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Our view of pain has changed over the centuries as our understanding of this universal condition has improved. Early humans viewed pain as a punishment from the deities for a variety of sins as exemplified by the legend of Prometheus. Prometheus was sentenced by Zeus to eternal torture for giving the fire reserved for the gods to mortals Artist's depiction of Prometheus The seventeenth-century scientist and philosopher, Descartes(Fig. 17.2), changed this view in a single instant by his drawing of a fire burning the foot of a man. Descartes postulated a rational basis for pain premised on the then radical notion that pain was sensed in the periphery and then carried via the nerves and spinal cord to the brain (Fig. 17.3). In 1965, Melzack and Wall2 proposed the gate control theory of pain. The final model, depicted in Figure 1.1D in the context of earlier theories of pain, is the first theory of pain that incorporated the central control processes of the brain. The gate control theory of pain2 proposed that the transmission of nerve impulses from afferent fibers to spinal cord transmission (T) cells is modulated by a gating mechanism in the spinal dorsal horn. This gating mechanism is influenced by the relative amount of activity in large- and small-diameter fibers, so that large fibers tend to inhibit transmission (close the gate), whereas small fibers tend to facilitate transmission (open the gate). In addition, the spinal gating mechanism is influenced by nerve impulses that descend from the brain. Pain may be roughly divided into two broad categories: physiologic and pathologic pain. 1. Physiologic (acute, nociceptive) pain is an essential early warning sign that usually elicits reflex withdrawal and thereby promotes survival by protecting the organism from further injury. 2. In contrast, pathologic (e.g., neuropathic) pain is an expression of the maladaptive operation of the nervous system; it is pain as a disease. Physiologic pain is mediated by a sensory system consisting of primary afferent neurons, spinal interneurons and ascending tracts, and several supraspinal areas. Trigeminal and dorsal root ganglia give rise to high-threshold Aδ and C fibers innervating peripheral tissues (skin, muscles, joints, viscera). These specialized primary afferent neurons, also called nociceptors, transduce noxious stimuli into action potentials and conduct them to the dorsal horn of the spinal cord When peripheral tissue is damaged, primary afferent neurons are sensitized or directly activated (or both) by a variety of thermal, mechanical, and chemical stimuli. Examples are protons, sympathetic amines, adenosine triphosphate (ATP), glutamate, neuropeptides (calcitonin gene–related peptide, substance P), nerve growth factor, prostaglandins, bradykinin, proinflammatory cytokines, and chemokines. These agents lead to opening (gating) of cation channels in the neuronal membrane. Such channels include the capsaicin-, proton-, and heat-sensitive transient receptor potential vanilloid 1 (TRPV1) or the ATP-gated P2X3 receptor. Gating produces an inward currentof Na+ and Ca2+ ions into the nociceptor terminal. If this depolarizing current is sufficient to activate voltage-gated Na+ channels (e.g., NaV1.8), they too will open, thus further depolarizing the membrane and initiating a burst of action potentials that are then conducted along the sensory axon to the dorsal horn of the spinal cord. Thereafter, these impulses are transmitted to spinal neurons, the brainstem, the thalamus, and the cortex. Transmission of input from nociceptors to spinal neurons that project to the brain is mediated by direct monosynaptic contact or by multiple excitatory or inhibitory interneurons. The central terminals of nociceptors contain excitatory transmitters such as glutamate, substance P, and neurotrophic factors that activate postsynaptic N-methyl-D-aspartate (NMDA), neurokinin, and tyrosine kinase receptors, respectively. Repeated nociceptor stimulation can sensitize both peripheral and central neurons (activitydependent plasticity). In spinal neurons such a progressive increase in