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Chapter 10
PATIENT-CONTROLLED ANALGESIA Jennifer A. Elliott
INTRODUCTION Patient-controlled analgesia (PCA) has been in use for the management of pain since the early 1970s. This technique has historically been used in the provision of intravenous opioids for pain control. Since the late 1990s, a variety of new forms of PCA have been developed, including patient-controlled epidural analgesia (PCEA), patient-controlled regional analgesia (PCRA), patientcontrolled oral and intranasal analgesia, and patient-controlled transdermal fentanyl (currently in development). Just as options for patient-controlled delivery have expanded, monitoring capabilities for the prevention of adverse events related to the use of these techniques have become more sophisticated. PCA is employed in the management of pain from a variety of conditions, including surgical pain, cancer-associated pain, and pain related to disorders such as sickle cell anemia and pancreatitis. These techniques can be used in a wide array of patients, including those at extremes of age. It is important to recognize that whereas these techniques typically allow for excellent pain control and patient satisfaction, they are not without risk. Certain patient populations—such as those with obstructive sleep apnea, chronic obstructive pulmonary disease, and renal dysfunction—may be more predisposed than others to potential adverse events with the use of PCA. Likewise, these techniques may not be appropriate for some individuals such as those with significant cognitive dysfunction. When selecting a PCA technique, the practitioner must do so with an understanding of the pharmacokinetics of the agent employed and of patient characteristics that may increase the potential for adverse events. In addition, caregivers must be alert to potential technical and programming errors that may occur and must appropriately monitor for evidence of adverse effects. PCA can be very satisfying for both patient and provider if these principles are observed.
PATIENT SELECTION AND POTENTIAL ADVANTAGES OF PCATHERAPY PCA can be a highly effective means of pain reduction. Successful use of this modality depends upon proper education of both prescriber and patient. Practitioners must appropriately select dosing parameters, and patients must understand how to use the device in order to achieve desired levels of analgesia. This mode of analgesia has been used with success in a wide range of populations including those at extremes of age.1,2 When PCA is considered for use in a patient, it must be ascertained that the individual understands how to use the device and is physically capable of activating the demand button. Practitioners must also take into consideration some psychological factors that may influence a patient’s satisfaction with this type of analgesia.
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Some patients find the autonomy involved in self-directed analgesia to be comforting, whereas others may prefer nurse-delivered analgesia and may find the idea of self-delivered analgesia to be anxiety provoking. Fear of addiction or inadvertent overdosage may also cause underutilization of PCA by some individuals, which may thereby result in inadequate analgesia.3 Traditional intermittent (as-needed) parenteral analgesia involves the administration of relatively large doses of opioid in order to achieve sustained serum opioid levels above the minimum effective analgesic concentration prior to the next dosing interval. Unfortunately, this technique results in wide fluctuations in serum opioid concentration. As a consequence of these wide swings in serum opioid concentrations after intermittent parenteral administration, patients may experience adverse effects of nausea or sedation as opioid concentrations peak and inadequate analgesia as opioid concentrations drop off prior to the next dose. PCA allows for more frequent administration of smaller analgesic doses and, thereby, may reduce the degree of fluctuation in serum opioid concentrations and attendant undesired effects.4 Many studies have been performed to evaluate whether there are advantages to the use of PCA over those of conventional intermittent intramuscular opioid administration for postoperative pain management.5–8 Several of these studies do not seem to indicate significant differences between these two modalities when assessing opioid consumption, adverse effects, or length of postoperative hospitalization. However, the vast majority do demonstrate increased patient satisfaction with use of PCA. Some studies indicate that postoperative pulmonary complications may be reduced when PCA is employed, and patient participation in postoperative rehabilitation may be enhanced as well.9–11 Some drawbacks to intramuscular analgesia that have been cited include unpredictable drug absorption and pain with administration that might result in decreased usage, especially among pediatric patients. These factors may result in suboptimal postoperative analgesia.12
PCA DEVICES PCA devices consist of a pump connected to a timer. The medication to be delivered is housed in a secure portion of the device that is accessible with the use of a key or the entry of a numerical combination on a keypad. The medication is delivered to the patient via tubing connected from the medication syringe or cartridge to an intravenous (or other applicable) catheter. The patient is able to use the device by activating a button connected to the PCA pump by a cord. Safety features incorporated into PCA devices include alarms to alert to the presence of an empty syringe, low battery, tubing occlusion, or air entrainment. The keypad used by health care professionals to program the PCA device is locked during device use to prevent dose tampering by patients or visitors. Reprogramming the device to reflect changes in the analgesic prescription typically requires use of a key or the keypad entry of a numerical combination.
