COMPARISON OF 0.125 % BUPIVACAINE WITH FENTANYL 2µg/ml AND 0.125% ROPIVACAINE WITH FENTANYL 2 µg/ml FOR
EPIDURAL LABOUR ANALGESIA
A DISSERTATION SUBMITTED TO
THE TAMILNADU DR.M.G.R MEDICAL UNIVERSITY In partial fulfillment of the regulations for the award of the degree of
M.D. ANAESTHESIOLOGY – BRANCH X Reg. No. 201720108
DEPARTMENT OF ANAESHESIOLOGY
GOVERNMENT MADURAI MEDICAL COLLEGE AND HOSPITAL
THE TAMILNADU DR.M.G.R MEDICAL UNIVERSITY CHENNAI
MAY 2020
INSTITUTE OF ANAESTHESIOLOGY, MADURAI MEDICAL COLLEGE,
MADURAI
CERTIFICATEBY GUIDE
This is to certify that this dissertation entitled “COMPARISON OF 0.125% BUPIVACAINE WITH FENTANYL 2µg/ml AND 0.125%
ROPIVACAINE WITH FENTANYL 2µg/ml FOR EPIDURAL LABOUR ANALGESIA” is a bonafide and genuine research work done by Dr.RAGUL.A in partial fulfillment of the requirement for the degree of MD in Anaesthesiology and Critical care.
Dr. M.P. SANTHANA KANNAN M.D., Assistant Professor
Institute of Anaesthesiology
Madurai Medical College, Madurai-20.
DR.M. KALYANASUNDARAM, M.D., Professor
Institute of Anaesthesiology
Madurai Medical College, Madurai-20
INSTITUTE OF ANAESTHESIOLOGY, MADURAI MEDICAL COLLEGE, MADURAI
CERTIFICATEBY HEAD OF THE DEPARTMENT
This is to certify that this dissertation entitled “COMPARISON OF 0.125% BUPIVACAINE WITH FENTANYL 2µg/ml AND 0.125%
ROPIVACAINE WITH FENTANYL 2µg/ml FOR EPIDURAL LABOUR ANALGESIA” is a bonafide and genuine research work done by Dr.
RAGUL.A in partial fulfillment of the requirement for the degree of MD in Anaesthesiology and Critical care under the guidance of Prof.Dr.M.
KALYANASUNDARAM, M.D., Institute of Anaesthesiology and critical care.
Prof. Dr.M. KALYANASUNDARAMM.D., Director
Institute of Anaesthesiology,
Govt.Rajaji Hospital & Madurai Medical College
Madurai-20.
ENDORSMENT BY THE DEAN
GOVERNMENT RAJAJI MEDICAL COLLEGE AND HOSPITALS
This is to certify that this dissertation entitled “COMPARISON OF 0.125% BUPIVACAINE WITH FENTANYL 2µg/ml AND 0.125%
ROPIVACAINE WITH FENTANYL 2µg/ml FOR EPIDURAL LABOUR ANALGESIA” is a bonafide and genuine research work done by Dr.RAGUL.A in partial fulfillment of the requirement for the degree of MD in Anaesthesiology and Critical care under the guidance of Professor Dr.M. KALYANASUNDARAM, M.D., Institute of Anaesthesiology and critical care, Professor, Institute of Anaesthesiology and critical care.
Dr. VANITHA,M.D., DCH., Dean
Govt.Rajaji Hospital Madurai Medical College Madurai.
Date:
Place: Madurai
DECLARATION
I, Dr.RAGUL.A solemnly declare that, this dissertation titled
“COMPARISON OF 0.125% BUPIVACAINE WITH FENTANYL 2µg/ml AND 0.125% ROPIVACAINE WITH FENTANYL 2µg/ml FOR EPIDURAL LABOUR ANALGESIA” has been done by me. I also declare that this bonafide work or a part of this work was not submitted by me or any other for any award, degree or diploma to any other University or board either in India or abroad.
This is submitted to The Tamilnadu DR.M.G.R Medical University, Chennai in partial fulfillment of the rules and regulations for the award of Doctor of Medicine degree branch X (Anaesthesiology) to be held in MAY 2020.
DATE:
Place: Madurai Dr. RAGUL.A
ACKNOWLEDGEMENTS
With great reverence, I extend my deep sense of gratitude to respected guide Dr.M. KALYANASUNDARAM, M.D., Professor, Institute of Anaesthesiology and critical care, for his advice, able guidance, constant inspiration, constructive criticism and novel suggestions throughout my post graduate study, without whose initiative and enthusiasm, this study would not been completed.
My sincere thanks to Dr.M.KALYANASUNDARAM M.D., DIRECTOR, Institute of Anaesthesiology and critical care who supported and guided me in each and every step of my work.
My sincere thanks to Dr.M.P. SANTHANA KANNAN, M.D., Assistant professor, Institute of Anaesthesiology and critical care who supported and guided me in each and every step of my work.
I am thankful to all my Assistant Professors, Professors, My Colleagues, Seniors, Juniors and All Other Staff Members Institute of Anaesthesiology And Critical Care for their constant support and guidance in completing this study.
I thank my Parents, wife and Family members for their support during the course of study.
I also thank my collaborating department, Department of OBSTETRICS AND GYNAECOLOGY who allowed me to perform my study at their theatre.
I thank The Dean, Government Rajaji Hospital and Madurai Medical College, Maduraifor permitting me to utilize the college and hospital for my study.
Lastly, I sincerely thank all of my patients for their kind cooperation during the course of the study.
Date:
Place: Madurai DR.RAGUL.A
S.NO TITLE PAGE NO
1. INTRODUCTION 1-45
2. AIM AND OBJECTIVES 46
3. REVIEW OF LITERATURE 47-49
4. MATERIALS AND METHODS 50-60
5. RESULTS 61-82
6. DISCUSSION 83
7. CONCLUSIONS 85
ANNEXURES BIBLIOGRAPHY PROFORMA MASTER CHART
ETHICAL COMMITTEE APPROVAL LETTER PLAGIARISM CERTIFICATE
TABLE OF CONTENTS
INTRODUCTION
Labour is an extremely painful process. Pain during labour is severe in nature and most painful experience in her life. It has deleterious effect on both mother and fetus(1),(2). Labour pain increase the stress response which is neither beneficial for mother nor for fetus. Maternal disorders such as maternal hypertension, dystocia, meconium staining liquor and fetal distress are stress related(3) .
Providing adequate pain relief during labour produce physiological and psychological benefits for mother and improve fetal oxygenation by increasing the uteroplacental blood flow(4).Among the several methods of labour analgesia, regional analgesia is a safe and effective method (1),(2). Among the various methods of regional analgesia epidural labour analgesia is most popular and most effective method (5).
Epidural labour analgesia improve cardiovascular , pulmonary functions in mother with respiratory,and cardiovascular compromise(6), During epidural labour analgesia mother is awake, cooperative, and actively participate in labour proceses(7) Compared with other methods of pain relief, epidural labour analgesia is associated with the highest level of maternal satisfaction(8).
Despite providing excellent pain relief during epidural labour analgesia if we use local anesthetic alone and in higher concentration will produce motor block, associated with prolonged second stage and increased incidence of instrumental delivery that will reduces the maternal satisfaction(9).When we are use opioids alone
is not satisfactory throughout the labour. Adding an opioid to local anesthetic solution can increase the duration, quality of analgesia and sparing or reduction in motor block contribute to good progress of labour , vaginal delivery, and reduces local anesthetic dose requirement also (10)
So in this study we use minimal local anesthetic concentration(MLAC), minimal local anesthetic volume(MLAV),minimal local anesthetic dose(MLAD) were used with opioids to improve the quality of analgesia to avoid or reduce the motor blockade,to avoid local anesthetic toxicity and to maintain maternal hemodynamic stability. Mother can walk during this procedure(Walking Epidural) result in higher vaginal delivery when giving epidural bolus if the study solution is inadvertently injected intravascularly, it will not produce local anesthetic toxicity. Our aim of this study is to increase the safety of mother and fetus without affecting the progress of labour during epidural analgesia.(11),(12).