output in response to persistent nociceptor excitation has been termed “wind-up.” Later, sensitization can be sustained by transcriptional changes in the expression of genes coding for various neuropeptides, transmitters, ion channels, receptors, and signaling molecules (transcription-dependent plasticity) in both nociceptors and spinal neurons. INFLAMMATION/NOCICEPTIVE Peripheral Sensitization Central Sensitization Damaged Zone ALLODYNIA HYPERALGESIA Sensitization and activation COX1 - COX2 BK2 - BK1 PGs, H+ CNS ATP NGF blood vessel C-fibre SP, CGRP BK 5HT Vasodilation+plasma extravasation Transmitter release - neuronal excitability Spike firing frequency After Before Increased suprathreshold firing Spontaneous firing Stimulus intensity Reduced threshold Tissue damage Hyperalgesia PERIPHERAL ACTIVITY Nerve damage Spontaneous pain Allodynia CENTRAL SENSITIZATION Decreased threshold to peripheral stimuli Increased Expansion of spontaneous activity receptive field Important examples include the NMDA receptor, cyclooxygenase-2 (COX-2), Ca2+ and Na+ channels, and cytokines and chemokines expressed by neurons and glial cells. In addition, physical rearrangement of neuronal circuits by apoptosis, nerve growth, and sprouting occurs in the peripheral and central nervous systems. Concurrent with the events just described, powerful endogenous mechanisms counteracting pain unfold both in the periphery and in the central nervous system. In injured tissue this occurs by interactions between leukocyte-derived opioid peptides and peripheral nociceptor terminals carrying opioid receptors [10] [11] and by the action of anti-inflammatory cytokines. Inflammation of peripheral tissue leads to increased expression, axonal transport, and enhanced G protein coupling of opioid receptors in neurons of the dorsal root ganglia. These phenomena are dependent on sensory neuron electrical activity, production of proinflammatory cytokines, and the presence of nerve growth factor within the inflamed tissue. In parallel, opioid peptide–containing immune cells extravasate and accumulate in the inflamed tissue. These cells upregulate the gene expression of opioid peptide precursors[15] and the enzymatic machinery for their processing into functionally active peptides. In response to stress, corticotropin-releasing factor, cytokines, chemokines, or catecholamines, leukocytes secrete opioids, which then activate peripheral opioid receptors and produce analgesia by inhibiting the excitability of nociceptors or the release of excitatory neuropeptides, or both The clinical relevance of these mechanisms has been shown in studies demonstrating that patients with knee joint inflammation express opioid peptides in immune cells and opioid receptors on sensory nerve terminals within synovia .After knee surgery, such patients exhibited significantly enhanced postoperative pain and analgesic consumption when the interaction between opioid peptides and receptors was blocked by intra-articular application of the antagonist naloxone. In the spinal cord, inhibition is mediated by the release of opioids, γ-aminobutyric acid (GABA), or glycine from interneurons, which then activate presynaptic opioid or GABA receptors (or both) on central nociceptor terminals to reduce the release of excitatory transmitters. In addition, opening of postsynaptic K+ or Clchannels by opioids or GABA, respectively, evokes hyperpolarizing inhibitory potentials in the dorsal horn neurons. During ongoing nociceptive stimulation, spinal interneurons upregulate gene expression and the production of opioid peptides. Powerful descending inhibitory pathways from the brainstem also become active by operating mostly through the noradrenergic, serotonergic, and opioid systems. A key region is the periaqueductal gray matter. It projects to the rostral ventromedial medulla, which then projects along the dorsolateral funiculus to the dorsal horn. Integration of signals from excitatory and inhibitory neurotransmitters with cognitive, emotional, and environmental factors (see later) eventually results in the central perception of pain. When the intricate balance among biologic, psychological, and