised controlled study and compared postoperative analgesia in patients undergoing lower limb surgeries using intrathecal 0. 5%
hyperbaric Bupivacaine with 0.5% isobaric Ropivacaine. They observed that Ropivacaine provide shorter duration of sensory and motor blockade with minimal intraoperative and postoperative side effects.
9. Chari VRR, Goyal A (2013) et al did a randomised double blind controlled study and compared intrathecal 0.75% isobaric Ropivacaine and 0.5%
hyperbaric Bupivacaine in infra umbilical surgeries. They found that plain intrathecal Ropivacaine is superior to Bupivacaine in terms of longer sensory blockade with shorter duration of motor block.
10. Dr Kumkum Gupta, Surjeet Singh we're all conducted a prospective study based on Intrathecal Fentanyl as an adjuvant to 0.75% Isobaric Ropivacaine for infraumbilical surgery under subarachnoid blockade. One hundred and sixty
patients of ASAP 1and 2 were randomly divided into two groups. One group ( n= 80) have to receive either intrathecal 4 ml of 0.75% Ropivacaine with 0.4 ml
of 0.9% sodium chloride (Group RC) or Fentanyl 20mcg (Group RF). They monitored the hemodynamic parameters, onset as well as duration of sensory and motor blockade, peak block height, time to achieve peak block height and
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complications. Their observation interepretations were: The mean onset time of
sensory and motor blockade in both groups were statistically insignificant (p value <0.05).
The mean time taken to reach maximum sensory height of T6 was statistically insignificant in two groups with p < 0.05. The mean total duration of sensory analgesia in Group I was 316 minutes and Group II was 359 minutes. The mean difference observed regarding motor blockade in two groups was statistically significant with p value>0.05.
They concluded that intrathecal Fentanyl as an adjuvant to 0.75% Ropivacaine provides prolonged duration of sensory blockade with early motor recovery.
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OBSERVATION AND RESULTS Data Analysis:
Descriptive statistics was done for all data and reported in terms of mean values and percentages. The collected data were analysed with IBM. SPSS statistics software 23.0 Version. To describe about the data descriptive statistics frequency analysis, percentage analysis were used for categorical variables and the mean and S.D were used for continuous variables. To find the significant difference between the bivariate samples in Independent groups the Unpaired sample t- test was used. To find the significance in categorical data Chi-Square test was used. In both the above statistical tools the probability value0. 05 is considered as significant level.
Groups
Group Name Interventions
Group R 0.75%Isobaric Ropivacaine with Fentanyl
Group B 0.5%hyperbaric
Bupivacaine with Fentanyl
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In our study we compared the following parameters between the two groups.
Age
Gender
Mean weight
Mean Height
ASA Physical Status
Peak block height
Onset of sensory and motor blockade
Time to Peak block height
Time for two segment regression
Time for regression to L1
Time for complete regression to S2
Time to motor blockade Bromage 3
Time to Bromage 0
Rescue Analgesia
Postoperative Numeric scoring system
Postoperative complications
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Table 1: Age distribution of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20)
Group Bupivacaine
(N=20) P
value
n % n %
Age group (years)
36 to
40 5 25 5 25
0.651 41 to
45 5 25 5 25
46 to
50 5 25 7 35
51 to
55 1 5 2 10
above
50 4 20 1 5
Comments: The age distribution of study subjects in both groups were similar and only minor difference was observed.
Table 2: Comparison of mean age of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20)
Group Bupivacaine (N=20)
P value
Mean SD Mean SD
Age (years) 46.2 7.0 45.1 5.4 0.583
Comments: The minor difference in mean age between the two groups was not statistically significant (p>0.05) and hence both the groups were comparable.
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Fig 1: Age distribution of the study sample (n=40)
Table 3: Gender distribution of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20)
Group Bupivacaine
(N=20) P
value
n % n %
Sex Male 11 55 10 50
0.752
Female 9 45 10 50
Comments: The gender distribution of study subjects in both groups can be considered as similar as the minor difference observed was not statistically significant (p>0.05). Hence both the groups were comparable.
25 25 25
5
20
25 25
35
10
5
0 5 10 15 20 25 30 35 40
36 to 40 41 to 45 46 to 50 51 to 55 above 50
%
Age group
Group Ropivacaine Group Bupivacaine
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Fig 2: Gender distribution of the study sample (n=40)
Table 4: Comparison of mean weight of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20) Group Bupivacaine (N=20)
P value
Mean SD Mean SD
Weight (kg) 63.4 5.2 63.4 7.2 0.980
Comments: The minor difference in mean weight between the two groups was not statistically significant (p>0.05) and hence both the groups were comparable with regards to body weight.
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50 45
50
0 10 20 30 40 50 60
Group Ropivacaine Group Bupivacaine
%
Male Female
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Table 5: Comparison of mean height of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20) Group Bupivacaine (N=20)
P value
Mean SD Mean SD
Height (cm) 157.3 5.2 156.3 5.5 0.564
Comments: The minor difference in mean height between the two groups was not statistically significant (p>0.05) and hence both the groups were comparable with regards to height.
Table 6: Comparison of ASA category of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20)
Group Bupivacaine
(N=20) P
value
n % n %
ASA PS Category
ASA PS 1 11 55 8 40
0.150 ASA PS 2
9
45 12 60
Comments: The minor difference in the distribution of ASA category was not statistically significant (p>0.05) and hence both the groups were comparable with regards to ASA category.
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Fig 3: Distribution of ASA category of the study sample (n=40)
Table 7: Comparison of peak block height of the study sample (n=40)
Characteristics
Group Ropivacaine (N=20)
Group Bupivacaine
(N=20) P
value
n % n %
Peak block height
T6 6 30 8 40
0.796
T8 9 45 8 40
T10 5 25 4 20
Comments: The minor difference in the peak block height between the groups was not statistically significant (p>0.05) and hence both the groups were comparable with regards to peak block height.
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40 45
60
0 10 20 30 40 50 60 70
Group Ropivacaine Group Bupivacaine
%
ASA PS 1 ASA PS 2
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Fig 4: Comparison of peak block height of the study sample (n=40)
30
40 45
40
25
20
0 5 10 15 20 25 30 35 40 45 50
Group Ropivacaine Group Bupivacaine
%
T6 T8 T10