In recent years Bupivacaine is increasingly replaced by Ropivacaine in Labour.
Epidural Analgesia because Ropivacaine has similar analgesic property, less motor blockade ,less cardiovascular and less central nervous system toxicity(13).
In this study we are using more diluted solution of Bupivacaine 0.125% and Ropivacaine 0.125% with fentanyl 2µg/ml and compared for their analgesic efficacy, motor blockade, hemodynamic stability, labour outcome, and fetal outcome.(14)
HISTORY:(8),(15),
On 1847 James Joung Simson obstretician used ether for delivery.
On 1853, John Snow used chloroform for birth of Prince Leopold eighth child of Queen Victoria. He gave 15 doses of chloroform intermittently with handkerchief
On1898 Augest Bier prformed first spinal anaesthesia
On1901 The first caudal anaesthesia was described by Jean Anthanase Siccard and Fernand Cathleen.
On1921,Fidel Pages first described Lumbar epidural anaesthesia in human.
On 1930, Dogliotti first performed the loss of resistance technique.
On1931, Eugene Bogden Aburel injecting Local anesthetic via silk catheter into the. Lumbar Epidural space.
On 1933 Ruiz,and Gutrieuz performed epidural by hanging drop method On1949 continuous lumbar epidural analgesia by Manuel Martinez Cuberlo.
On 1962 Lee introduced closed tip with lateral hole epidural catheter.
On 1963, Bupivacaine first introduced.
On1979, Cooper et al demonstrated addition of opioid to Local anesthetic On1980, opioids was first used in labour analgesia.
On1988, Gambling performed first patient controlled epidural analgesia.
On 1993, Morgan introduced combined spinal epidural analgesia for labour.
On 1993 Collins and Morgan described Walking Epidural in Queen Charlotte hospital in London
ANATOMY OF THE EPIDURAL SPACE(16),(17)
THE EPIDURAL SPACE
The epidural (extradural, peridural) space with in the spinal canal and external to the dura mater. It lies between the dura mater and the periosteum lining the canal, and corresponds to the very restricted space within the skull between the two layers of the cranial duramater enclosing the venous sinuses.
BOUNDARIES
·Anteriorly:By vertebral bodies and posterior longitudinal ligaments
·Posteriorly: Vertebral arches and ligamentum flavum Lateraly: pedicle ,intervertebral foramen
·Superiorly: Fusion of dura with periosteum at foramen magnum
·Inferiorly: Sacrococcygeal ligament at sacral hiatus
The epidural space extends from the Foramen magnum to sacral hiatus. The upward spread of drugs is limited by the attachment of duramater to the circumference of the foramen magnum The anterior and posterior nerve roots with their dural coverings pass across the very narrow space to unite in the intervertebral foramen to form the segmental nerves. anterolaterally where it is continuous with the pads of fat surrounding the spinal nerves in the intervertebral foramina.Between the postero- lateral walls of the lumbar vertebral canal and the dura, the space is narrower, and the fat less evident. Anteriorly in a thin subject, the space is only potential, since here the
dura lies close to the posterior longitudinal ligament on the posterior aspect of the vertebral bodies
Contents:spinal nerve roots,lymphatics,loose connective tissue,fatty tissue,small arteries,internal vertebral venous plexuses(Batson plexus)
The spread of the local analgesic solution injected into the epidural space is not accurately predictable, because of the resistance offered by the fatty areolar tissue and the numerous foramina through which the fluid can leak. A dorsomedian fold of dura mater was demonstrated in a few cases, which sometimes divides the epidural space into a ventral and two dorso-lateral compartments, not necessarily freely communicating with each other. The median thickness of the space might be only 2 mm. These observations explain the occasional patchy analgesia and inadvertent dural puncture when the midline approach is used.
The space occupied by the venous plexus varies with the amount of the venous distention and is related to the intra-thoracic pressure.
FIGURE1. shows Epidural space with Local Anesthetic
Lumbar vertebrae:
Body: shape largest than other vertebrae Vertebral foramen: Triangular
Pedicles: Short and thick directed backward laterally Laminae: Short broad and do not overlap
Spinal process: Large quadrangular, more or less horizontal Lumbar epidural space:
Depth: Average 5cm from the skin
Thickness of lumbar epidural space: 4-7mm
FIGURE 2.Cross section of spinal cord shows epidural space and it’s relationship
PRESSURE AND VOLUMES OF THE EPIDURAL SPACE(18)
Differences between pregnant and non-pregnant patient. Pressure and volume changes in the epidural space during pregnancy are mainly due to the mechanical effects of gravid uterus over the inferior vena cava The return of blood from the lower part of the body is mainly via the inferior vena cava in case of venacaval obstruction.
In pregnancy epidural veins are an alternate of returning the lower limb blood. So the epidural veins are dilated and the actual size of the epidural, subarachnoid spaces are reduced.
Reduced size of epidural space can cause following effects
The volume of local anaesthetic required to provide an extensive block is reduced in pregnancy.
There is an increased risk of puncture of the distended veins by either the
Distension of dura is likely to be maximum in the sitting position and pressure in the epidural space is also increased particularly in the sitting position because of negative epidural pressure become positive.
During a uterine contraction, as the blood expelled from the contracting uterus passes to the epidural venous plexus, the pressure in the epidural space may rise by 4- 10 cmH2O. For this reason that injections of local anesthetics should be with held during a contraction, as the spread may be unpredictable and probably excessive. The engorgement of the epidural veins would appear to be increased in the sitting position due to gravity than lateral position. Chances of dural and venoue puncture are increased in sitting position than lateral position . so we preferred lateral position in this study.
PHYSIOLOGICAL CONSIDERATIONS DURING PREGNANCY AND LABOUR(19),(20)
Maternal changes in pregnancy occur as a result of hormonal alterations, mechanical effects of the gravid uterus, increased metabolic and oxygen requirements of the fetoplacental unit, and hemodynamic alterations associated with the placental circulation. These adoptive changes useful to the mother tolerating the stresses during pregnancy,labour and pain.Such changes become more significant as pregnancy progresses, and they have major implications for labour analgesia and anesthesia especially in high-risk parturients.
RESPIRATORY SYSTEM
During labour, particularly in the late first stage and second stage, the pain from episodic uterine contractions produce corresponding increases in maternal minute ventilation (as much as 300% over that of non pregnant women) and oxygen consumption.
The most impressive change in maternal lung dynamics is a decrease in functional residual capacity (FRC), which at term may have changed by as much as 20% of pre-pregnancy values. Minute ventilation increases by 45%, primarily as a result of an increase in tidal volume because the respiratory rate is essentially unchanged. Hormonal changes and an increase in the rate of carbon dioxide production are responsible for the increase in ventilation. Progesterone sensitizes the respiratory center to carbon dioxide. PaCO2 falls to approximately 30 mm Hg by the 12th week of gestation, and it remains at this level for the remainder of pregnancy.