social factors becomes disturbed, chronic pain can develop. Clinical definition of pain1 “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage... 1. IASP Pain Terminology. In Merskey H & Bogduk N eds. Classification of Chronic Pain, Second Edition, IASP Task Force on Taxonomy. IASP Press, Seattle 1994:209-14. درد یک ترکیب فیزیولوزی و رویداد احساسی است و یک حس ساده و آسان نیست. درد شامل: تجربه حسی ناخوشایند رویداد عاطفی ناخوشایند ترکیبی از عناصر اجتماعی-روحی و معنوی ایجاد دپرشن برانگیختن اضطراب تداخل با عملکرد اجتماعی تاثیر منفی بر توانایی جسمی ممانعت از حرفه و شغل کاهش درآمد ترغیب به انزوا و گوشه گیری آسیب به کیفیت روابط اجتماعی ایجاد ناهماهنگی و استرس در خانواده ایجاد تزلزل در ایمان و اعتقاد Good pain management will aid the treatment of future pain Physical Pain Previous/multiple or Progressive pains Other Physical Symptoms Psychological Problems Failure to recognise & treat psychological distress is a common cause of unrelieved pain Palliation of other symptoms will improve pain control Social Difficulties Spiritual Concerns Cultural Issues Clinical Pain What the patient says it is What must be treated Culturally appropriate management & circumvention of language barriers may lessen pain دردی است ناشی از تحریک اعصاب محیطی که با یک سیستم عصبی غیرمعیوب منتقل شده.ایمپالس های درد وارد طناب نخاعی می شوند در مسیر شاخه دورسال جایی که به مراکز باالتر در مغز صعود می کنند.ایمپالس های مهارکننده ,انتقال در شاخه دورسال در طناب نخاعی را بلوک می کنند و از انتقال بعدی ایمپالس های درد جلوگیری می کنند.این دردها معموال به اپیوئیدها حساس می باشند و پاسخ نشان می دهند شامل: :Peripheral pain درد نوروپاتیک محیطی توسط آسیب سیستم عصبی محیطی ایجاد شده و اغلب اطراف عصبی که آسیب دیده ,منطقه ای با حساسیت تغییر یافته وجود دارد. :Central pain درد نوروپاتیکی است که ناشی از آسیب سیستم عصبی مرکزی می باشد و معموال یک ناحیه با حساسیت تغییر یافته آمیخته با ناحیه درد وجود دارد.یک حادثه سربرو واسکوالر یا آسیب طناب نخاعی ممکن است مرتبط با درد سنترال باشد Nociceptive pain Transient pain in response to noxious stimuli › Inflammatory pain Spontaneous pain and hypersensitivity to pain in › response to tissue damage and inflammation Neuropathic pain Spontaneous pain and hypersensitivity to pain in › association with damage to or a lesion of the nervous system Woolf. Ann Intern Med. 2004;140:441-451. Is responsive to NSAID’s, coxibs, and opiates Noxious paracetamol Peripheral Stimuli Pain-Autonomic Response Heat - Withdrawal Reflex Cold Intense Mechanical Force Nociceptor Sensory Neuron Brain Chemical Irritants Spinal Cord Woolf. Ann Intern Med. 2004;140:441-451. Is responsive to NSAID’s,coxibs, paracetamol, and opiates Inflammation Macrophage Mast Cell Neutrophil Granulocyte Spontaneous Pain Pain Hypersensitivity -Allodynia -Hyperalgesia Nociceptor Sensory Neuron Brain Tissue Damage Spinal Cord Woolf. Ann Intern Med. 2004;140:441-451. Spontaneous Pain Pain Hypersensitivity Peripheral Nerve Damage May respond to• local anaesthetic• anticonvulsants• antidepressants • Brain Stroke Less responsive to opioids• Spinal Cord Injury No response to NSAID’s, coxibs, or • paracetamol . Woolf. Ann Intern Med. 2004;140:441-451 Perception Is responsive to NSAID’s,coxibs, paracetamol and opiates Modulation Transmission Transduction Reuben et al. J Bone Joint Surg. 2000;82:1754-1766. Acute Pain Increased sympathetic activity GI effects Splinting, shallow breathing Increased catabolic demands Anxiety and fear Peripheral/ central sensitization Myocardial O2 consumption GI motility Atelectasis, hypoxemia, hypercarbia Poor wound healing/muscle breakdown Sleeplessness, helplessness Available drugs Myocardial ischemia Delayed recovery Pneumonia Weakness and impaired rehabilitation Psychological Chronic pain Courtesy of Sunil J Panchal, MD Pain pathway and modulation1 Ascending nociceptive pathways Interpretation in cerebral cortex: pain Activation of serotoninergic and noradrenergic pathways Stimulation of nociceptors (A and C fibers) / Release of neurotransmitters and neuromodulators (i.e. PG) Histamin,bradikinin, serotonin Descending inhibitory controls / Diffuse noxious inhibitory controls Injury Release of serotonin, noradrenalin and enkephalins at spinal