Tidal volume increases by 50%, with half of this increase occurring during the first trimester. The parturient's breathing pattern changes; it becomes more diaphragmatic as pregnancy progresses because of the effects of the gravid uterus and limitation of thoracic cage movement. Closing capacity (CC), however, remains unchanged. The resulting decrease in the FRC/CC ratio causes faster small-airway closure when lung volume is reduced, thus parturients can desaturate at a much faster rate than non pregnant women .The rapid development of hypoxia as a result of decreased FRC, increased oxygen consumption, and airway closure may be minimized by administration of 100% oxygen for 3 to 5 minutes before the induction of anesthesia.
sufficient. During pregnancy, capillary engorgement of the mucosa occurs throughout the respiratory tract, potentially causing oedema in the nasopharynx, oropharynx, larynx and trachea. Therefore manipulation of the upper airway requires extreme care. Regional analgesia abolishes the requirement of airway manipulation and hence avoids the dangers involved in general anesthesia
CARDIOVASCULAR SYSTEM
The cardiovascular system is progressively stressed during pregnancy and parturition. Many of the changes appear during the first trimester of pregnancy increases in cardiac output of 22% and decrease in systemic vascular resistance by 30% at 8 weeks gestation. The changes continue into the second and early third trimester of pregnancy, when cardiac output increases to approximately 30-40% of non-pregnant values. The increase in cardiac output during pregnancy is primarily a result of increase in stroke volume (by about 30%) with a more modest increase in heart rate(10-15 beats/min). Arterial blood pressure does not change during normal pregnancy because of a decrease in peripheral vascular resistance.
Cardiovascular changes in pregnancy Heart rate Increased by 20–30%
Stroke volume Increased by 20–50%
Cardiac output Increases by 30–50%
Central venous pressure remain Unchanged
Pulmonary capillary wedge pressure remain Unchanged
Systemic vascular resistance Decreased by 20%
Systemic blood pressure Slight decrease in Mid-trimester 10–15 mmHg,then rises Pulmonary vascular resistance Decreased by 30%
Pulmonary artery pressure Slight decrease
Clinical examination of a pregnant woman may reveal a wide, loud split first sound and a soft ejection systolic murmur, caused by the increased blood flow and vasodilatation. The elevated diaphragm usually alters the position of the heart at term, so that the point of maximum impulse is felt a little to the left. The axis on the ECG is also shifted to left. ECG may show non-specific ST, T and Q wave changes and benign arrhythmias.
The pain and apprehension of labour adds to cardiac work during pregnancy and increases stroke volume and cardiac output by 45% over prelabour values. Blood pressure increases during painful labour. Additional stresses are imposed by uterine contractions, which cause, in effect an autotransfusion. With each uterine contraction, blood from the body of the uterus is pushed into the central circulation and blood volume and cardiac output increase by 10-25%. After delivery also the same auto transfusion occurs. In addition to increase in central blood volume, obstruction of the venacava is relieved. As a result there is a marked increase (upto 80% of pre labour values) in stroke volume and cardiac output in the immediate post partum. Patients with limited cardiac reserve may experience cardiac failure at this time.
Despite the increase in blood volume and cardiac output, the parturient at term is susceptible to hypotension in supine position. ‘When the patient is supine, the gravid uterus partially or completely compresses the aorta and inferior vena cava, leading to decreased venous return, decreased cardiac output,hypotension and reduced uterine blood flow. Up to 10% of pregnant patients near term develop signs of shock (hypotension, pallor, sweating, nausea, vomiting,changes in cerebration) when they assume this position. Compensatory mechanisms include increased sympathetic tone and collateral routes (paravertebral veins to azygos vein) to improve venous return during obstruction of the vena cava. Caval compression also increases uterine venous back pressure, which further decreases uterine blood flow. Compression of the aorta is not associated with maternal symptoms but does cause arterial hypotension in the lower extremities and uterine arteries, which can further decrease uterine blood flow and impair utero-placental perfusion.
The anesthesiologist must recognize the importance of the aortocaval compression syndrome and the potential for its adverse effects to be exaggerated by anaesthesia. Drugs causing vasodilatation such as potent inhalational agents and particularly anesthetic techniques causing sympathetic blockade (subarachnoid or epidural anesthesia) exacerbate decreased venous return to the heart when the vena cava is obstructed. Aortocaval compression must be prevented. Displacement of the uterus, off the great vessels can be accomplished by manually displacing the uterus to the left. During labour the patient should be positioned either on her side or with a left tilt. During delivery the operating or the delivery table can be tilted laterally to the left
or a small pillow or foam rubber wedge can be used to elevate the patient’s right buttock and back to about 10-15 cms.
The pregnant woman at term is in a hyper coagulable state owing to increase in factors VII, VIII, X and plasma fibrinogen. Estimation of blood loss at delivery vary but may be around 500ml for an uncomplicated vaginal delivery. Blood loss during caesarean section varies widely with 500 to 1400 ml, being reported.
GASTRO INTESTINAL CHANGES
During pregnancy, the secretion of gastric acid can increased. During late pregnancy gastric emptying is slowed as a result of displacement of pylorus by the enlarged uterus. Pain, anxiety and use of opioid analgesia during labour contribute to impaired of gastric emptying. Intra-gastric pressure is increased and lower oesopahgeal sphincter tone is decreased during pregnancy. All these changes increase the risk of regurgitation and aspiration during either during general anaesthesia or during the state of impaired consciousness from any other cause.
CENTRAL NERVOUS SYSTEM
Pregnancy reduces anesthetic requirements during regional and general anesthesia. During spinal or epidural anesthesia, less local anesthetic is required to produce a required level of anesthesia. This was thought to be due to the mechanical effects of increased intra-abdominal pressure,can cause epidural venous engorgement and reduction of both the epidural and subarachnoid space. Reduced Minimal Alveolar Concentration is seen during early pregnancy and immediate postpartum
HEPATIC CHANGES
Total protein concentration and the albumin- globulin concentration ratio decrease. Although plasma cholinesterase activity is reduced during pregnancy and in the immediate post partum period, moderate doses of Succinylcholine are usually metabolised easily.
RENAL CHANGES
Renal blood flow and glomerular filtration rate are increasing rapidly during pregnancy it will reflect the changes in cardiac output. During the third trimester, they slowly return to normal. Creatinine clearance usually increases and therefore the upper limits of normal blood urea nitrogen and serum creatinine are lower in the pregnant woman.
HEMATOLOGICAL CHANGES
Pregnancy associated with hypercoagulable state may be beneficial in limiting blood loss at delivery.Factors VII,VIII,IX,X and IX are increased. Factor IX may be decreased.In third trimester accelerated fibrinolysis is observed in late.Dilutional anaemia,leukocytosis(up to 21000/µl) , 10% decrease in platelet count and iron, folate deficiency also observed in third trimester.
METABOLIC CHANGES:
Complex metabolic and hormonal changes Metabolic changes resemble starvation altered carbohydrate, fat, protein metabolism, Blood glucose, amino acid levels are low ,free fatty acid, ketones, triglyceride levels are high.
Pregnancy is a diabetogenic state although insulin level are steadily raising in pregnancy.Human placental lactogen is responsible for insulin resitance also called as human chorionic somatomammotropin.
Secretion of human chorionic gonodotropin and increased level of estrogen can cause hypertrophy of thyroid gland and increase in T3,T4 but free T3,T4level, but thyrotropin(TSH) remain normal.
MUSCULOSKELETAL CHANGES:
Elevated level of relaxin can relaxing the pubic sympysis,pelvic joints,and spinal ligaments may be the cause for higher incidence of back pain.
UTEROPLACENTAL CIRCULATION:
Normal uteroplacental circulation is important for development and maintenance of healthy fetus, uteroplacental insufficiency cause intra uterine growth retardation and fetel death. Integrity of uteroplacental circulation depends on uterine blood flow and placental function
UTERINE BLOOD FLOW(21)
Uterine blood flow in the parturient at term is approximately 700ml/min and is determined by the following relationship: Uterine blood flow = (Uterine arterial pressure)-(Uterine venous pressure)/(Uterine vascular resistance). There is autoregulation of uterine blood flow. The vessels are maximally dilated during pregnancy. As such in the absence of aortic compression, uterine arterial pressure
decreases during maternal hypotension (sympathetic block,hypovolemia, haemorrhage, compression of the inferior vena cava), in circumstances in which uterine venous pressure is increased (compression of the inferior venacava, abruption placenta), and with increases in uterine vascular resistance (maternal hypertensive disorders, a agonists, uterine hypercontractility). Due to increased maternal mean arterial pressure and a concomitant decrease in uterine blood flow can produce deleterious effects on the fetus. After epidural analgesia uterine blood flow increases, mean arterial pressure stabilizes and placental blood flow is increased by either a reduction in extrinsic vascular tone (uterine tone) or a decrease in intrinsic vascular resistance (placental vasodilatation). Conditions that increase the frequency or duration of uterine contractions (e.g. an over dose of oxytocin or abruption placentae) also decrease uterine blood flow.
STAGES OF LABOUR:
There are three stages in labour First stage:
Stage of cervical dilatation and effacement onset of true labour pain to full cervical dilatation (10cm), full effacement(100%)
Primi 8-12 hours Multigravida 4-6 hours
Second stage;
Stage of Expulsion
Full cervical dilatation to delivery of fetus
Primi 1-2 hour
Multigravida half an hour to 1 hour
Third stage:
Stage of Placental delivery
Delivery of fetus to complete expulsion of placenta Few minutes to 15 minutes
FIGURE 3 . Shows three stages of Labour
LABOUR PAIN
During uterine contractions there is intermittent reduction of the intervillous blood flow and during a peak of contraction, there may be a temporary decrease in the placental gas exchange.
Primipara unprepared for child birth experiencing pain during labour is similar to amputation of digit without anesthesia
FIGURE 4 . Shows comparision of Labour pain with chronic pain syndromes and Trauma pain
PHYSIOLOGY OF PAIN IN LABOUR(2),(19) Labour Pain Pathways And Mechanism(1)
Pain perception by the parturient is a dynamic process that involves both peripheral and central mechanisms.Many factors have an effect on the degree of pain experienced by a woman during labour. Including psychological preparation, emotional support during labour,past experiences, the patient's expectations of the birthing process, and augmentation of labour with oxytocin. An abnormal presentation (such as occipitoposterior)may also cause early labour pain to be more intense.
Figure 5 .Shows nerve supply of birth canal and various methods of Regional analgesia
PAIN IN THE FIRST STAGE OF LABOUR(22),(23)
During the first stage of labour, pain impulses arise primarily from the uterus.Uterine contractions may result in myometrial ischemia, which ultimately causes the release of bradykinin, histamine, and serotonin. In addition, stretching and distention of the lower uterine segment and cervix may stimulate mechanoreceptors.
These noxious impulses follow the sensory nerve fibers that accompany sympathetic nerve endings, they travel through the paracervical region and the hypogastric plexus to enter the lumbar sympathetic chain.
Uterine contractions cause stretching, tearing and distortion and possibly ischemia of the uterine tissues, whilst simultaneously dilating the cervix and stretching the lower uterine segment. The intensity of the pain increases progressively with the raising strength of the contractions. In early labour only the nerve roots of T11 and T12 are involved, but as the intensity of contractions are increases, then the T10 and L1 are recruited.
Backache is a frequent complaint during labour and may be caused by one or other of two mechanisms. Pain originating in the uterus or cervix may be referred to the cutaneous branches of the posterior divisions of T10-L1, which migrate caudally for an appreciable distance before they innervate the skin overlying the vertebral column.
PAIN IN THE SECOND STAGE OF LABOUR(23)
The pain caused by the distension of the pelvic structure and perineum following descent of the presenting part is added to the pain of uterine contractions, although once cervical dilatation is complete the pain induced by uterine contractions may become less severe. The uterine pain continues to be referred to T10-L1, while the pain produced by stretching or pressure exerted on intra pelvic structures, including the peritoneum, bladder, urethra and rectum is referred to sacral segments.
Pressure on the roots of the lumbosacral plexus may manifest itself, as pain felt low in the back or in the thighs. Pain produced by stretching of the perineum is transmitted by the pudendal nerve (S2,3,4) and in part by the posterior cutaneous nerve of the thigh(S2,3), the genitofemoral nerve(L1,2) and the ilio-inguinal nerve (L1).
INNERVATIONOF BIRTH CANAL Anesthetic implication:
During the first stage of labour, a block limited to the T11-T12 segments at the beginning and later extending to involve T10 and L1 will usually be sufficient to provide excellent pain relief whilst avoiding neural blockade of the sacral segments.
Premature sacral blockade can result in the loss of the stimulating effect upon contractions of Ferguson’s reflex and the loss of pelvic muscle tone,which aids the rotation of the presenting part.
Later in the first stage and during the early part of the second stage, pain is often experienced in lower lumbar and upper sacral segments, so that the block will
segments need to be performed only when perineal pain becomes intense. Epidural block will interrupt the preganglionic sympathetic fibres and leave the postganglionic fibres intact.
RELAY OF PAIN.
Pain from the peripheral nociceptive field is transmitted to the cortex by the afferents arising from the dorsal root ganglion the first order neurons. The majority of these first order neurons passes to the contralateral side as the spinothalamic tract and gives afferents to the medullary centre, reticular activating system, hypothalamus and reach the post central gyrus in the cortex. The efferent impulses reach the segmental area through the corticospinal and rubrospinal tracts.Some of the first order neurons communicate through the internuncial neurons and give efferent impulses to the peripheral nociceptive areas from the segmental autonomic reflexes.
Labour and vaginal delivery produces tissue damage, and like tissue injury from any cause, result in pain and local segmental, suprasegmental and cortical responses Epidural analgesia extended to relieve both uterine pain and pain related to distension of the lower birth canal, thus providing analgesia for instrumental delivery or caesarean section. Regional analgesia minimizes or completely avoids the problems of maternal aspiration, as well as neonatal drug depression due to general anesthesia.
PHYSIOLOGICAL EFFCETS OF LABOUR PAIN(1),(17)
Placental gas exchange is worsened by maternal hyperventilation due to severe pain. Respiratory alkalosis in the mother results in the following:
A shift of the mother’s oxygen dissociation curve to the left,diminishing transfer of oxygen from mother to the fetus.
Maternal hypoxia during uterine relaxation and in between contraction
Umbilical vasoconstriction causing a diminution of umbilical blood flow
A reduction in uterine blood flow due to elevations in noradrenaline levels and Fetal hypoxia
Normally maternal blood receives acid metabolites and carbon dioxide from fetal blood and the pH decreases so that there is shift in the maternal oxyhaemoglobin dissociation to the right maintaining increased oxygen delivery to the fetus. At the same time in fetal blood, the pH increases leading to a shift in fetal oxygen dissociation curve to the left. This effect is known as thedouble Bohr effect.
In prolonged labour maternal hyperventilation leads to alkalosis and with diminishing maternal PaCO2, the Bohr effect may be attenuated and cause hypoxia in conditions of fetal stress. Thus maternal hyperventilation as a result of pain decreases fetal oxygenation, presumably by shifting the maternal oxygen dissociation curve to the left and by reducing umbilical blood flow.
PSYCHOLOGICAL EFFECTS OF LABOUR PAIN
Post partum depression
Post traumatic stress disorder
THE STRESS RESPONSE TO PAIN IN LABOUR(24),(25)
Segmental and supra-segmental reflex-responses from the pain of labour may affect respiratory, cardiovascular, gastro-intestinal, urinary and neuro-endocrine functions.
Respiratory - Pain in labour initiates hyperventilation leading to maternal hypocarbia respiratory alkalosis and subsequent compensatory metabolic acidosis. The oxygen dissociation curve is shifted to the left and thus reduces tissue oxygen transfer, which is already compromised by the increased oxygen consumption associated with labour.
Cardiovascular - Labour results in a progressive increase in maternal cardiacoutput, primarily due to an increase in stroke volume, and, to a lesser extent,maternal heart rate. The greatest increase in cardiac output occurs immediately after delivery, from the increased venous return associated with relief of venocaval compression and the autotransfusion resulting from uterine involution.