level The Anatomy and Physiology of Labor Pain ‘LABOUR can be defined as spontaneous painful uterine contractions associated with the effacement and dilatation of the cervix and the descent of the presenting part’ Pain is a noxious and unpleasant stimulus— produces fear and anxiety. Unrelieved stress in labour produces increased plasma cortisol and catecholamine concentrations. Leads to reduction in utero-placental blood flow. Effective pain relief reduces plasma noradrenaline, prevents the rise during first & second stage of labour. Prevents metabolic acidosis by reducing the rate of rise of lactate and pyruvate. Decreases maternal O2 consumption by 14%. First stage pain is due to uterine contractions causing stretching, tearing and possibly ischaemia of the uterus and dilatation of the cervix. Second stage pain is caused by distension of pelvic structures and perineum following descent of the presenting part. First stage: early, active, transition Dilatation › Second stage Pushing and birth › Third stage Delivery of placenta › Fourth stage Postpartum › Uterine contractions: o Myometrial ischemia o Causes release of potassium, bradykinin, histamin, serotonin Distention of lower uterine segments and o cervix Stimulates mechanorecoptors o Impulses follow sensory-nerve fibers from paracervical and hypogastric plexus to lumbar sympathetic chain Enter dorsal horn of spinal cord at T10-12, L1 Transition associated with greater o nocioceptive input related to increased somatic pain from vaginal distention Distention of vagina, perineum, pelvic floor, o stretching of pelvic ligaments Pain signal transmitted to spinal cord via S2-S4 o (includes pudendal nerve) Pathways of Placement of Anesthetics for Labor Pain Eltzschig H et al. N Engl J Med 2003;348:319-332 From onset of regular uterine contractions to full dilation of cervix. .I From full cervical dilation to delivery of the fetus. .II From delivery of the fetus to delivery of the placenta. .III METHODS OF PAIN RELIEF IN LABOR NON-PHARMACOLOGICAL METHODS PHARMACOLOGICAL METHODS ADVANTAGES—Drugs administered may cross the placenta and depress the fetus. Any method that avoids or restricts their use deserves attention. LAMAZE Preparation It is not just a birthing method but a birthing philosophy. A psycho prophylaxis in labor. HYPNOSIS based on the power of suggestion. self-hypnosis or receive assistance from a hypnotherapist. training sessions are required. Many methods are based on the work of Grantly DickRead, MD, ACUPUNTURE Generally two local points and two distal points on the arms or on the legs are selected. Begin Acupuncture 4 weeks before the expected time of delivery. Needles are placed once a week using the specific points. Points LI.4 Hegu, SP.6 Saninjiao, Extra Neima PC 6 (Neiguan), Du.20,Du.2,Du6, GB.21, He.7(shenmen) Beneficial in patients with moderate to severe contraction pains in an otherwise reasonably normal labor. Very popular in Europe. Easy to apply, non-toxic and frequently effective. 4 electrodes are placed one on either side of the spine in the lower thoracic region (T 10) and one on either side of the spine in the sacral area. The patient may control up to 3 levels of intensity of stimuli, and she can switch it off if she wishes. Mechanism of action: Inhibits transmitter release along pain pathway by stimulating the myelinated Aβ fibres of the spinal nerve roots T10-L1 & S2-4. Neuronal release of Endorphins in to the CSF may result in a feeling of well being as well as analgesia. Regional Analgesia SPINAL ANALGESIA EPIDURAL ANALGESIA COMBIND SPINAL EPIDURAL CAUDAL PUDENDAL PARACERVICAL Systemic Analgesia Intra Venous Analgesia Inhalational Analgesia Entonox (50:50 N2O/O2) Isoflurane ( 0/2%) Enflurane (0/2%) Desflurane (0/2%) LIMITED USE Drowsiness ,Unpleasant smell, High cost, Accidental overdose N2O does not interfere with uterine contractions. No effect on fetus too. Premixed nitrous oxide &oxygen. N2O 50% and O2 50%. ENTONOX-cylinders with a capacity of 500 L are available. Inhalation should begin 45 seconds before the onset of pain. If the patient holds her mask -it will fall from her hand, should unconsciousness supervene . (safety factor) OPIOIDS PETHIDINE (MEPERIDIN) FENTANYL SUFENTANIL REMIFENTANIL MORPHINE PENTAZOCINE NALBUPHINE TRAMADOL SEDATIVE-TRANQUILIZER BENZODIAZPINES BARBITURATE KETAMINE PROMETHAZINE Ketamine 0.5 to 1 mg/kg every 5 min Remifentanil 0.4 μg /kg lockout 1 min Promethazine 25-50 mg Tramadol 1 mg/kg/Im Active phase, dilatation 3-4cm, fully effaced A. Sympathetic From T 6- L 2. Motor to upper uterine segment via splanchnic nerves & coeliac, aortic, renal &hypogastric plexuses and then to great cervical ganglion of Frankenhauser. B. Visceral afferent T 11-L 1 Sensory from uterus Block of these eases pain of first stage of labour. C. Visceral afferent & efferent Parasympathetic Sensory and Motor to cervix Inhibitory to uterus S2,3,4. The 33 articles selected included 14 studies, 1 metaanalysis, and 2 systematic reviews obstetrics in rural and small urban centers might find single-dose ITN a useful alternative to parenteral or epidural analgesia for appropriately selected patients. A combination of 2.5 mg of bupivacaine, 25 μg of fentanyl, and 250 μg of morphine intrathecally usually provides a 4 hour painless window. The Cochrane Library Date review completed: pre 2004 Number of trials included: 16 Control group: various non-epidural analgesic interventions Main outcomes: pain relief better than cobntrol group Placement of epidural catheter Test dose 3ml of lidocaine 1.5% with adrenaline (?) Initial loading dose 10ml of bupivacaine 0.25% or lidocaine 1% and fentanyl 50 μg . Does Epidural Analgesia Increase the Incidence of Cesarean Section? NO Does Epidural analgesia prolong labor ? NO American Journal of Obstetrics and Gynecology 171(5), 1994, 1398 Anesthesiology 80(6), 1201-1208, 1994 American Journal of Obstetrics and Gynecology 185(1), 2001, 182-134 Test dose : 3 ml of 0.125% Bupivacaine Blouse : 8ml of 0.125% Bupivacaine + 50 μg of Fentanyl. Maintenance: 0.125% Bupivacaine +2 μg /ml Fentanyl at the rate of 10ml/h 3ml/5min P.R.N 3 times for breaking through pain upon patient request PATIENT CONTROLLED ANALGESIA EPIDURAL (PCEA) INTRAVENOUS (PCA) COMBINED SPINAL EPIDURAL (CSE) Advantages: Ability to minimize drug dosage .1 Flexibility and benefits of self-administration .2 Reduced demand on professional time .3 0.0625% Bupivacaine +Fentanyl 2 μg /ml Demand dose: 3ml , Lockout interval 6 min Background infusion 6 ml/h 3ml/5min P.R.N 3 times for breaking through pain upon patient request 0.125% Bupivacaine with 1:400,000 Epinephrine Plus Fentanyl 2 μg /ml 2ml bolus /10min lockout interval 3ml bolus/15min lockout interval 4ml bolus/20min lockout interval 6ml bolus/30min lockout interval Needle” through “Needle” “ Back “ eye” Needle” through “Needle” technique is the best Can be placed in lateral or sitting position Walking Epidural possible Rapid onset of analgesia Reliable, fewer failed or patchy blocks Effective sacral analgesia in advanced labor Less motor block Better patient satisfaction Aids epidural localization in difficult backs Faster cervical dilation in early nulliparas Placement of epidural catheter Test dose 3ml of lidocaine 1.5% with adrenaline (?) Initial loading dose 10ml of bupivacaine 0.25% or lidocaine 1% and fentanyl 50 μg . Start the infusion as soon as adequate anesthesia is achieved. Initial infusion rates are - bupivacaine 0.25% 8-12 ml/hr or lidocaine 0.5% 10-15 ml/hr. PCEA: 20ml BUP 0.125% + fentanyl 2mcg/ml, then 6 ml/hr infusion, 6ml bolus, 15min lockout CSE: 2.5mg BUP + fentanyl 25mcg No test dose, start PCEA PCEA: 0.0625% + 2 mcg/ml fentanyl. 15ml/hr basal infusion, 5ml bolus, 10min lockout, 30ml/hr max. If patient requires manual rebolusing they change to 0.11% BUP CSE: early labor 25mcg fentanyl + test dose Regular labor or multip: 15mcg fentanyl + › 2.5mg BUP + test dose. Start PCEA CSE: 2.5mg BUP + 25mcg fentanyl No test dose Infusion started Ropivacaine 0.1% + SUF 0.5mcg/ml Test dose + 5ml loading dose › PCEA: 4ml doses, 20min lockout › CEI: 6ml/hr › Rescue: 5ml if VAS > 5 › No epidural before cervical dilatation of 4 cm No epidural in the second stage IV hydration before/during epidural Bupivacaine 0.0625% ± fentanyl 2μg/ml Infusion rate 8~15 ml/hr ± initial loading 