Hormonal - Stimulation of pain results in the release of beta-endorphine and ACTH from the anterior pituitary. Associated anxiety also initiates further pituitary response.Pain also stimulates the increased release of both adrenaline and noradrenaline from the adrenal medulla which may lead to a progressive rise in peripheral resistance and cardiac output. Excessive, sympathetic activity may result incoordinate uterine action, prolonged labour and abnormal fetal heart-rate patterns.
Activation of the autonomic nervous system also delays gastric emptying and reduces intestinal peristalsis.
Metabolic - Maternal: During labour, glucagon, growth hormone, renin and ADH level increases while insulin and testosterone level decreases. Circulating free fatty acids and lactate also increase with a peak level at the time of delivery.
Fetal: Maternal catecholamines secreted as a result of labour pain may cause fetal acidosis due to low placental blood flow.
FIGURE 6:Shows physiological effect of Labour pain on mother and fetus
Pharmacological Methods Non Pharmacological Methods 1. Systemic
Analgesic Parentral Inhalational
2. Regional Analgesia a. Neuraxial blocks
Spinal Epidural
CSE
b. Non Neuraxial blocks Paracervical block Pudendal N block Perineal infiltration
Psychopropylaxis
Continuous labour support Prepared Child birth Touch and massage
Therapeutic use of heat,cold Hydrotheraphy
Vertical position
Intadermal water injection TENS
Acupuncture/Acupressure Hypnosis
LABOUR ANALGESIA(26),(27) Methods of Labour Analgesia
ADVANTAGESOF REGIONAL ANALGESIA
Superior Analgesia without loss of conciousness
No sedation, nausea and vomiting, Respiratory depression
Sympathetic blockade inhibit stress response syndrome
Coherant uterine action promote vaginal delivery
Increase the utero placental blood flow can cause better fetal acid base status and APGAR score
Allow awake mother immediately interact with baby No risk of pulmonary aspiration of gastric content
EPIDURAL LABOUR ANALGESIA(27) INDICATION
Maternal request
Proteinuric pregnancy induced hypertension, pre eclampsia
Twins, breech,premature infants
Inco-ordinate uterine actions and cervical dystocia
Trial of labour
Elective forceps,
Cardiac and respiratory disease
In operative delivery Lower (LSCS) when full stomach ,with intubation difficulties
CONTRAINDICATIONS
Coagulation defect
Uncorrected hypovolemia and shock
Previous severe allergy to Local Anesthetic
Local infection at the site of insertion
Spina bifida occulta
Raised intracranial pressure
Fixed cardiac output state (AS)
BENEFITS OF EPIDURAL ANALGESIA(28) Maternal Benefits
Safe and effective analgesia
Minimal Hypotension
Minimal motor blockade pt can be ampulated
Provide continuous and prolonged pain relief
Less post dural puncture headache
In severe pre-eclampsia, as an adjuant to antihypertensive therpy, to stabilise blood pressure.
For women with cardiac, respiratory ,neuro muscular and neurological disease, pain control may have some benefits
Provide extended analgesia or anaesthesia for episotomy, Instumental vaginal delivery, and caesarean section
All benefits of Regional Analgesia
Foetal and neonatal benefit
Better APGAR score, minimal respiratory depression compared with systemic opioids
Compared with no analgesia labour ,better acidbase status
In compromised fetus uteroplacental blood flow is increased (IUGR, Severe preeclamsia)
In the premature Labour ,breech presentation, multiple pregnancy assist a controlled birth
Timing of Intervention(29),
It is uncommon for spontaneously labouring parturients to request epidural analgesia before 3 cm of cervical dilation. However, women receiving augmentation of labour with oxytocin may request analgesia at minimal cervical dilation. In this study we activate labour analgesia at active phase of first stage of labour with 3-5 cm cervical dilataion. Too early activation can prolong the duration of labour .Too late iniation may produce ineffective analgesia
Friedman plotted a graph cervical dilatation inX axis ,time in Y axis obtain a S shaped curve indicating normal progress of labour
FIGURE 7.Shows Friedman curve shows cervical dilatation and desent of head in First stage of Labour
FIGURE 8.Shows cervical dilatation in various stages of Labour andFetal head desent
INDUCTION AND MAINTENANCE OF ANALGESIA(19)
The anesthesiologist's goal during the first stage of labour should be to provide segmental sensory anesthesia of the T10-L1 dermatomes. The dose of local anesthetic necessary to achieve effective labor analgesia will depend on the intensity and location of the patient's pain. These in turn depend on the amount and rate of cervical dilation; the strength, frequency and duration of uterine contractions, and the position of the fetal head at the time epidural analgesia is requested. Approximately 10 mL of 0.125 to 0.25percent bupivacaine or 0.125 to 0.25 percent ropivacaine, with or without
a small ldose of a lipid-soluble opioid (e.g., fentanyl or sufentanil), establishes effective analgesia with minimal motor block. Thereafter, maintenance of epidural analgesia may be achieved with either intermittent bolus injections, or continuous epidural infusion or patient-controlled epidural analgesia. In most cases, analgesia may be maintained with a solution of local anesthetic more dilute than that used for induction.
The supine position is contraindicated in women receiving epidural analgesia during labour. Compression of the abdominal aorta and the inferior vena cava (aortocaval compression) by the term gravid uterus may concurrently decrease uterine arterial pressure and increase uterine venous pressure. Consequently,uterine perfusion pressure (uterine arterial pressure minus uterine venouspressure) may be substantially reduced even in the presence of normal brachial arterial blood pressure measurements (concealed aortocaval compression). When maternal hypotension occurs during epidural analgesia, it is essential to verify that the patient is not supine.
The onset of fetal descent causes substantial distention of the vagina and perineum, typically resulting in severe pain. It is important to ensure that the segmental extent of epidural analgesia has spread to include the S2-4 nerve roots to maintain analgesia during this stage of labor. Achieving adequate perineal analgesia is especially important in women in whom episiotomy or the application of forceps is probable. Complaints of rectal pressure with progressive descent of the fetal head should alert the anesthesiologist that sacral analgesia may be inadequate for delivery.
Women who progress into the second stage of labour soon after induction of epidural analgesia seldom have adequate sacral blockade and often require additional epidural boluses of local anesthetic before delivery. On the other hand, women who have been receiving continuous epidural analgesia for many hours often have excellent perineal analgesia at delivery.
FIGURE 9.Shows method of identification of epidural space and insertion of catheter
PHARMACOLOGY OF BUPIVACAINE(30)
Bupivacaine hydrochloride is a long-acting local anesthetic of the amide type.
STRUCTURE
Bupivacaine HCl which is chemically designated as 2 piperidinecarboxamide, 1-butyl-N-(2,6-dimethylphenyl)-, monohydrochloride, monohydrate and has the following structure:
Figure 10.Chemical structure of bupivacaine
CHEMISTRY
Bupivacaine occurs as a 50:50 racemic mixture of the R- and S-enantiomers and is commercially available as bupivacaine and levobupivacaine, the S-enantiomer of bupivacaine. Bupivacaine hydrochloride is a local anesthetic of the amide type with a long duration of action. Bupivacaine hydrochloride differs structurally from mepivacaine hydrochloride only in the substitution of a butyl group for the Nmethyl group. Bupivacaine hydrochloride occurs as a white, odorless, crystalline powder and is freely soluble in water and in alcohol. The pKa of bupivacaine hydrochloride is 8.1.
MECHANISM OF ACTION
The base form is in equilibrium with cationic form outside the axoplasmic membrane. Base form diffuses inside the cell and recalibrates with cationic form. It then reaches the local anesthetic receptor in the Na channel by reversing channel pore while it is in an open state. It prevents Na ions moving intracellularly. In addition to this simple sodium channel blockade, it also affects second messenger system such as adenylatecyclase and guanylatecyclase and also inhibits synaptic transmission by modification of post synaptic receptor (or)presynaptic calcium channel blockade in epidural / subarachnoid blockade.
PHYSIOCHEMICAL PROPERTIES Property Value
Molecular weight 288
Potency ratio 15
Toxicity ratio 10
pKa (25.C) 8.16 Protein binding in %
Maternal 95
Fetal 66
% non ionized at
pH 7.4 17
pH 7.2 11 Partition co-efficient
(25.C,pH7.4) 346
Anesthetic index 3.0-4.0
PHARMACOKINETICS OF EPIDURAL BUPIVACAINE
The uptake of local anesthetic into blood vessels in the area where it has been deposited and its subsequent transfer into systemic circulation is referred to as systemic absorption.
ABSORPTION
A biphasic absorption pattern has been found for epidural bupivacaine. The rapid initial absorption following epidural administration is most likely related to high concentration gradient between the drug in the solution and in the blood. In addition profound increases in epidural blood flow observed during epidural administration of bupivacaine may contribute to its fast initial absorption rate.Later on, after the local anaesthetic has been taken up into local tissues such as epidural fat, absorption will become dependent on tissue blood partitioning, resulting in marked slowing of absorption. Estimated total fraction of the dose ultimately absorbed into general circulation is 0.94 with mean absorption time 8.6hours.
Absorption of local anesthetic is directly related to the amount of drug injected,vascularity, site injected and tissue binding of local anesthetic at injection site.Bupivacaine will produce lower Cmax than less potent and less lipid soluble agents.
DISTRIBUTION
Distribution of local anesthetic has special emphasis in the pregnant patient, because one of the organs that will be exposed to the absorbed drug is fetoplacental
PHARMACOKINETICS OF BUPIVACAINE
Elimination half life t1/2 - 162 minutes
Volume of distribution VDSS - 73 litre
Clearance (litre/min) - 0.6
Hepatic extraction - 0.4
BIODEGRADATION AND ELIMINATION
Liver is the site of metabolism. Two major factors controlling the clearance of the amide linked local anesthetic are hepatic blood flow and hepatic function. The principal pathways are N-dealkylation, aromatic hydroxylation and amide hydrolysis.
CLINICAL CHARACTERISTICS OF BUPIVACAINE Property Value
Penetrance Moderate
Duration 6-8 hours
Infiltration 0.05%
Field block 0.1%
Pudendal/paracervical0.125%
Epidural analgesia 0.125-0.25%
Extradural motor 0.5-0.75%
Maximal dose 2mg/kg body weight
ADVERSE EFFECT AND COMPLICATIONS Central Nervous System Toxicity
Potentially toxic blood level can occur when a drug is injected intravenously, intra arterially or a large dose of drug is given into highly vascular area. Risk of CNS toxicity is more because bupivacaine is a highly protein bound drug. Pregnancy is associated with 30% reduction in protein binding. This allows for higher brain level of bupivacaine for a given dose of drug.
Symptoms
Slow speech, jerky movements, tremors, hallucination, and seizure.
Cardiovascular Toxicity
Dose dependant depression of contractility
Dose dependent depression of conduction and velocity in all conducting tissues. Progressive prolongation of ventricular conduction.
Predisposition to reentry phenomenon followed by sudden onset of ventricular fibrillation.
More affinity for cardiolipin Toxic plasma concentration is 4-5 μg/ml
STSTEMIC TOXICITY MANAGEMENT
Seizure occur ,treat with small doses of benzodiazepine Cardiae arrest occurs consider epinephrine 10-100 μg boluses then Lipid Emulsion Therapy 20% intralipid emulsion used treat the toxicity
Dose: 1.5 ml/kg bolus followed by 0.25 ml/kg/min infusion up to 10 mins after
PHARMACOLOGY OF ROPIVACAINE(31)
Ropivacaine is a amino amide local anesthetic drug ,S enantimer of buipivacaine. Its a pipecoloxylyl derivative Levorotatory form , S enantiomer Ropivacaine is less potent than Bupivacaine( 40% less)
CHEMISTRY
Ropivacaine chemicaly designated as levorotatory enantiomer from N-2,6- dimethylphenyl)-1-propyl-2-piperidinocarboxa mide, that is, a (S)-N-(2,6- dimethylphenyl)-1-propyl-2-pip eridinocarboxamide (31).
STRUCTURE
Figure 11.Chemical structure of Ropivacaine
STERIOSPECIFICITY
Enantiomers present in two spatial configuration like left and right handed cloves There are two enantiomers one is enantiomers R+ (clockwise rotation) dexarotatory,another is enantiomer S- (counterclockwise rotation) levorotatory.
Ropivacaine is optically pure S- enantiomer form. Compared with Bupivacaine which has butyl group
MECHANISM OF ACTION
Reversible inhibition of Na+ ion influx in nerve fibres.Ropivacaine is less lipophilic than bupivacaine and less likely to penetrate myelinated motor fibres So Ropivacaine produce less motor blockade than Bupivacaine.It has greater degree of motor, sensory differentiation. So it is very useful where motor block is undesirable
PHARMACODYNAMICS
CNS: Ropivacaine is less lipophilic than bupivacaine. so it has less CNS toxicity CVS:Ropivacaine is S- enantiomer ( levorotatory) has sterio selective properties So it has less cardiotoxicity
PROPERTY VALUE
Moleclar weight 27.4gm/mol pKa 8.1
Protein binding 94%
Melting point 144 to146 . C
% non ionized at
pH 7.4 17
Clinical uses
Infiltration 0.2-0.5%
PNB 0.5-1%
Partition coefficient 230
PHARMACOKINETIC OF EPIDURAL ROPIVACAINE ABSORBTION AND DISTRIBUTION
Slow onset
Volume of distribution 59Litres
Clearance 0.44 L/min
Elimination half life 108 min
Duration of action 240-480 min
Dose 3mg/kg
Maximum single dose for infiltration 200mg
Toxic plasma concentration >4 µg/ml
Plasma concentration of Ropoivacaine depends on total dose administration,route of administration,hemodynamic circulatoy condition of the patient, and vascularity of administered site.Protein binding is 94% mainly with α acid glycol protein Increased protein binding capacity lead to decrease in clearance of Ropivacaine Ropivacaine can cross the placenta. Plasma concentration of Ropivacaine is lower in fetal circulation because α glyco protein is more concentrated in maternal plasma
METABOLISM AND EXCRETION
Extremly metabolized in liver by two mechanism
Aromatic hydroxylation to 3 hydroxy Ropivacaine by cytochrome P450 1A2
N dealkylation to 2,6 pipecoloxylidide by cytochrome P450 3A4 Excretion mainly by kidney, terminal half life 1.8 ±0.7 hour for intravenous administration 4.2±1.0 hour for epidural administration
PHARMACOLOGY OF FENTANYL(32),(33).
Fentanyl is a synthetic phenylpiperidine-derivative opiate agonist.
STRUCTURE
Fentanyl citrate is N-(1-Phenethyl-4- piperidyl) propionanilide citrate (1:1).
Fentanyl is a highly lipophilic compound that is freely soluble in organic solventsand sparingly soluble in water (1:40). The molecular weight of the free base is336.5 (the citrate salt is 528.6). The pKa of the tertiary nitrogens are 7.3 and 8.4.
Figure 12.Chemical structure of fentanyl
PHARMACODYNAMICS OF FENTANYL CARDIOVASCULAR SYSTEM
Bradycardia — vagal stimulation in high doses.
No effect on cardiac contractility
Hypotension in large doses due to bradycardia, venodilation and suppression of central sympathetic out flow.
RESPIRATORY SYSTEM
Dose dependent respiratory depression through direct action on medullary Respiratory centre.
Apnoeic threshold increased.