5~10 ml Essentially nurse-control analgesia Van Gessel et al. demonstrated that 59% of dural punctures were performed 1 or 2 spaces higher than assumed Broadbent et al. demonstrated in a group of experienced anesthesiologists that when they believed they were at L3-L4, in 85% of the cases the space was 1 to as many as 4 segments higher A.ABSOLUTE Maternal refusal Coagulation disorders Local sepsis Patient on anti-coagulant therapy B.RELATIVE Shock Hypovolaemia Neurological disease Previous spine surgery Difficult anatomy C.MISCELLANEOUS Inexperienced anesthetist Inadequate supervision, facilities, apparatus and personnel Very obese patients Allergies to local anesthetic drugs Immediate Hypotension Urinary retention Local anestheticinduced convulsions Local anestheticinduced cardiac arrest Delayed Postdural puncture headache Transient backache Epidural abscess or meningitis A.MATERNAL Needle or catheter-insertion Wrong place Penetrates blood vessels,dura,neural tissue. Broken catheter. Injection Sub-arachnoid Intravascular Adverse reaction to local anesthetics Neural blockade Hypotension Motor blockade Bladder dysfunction Shivering. Inadequate Anaesthesia Total failure Partial failure Progress of labour Prolongs labour Increased instrumental deliveries. A. BLOODY TAP: Epidural venous plexuses are distended during pregnancy. Accidental intravenous injection causes— Hypotension .1 Convulsions .2 Unconsciousness. .3 B. DURAL PUNCTURE: Incidence-13% (in the hands of inexperienced anesthetist) Sequelae of dural puncture PDPH .1 Sub-dural or extradural haematoma .2 Total spinal block. .3 NEUROLOGICAL Injury to peripheral nerves Femoral & common peroneal nerve HEADACHE- Post-dural puncture headache (PDPH). Concentration (%) Dose (mg*segment-1) Onset (min) Duration (min) Chloroprocaine 2-3 45 5-15 30-90 Lidocaine 1-2 25 5-15 60-120 10-20 120-140 Bupivacaine 0.25-0.75 7 Ropivacaine 0.25-.75 9 10-15 120-160 Visceral pain comes from outer covering of abdominal viscera which are innervated by autonomic nervous fibres , pain is due to distension or muscular contraction of a viscera It is typically vague , dull and nauseating , percieved in areas corresponding to embryonic dermatome origin Somatic pain comes from parietal peritoneum which are innervated by somatic nervous fibres pain is due to irritation from inflammation ,infection , chemical It is typically sharp and well localised Referred pain is pain percived distant from its source and result from convergence of nerve fibres at spinal cord Usually performed by obstetrician Blocks the visceral afferent nerve fibres that pass through the paracervical ganglion of Frankenhauser Gives good analgesia without motor blockade Does not block the progress of labour Disadvantages: Does not provide perineal analgesia High incidence of fetal bradycardia-due to high levels of local anesthetic entering the uterine artery and reaching the fetus Trauma to fetal scalp or maternal vagina. Indirectly by changes in uterine blood flow Effect exerted directly by local anesthetic drugs Changes in uterine contractility Epidural blockade-produces fall in fetal oxygenation-if hypotension is allowed to develop If MAP remains<70mmHg for more than 3 hrsneonatal neuro – behaviour will be impaired. Usually performed by obstetrician Provides good analgesia for somatic perineal pain in the second stage of labour. Disadvantages: Trauma to mother & fetus Accidental intravascular injection into the adjacent pudental vessels Vaginal & ischiorectal haematoma Retropsoal & subgluteal abscess. Newer drugs for epidural: Sufentanil---- potent opioid Levobupivacaine—less motor blockade Ropivacaine----- less motor blockade Walking epidurals Increased maternal comfort Improved neonatal outcome Ability to walk & change positions in bed are supporting reasons for walking epidurals. CONTINUOUS SPINAL ANALGESIA Using micro catheters--- 28 G. Loading dose: 11ml Ropivacaine 0.2% Maintenance: 6ml/h Ropivacaine 0.1% plus Fentanyl 2 μg /ml Demand dose of 5ml,lockout interval 10min Maximum 31ml Epidural initiated: 8 ml 0.25% BUP 0.125% BUP PECA: 4 ml basal, 4 ml bolus, Lockout 20 min, 16 ml/hr max CIEA: 12 ml/hr infusion