Hypoxic drive decreased
Delayed respiratory depression.
CENTRAL NERVOUS SYSTEM
Analgesia, euphoria, sedation, hyponosis, miosis, nausea, vomiting.
GASTROINTESTINAL SYSTEM
Delays gastric emptying, produces biliary colic.
ENDOCRINE SYSTEM
Attenuation of stress response
PHARMACOKINETIC / PHYSIOCHEMICAL PROPERTIES Property Value
pKa 8.4
% unionized at pH 7.4<10
Percentage bound to plasma protein 84
t 1/2 μ l-2mins
t 1/2 α 10-30mins
t 1/2 β 2-4hour
Vdcc Litre/kg 0.5 - 1.0 Litre /Kg
Vdss Litre/kg 3-5 Litre/kg
Clearance 10-20 mI/kg/mt
Hepatic extraction ratio 0.8-1.0
CLINICAL PROPERTIES
Minimal CSF spread
Rapid onset
Short duration
Low CSF solubility Rapid analgesia
Decreased side effects
Ideal for PCEA
DISADVANTAGES
Systemic absorption
Brief single dose analgesia
When applied intraspinally these opioids should be injected as close as possible to the spinal segments where the previous nociceptive afferent, carrying the nociceptive impulses from the involved dermatomes enter the spinal cord. When this is accomplished small doses of the drug will produce significant analgesia.
PHARMACOLOGY OF EPIDURAL FENTANYL
Dose = 50 -200 μg
Onset = 5—15 minutes
SIDE EFFECTS
Pruritus, sedation, nausea and vomiting, urinary retention, apnoea and seizures,chest wall rigidity.
FACTORS ASSOCIATED WITH RESPIRATORY DEPRESSION
Elderly, poor general condition, concomitant use of other drugs (CNS depressants), the use of hydrophilic opioids. Naloxone 0.25µg/kg/hour attenuating the opioid induced side effects
COMPARISON OF BUPIVACAINE AND ROPIVACAINE(34)
Bupivacaine most widely used LA for Epidural labour analgesia because of its analgesic potency
Inspite of its benefit it can cause prolonged second stage and instumental delivery due to its motor blockade
When accidently injected in to vessel during epidural injection it can produce toxicity,
BUPIVACAINE TOXICITYAND MOTOR BLOCKADE CAN BE REDUCED BY FOLLOWNG METHODS
Bupivacaine can be used in lower conc and more diluted solution 0.0625-0.1%
Before injecting Bupivacaine boluses through epidural catheter exclude intravenous and intrathecal administration by
a. Aspiration of epidural catheter for blood and CSF b. Giving test dose
c. Fractionation of epidural bolus doses
Safe alternate drugs are used like Ropivacaine
Several author compared its efficacy with Bupivacaine in obstetric analgesia
AIM AND OBJECTIVES:
To compare and evaluate efficacy of 0.125% Bupivacaine with Fentanyl 2 µg/ml and 0.125% Ropivacaine with fentanyl 2µg/ml to providing effective Labor analgesia without affecting the progress of Labour.
The following parameters are compared:
Time of onset of analgesia(Min)
Quality of analgesia (VAS)
Sensory level
Motor block (Bromage score)
Maternal hemodynamics(SBP,DBP,SPO2)
Foetal heart rate
Progress of labour(cervical dilatation,Head station,uterine contraction)
Duration of labour analgesia time from epidural to delivery PRIMARY OBJECTIVES:
1. To compare analgesic efficacy of 0.125% Bupivacaine with Fentany 2µg/ml and 0.125% Ropivacaine with fentanyl 2µg/ml in Epidural labour analgesia 2. To compare level of sensory, motor blockade
3. To provide optimal Labour Epidural Analgesia with minimal local anesthetic Concentration
SECONDARY OBJECTIVES:
1. To compare and evaluvate maternal satisfaction, labour progress and outcome, fetal outcome , haemodynamic changes in mother and fetus and maternal satisfaction
2. To increase the margin of safety both mother and fetus during epidural analgesia
REVIEW OF LITERATURE
1. Chethanananda(35), T. N. et al. “Comparative Efficacy of Minimal Concentration of Racemic Bupivacaine (0.0625%) with Fentanyl and Ropivacaine (0.1%) with Fentanyl for Epidural Labor Analgesia.” Anesthesia Essays and Researches11.3 (2017): 583–588. PMC. Web. 18 Apr. 2018 prospective Randomized comparative study between two groups ,Group B(N=30) 0.0625%Bupivacaine and fentanyl 2µg/ml of 10ml, Group R (n=30) Ropivacaine 0.1% and fentanyl 2µg/ml of 10ml, 5ml fractionated doses 5min interval during labour analgesia. Quality of analgesia,haemodynamic variables ,mode of delivery,maternal satisfaction were compared
Conclusion: both Group B and Group R produced equalent analgesia for labour and well tolerated.There is no statistical difference in pain score,sensory level,motor block,mode of delivery,amount of LA consumed,side effects ,maternal satisfaction between the two groups
2. CHINMAYI SURENDRA PATKAR et al(36)
Sixty term primi or second gravida healthy parturients in labor requesting epidural analgesia were recruited in this study. Lumbar epidural catheter was inserted, and analgesia initiated with 0.2% ropivacaine. Patients were randomized to receive ropivacaine 0.1% with fentanyl 0.0002% via either continuous infusion (Group A) or intermittent boluses (Group B) on an hourly basis. If the parturient complained of pain and visual analog scale (VAS) score was >3, an additional bolus of the study drug was
were frequently monitored . Side effects, mode of delivery and neonatal outcome were noted
Conclusion: Intermittent bolus administration provides a more efficacious route of drug delivery when compared to continuous infusion by significantly decreasing the total amount of local anesthetic plus opioid without adversely affecting patient safety or maternal satisfaction
3.M Dressner et al (2000)(37), conducted a randomised double blind study and among 203 parturients and compared 0.1 % bupivacaine and 2mcg/ml fentanyl with 0.22 % ropivacaine and 2mcg/ml of fentanyl. Both groups received 15 ml of loading dose followed by 8 ml/hr of continuous infusion and topups of 10 ml.
Breakthrough pain were treated with escape topups of 10 ml 0.25% bupivacaine Conclusion:ropivacaine group received fewer routine topups and escape topups and there were no differences in motor blockade or mode of delivery between
4. Jaime Fernandez et al (2001)(11), conducted a prospective blind study among 98 labouring parturients who received 0.0625 % bupivacaine and 2mcg/ml fentanyl with 0.1 % ropivacaine and 2mcg/ml fentanyl as infusion .The dose used in both groups were 15ml/hr and topup doses of 5ml if patient perceived pain.
Conclusion: there were no differences in intensity of pain, level of sensory blockade , degree of motorblockade, hemodynamics parameters,
5. SUMIT KALRA et al (2010)(38) compared the efficacy of low concentration of Bupivacaine with Fentanyl and Bupivacaine with Sufentanyl for
epidural labour analgesia. 50 full term parturients received a initial bolus dose of a 10ml of 0.125% Bupivacaine. The patients were randomly divided into two groups:
Fentanyl group (F) received 0.0625% Bupivacaine + 2.5µg/ml Fentanyl. Sufentanyl group (S) received 0.625% Bupivacaine + 0.25µg/ml Sufentanyl. Verbal analogue pain scores, need of supplementary boluses, mode of delivery and maternal satisfaction neonatal APGAR scores were recorded. No significant difference was observed in the 2 groups.
Conclusion:both Fentanyl and Sufentanyl were equally effective in providing labour analgesia with hemodynamic stability, maternal satisfaction without serious maternal / fetal side effects.
MATERIALS AND METHODS
STUDY CENTRE: Government Madurai Medical College, Madurai.
STUDY PERIOD: 6 months
SOURCE OF DATA: Primi gravidacoming for delivery at Government Madurai Medical College Hospital, Madurai.
SAMPLE SIZE: 60 Patient, 30 in each group
STUDY DESIGN: Prospective randamized double blinded comparative study STUDY POPULATION:
Sixty parturients who were admitted to the antenatal ward and who requested pain relief during labour and who fulfilled the criteria were selected for the study. The procedure was explained to them in detail and written consent was obtained from them
ETHICAL REQUIREMENT:
Ethical approval of the study protocol was obtained from the Ethical Committee at the institution before the study was undertaken.
INFORMED CONSENT:
Written informed consent was obtained from each patient in the prescribed format prior to performance of any study related procedures, before physical examination, laboratory screening or any other investigational procedure and before administration of any study related medication. The patients were explained in detail about the nature, procedure and importance of the study.
INCLUSION CRITERIA:
1. primi gravida aged 18-40 Years
2. Adequate pelvis, no cephalopelvic disproportion 3. Single pregnancy with vertex presentation 4. First Stage , Cervical dilatation 3-5cm
5. ASA I & II
EXC LUSION CRITERIA
1. Contrindication to Epidural block
Patient refusal
Hypersensitivity to LA
Infection at insertion site
Coagulopathy 2.Preterm Pregnancy 3.Multiple Pregnancy
4.Previous caesarean section 5.Failed Epidural
PRE PROCEDURAL EVALUATION HISTORY
Obstetric
previous Anaesthesia
Medical diseases
PHYSICAL EXAMINATION Vital Signs- BP, HR, SPO2,RR
SYSTEMICEXAMINATION - RS CVS CNS Airway Spine INVESTIGATIONS
Hemoglobin.
Urine routine examination.
Blood Grouping and typing
Coagulation profile
PRE PROCEDURAL PREPARATION 1.Informed consent
2.Preparaion of mother
Anxiety and fear due to ignorance activate sympathetic system. So giving information regarding labour, delivery, how to feel the painless contraction and how to bearing down during contractions will reduce the anxiety, fear and make the mother actively participate in labour. Before procedure patient should empty her bladder.
3. IV access; 18G intravenous cannula placed in forearm ,500ml Ringer Lactate Started for maintenance
4. Preparation of drugs
Local Anesthetic drugs and opioid
Drugs for hypotension management
Drugs for emergency intubation
Drugs for resusitation
4. Preparation of equipments
Positive PressureVentilation Machine with O2 source
Airway equipments
Ambubag
Defibrilator
Multiparameter monitor
Cardiotocogram
Tilting bed
STUDY PROCEDURE
Patient are randomized into two groups by using computer generated randamization table. Study solution was prepared by the qualified anaesthesiologist who was not involved in patient monitoring or management .Coding was done and same code was written on the drug vial and parturient case record. The study solution was handed over to the investigator. Epidural placement, initial and topup bolus was administered by the investigator. Hemodynamic parameters like blood pressure, heart rate, onset of pain, level of sensory and motor block ade was recoded by a MD Anaesthesia post graduate student who was blinded about the local anaesthetic solution given epidurally. The procedure was clearly explained to the patient.
Anaesthesia machine was checked and all emergency airway equipments like laryngoscopes,blades of different sizes, endotracheal tubes, laryngeal mask airways, oropharyngeal airways were kept ready. An emergency drug tray containing all the emergency drugs were also kept ready.
The patients were shifted to the operation theatre for insertion of the epidural catheter under aseptic precaution. After measuring baseline parameters maternal Bood pressure, peripheral oxygen saturation(spo2),fetal heart rate, uterine contractions, cervical dilatation, fetal head station, visual analogue pain score the patient is placed in lateral position. Under aseptic precaution. L3-L4 interspace skin infiltration was done with 1.5 ml of 2%lignocaine. The epidural space was identified by‘loss of resistance to air’ technique using a 18G Tuohy epidural needle
The depth of epidural space was measured from needle tip in the epidural space to length of epidural needle at skin level, it may be in the range of 3-5.5cm After confirmation by negative aspiration test for blood and CSF 20G epidural multi hole catheter was inserted through the epidural needle and the catheter tip was kept in epidural space 5 cms cranialy. Total length of catheter inserted into the epidural space at the level of skin is addition of epidural space depth plus 5cm. Catheter was tapped firmly to the back. The patient was turned to supine position and left uterine displacement was done and epidural analgesia was maintained with intermittent epidural boluses
TEST DOSE
Previously the test dose of 3ml of lignocaine 1.5% with 1:2,00.000 adrenaline injected through catheter after negative aspiration of blood and CSF. Intrathecal injection is detected by motor blockade within 5 min. Intravascular injection is detected by raise in maternal pulse rate 20-30 beats /min from baseline with in 20-40 seconds
A standard epidural test dose itself will result in augmentation of motor blockade and reduce the possibility of walking. Further, addition of epinephrine to confirm intravascular placement is not reliable in active labour.Intravenous adrenaline can cause uterine vasoconstriction and relaxation of uterine muscle. Test dose can be given for operative delivery(LSCS). Hence test doses were done away. Now recent concept was “EVERY DOSE IS A TEST DOSE” The initial bolus dose 10ml was given in divided doses with 5 minutes interval 3ml of prepared local anesthetic epidural mix ( Bupivacaine0.125% or Ropivacaine 0.125% with fentanyl 2µg/ml) was given as a test dose and look for any intrathecal and intravascular injection.If low dose local anesthetic solution injected intrathecaly it will produce onset of analgesia with in 5 minutes and higher level of sensory blockade it will block thoracic and lumbar and sacral segments. If injected intravascularly it will produce dizziness, ringing in the ears, perioral numbness, metallic taste in the mouth.
Before and after administration of local anesthetic solution check for vitals blood pressor, pulse rate, peripheral oxygen saturation(SpO2) if vitals are stable for 5minutes then give next 7ml of local anesthetic solution.
After initial dose of local anesthetic with the catheter in place mothers were shifted to the labour ward,where they were closely monitored in supine position with left uterine displacement or lateral position till delivery.Mother can change her position every hourly Epidural top-ups were not given till patient complains of pain or discomfort and aspirate before every injection, epidural bolus should be given after
During second stage of labour mother experiencing pain over the perineum that time the local anesthetic dose should be given in sitting position or reverse trendelenburg position to block the sacral segments, patient can be encouraged to push down when crowning of fetal head in the perineum
PARAMETERS MONITORED 1.Oxygen saturation(SPO2)
2.pulse rate (PR)
3.Non invasive blood pressure (NIBP) 4.Foetal heart rate (FHR)
5.Pain score-assessed by visual analogue scale(VAS) 6.Highest level of sensory block by alcohol swab 7.Degree of motor blockade assessed by Bromage scale
Above parameters are measured at 5, 10, 15,20,30,min after that every 30min until delivery
After delivery the following are noted 8. Total dose of Local Anesthetic used 9. Total dose of Fentanyl used
10. Patient satisfaction level 11. The mode of delivery
WALKING EPIDURAL Advantages of walking
Vertical position of uterus ,weight of foetus would dilate the cervix
No Aorto caval compression
Before we ambulate the patient she should be assessed for
Motor blockade
Sensory blockade
Postural hypotension
MOTOR ASSESMENT ABILITY TO AMBULATE
Before ambulation asses the mother for risk of fall by following sequential order 1. Straight leg raise test to asses the leg strength
2. Sit at bed side to rule out postural hypotension and syncope 3. Stand at bedside for leg strength, and hypotension
4. Partial knee bend for leg strength 5. Six unassisted steps for Ambulation
Mother should ambulated with assistant in constant attendance REMOVAL OF CATHETER
Can be done immediately after vaginal delivery epidural analgesia may be extended for operative procedures, instrumental delivery, ceasarean section manual removal of placent and perineal tear repair
AFTER REMOVAL