PCA SETUP When initiating PCA, the drug to be employed must be selected and several dosing parameters must be established.13 The settings that must be chosen when starting PCA include a loading dose, a demand dose, a lock-out interval, and a bolus dose
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Chapter 10 PATIENT- CONTROLLED ANALGESIA
(an additional dose that can be delivered by nursing personnel if pain is uncontrolled). In addition, a continuous infusion and 1- or 4-hour maximum dose limit can be selected if desired.
device, as might occur with sleep. Effective bolus doses usually amount to two to three times the programmed demand dose. Bolus doses may be given as often as necessary. If frequent bolus doses are needed, adjustment of the demand dose should be considered.
Medications Used in PCA Several opioids are currently available for use in PCA. The most commonly employed agents include morphine, fentanyl, hydromorphone, and meperidine. Methadone, oxymorphone, and alfentanil have also been administered via PCA. Factors that may influence the selection of opioid include patient disease states that might influence drug metabolism or enhance the risk for opioidrelated toxicity and any history of adverse effects from prior exposure to a particular opioid. In general, meperidine is not used by most pain management practitioners for PCA owing to potential adverse effects from one of its metabolites, normeperidine, with repeated exposure to this drug. Normeperidine accumulation can result in neuroexictatory activity, including seizures. The risk of such events occurring increases when meperidine is administered in large doses (>600 mg in 24 hr) and when it is repeatedly given over a period exceeding 24 hours. The risk of toxicity from this drug is most significant among patients with renal insufficiency, and therefore, use of meperidine in this patient population is not advised.
Loading Dose A loading dose is typically administered at the time of initiation of PCA as a means of quickly achieving a serum opioid concentration that provides effective pain control. After administration of a loading dose, patients can then self-administer additional opioid doses via the demand mode to maintain satisfactory analgesia. A loading dose should generally be prescribed when patients are experiencing significant pain upon starting PCA because use of the demand feature alone is unlikely to allow for timely establishment of sufficient analgesic serum opioid concentrations. Loading doses can be given before PCA is initiated as multiple small opioid doses, repeated at frequent intervals until adequate analgesia is achieved (e.g., in the postanesthesia care unit [PACU]). It is vitally important to understand that PCA should be initiated only after the patient has achieved pain relief that is ‘‘in the ballpark of adequate analgesia.’’
Demand Dose The demand dose is the dose of opioid delivered each time the patient activates the PCA button, except during the established lock-out interval. The size of the demand dose selected may be influenced by factors such as age, weight (in pediatric patients), and any preexisting opioid tolerance. In general, elderly patients may respond well to lower demand doses, whereas chronic opioid users will require higher demand doses than the average adult patient. Adjustment of the demand dose may be required if evaluation of the patient’s utilization of the PCA reveals a high rate of demands.
Bolus Dose A bolus dose is an extra dose of medication that can be delivered by nursing personnel for inadequately controlled pain. A typical scenario in which a bolus dose may need to be administered is movement-associated pain, such as when a patient participates in physical therapy. A bolus may also be necessary when a long period has elapsed between demand activations of the PCA
Lock-out Interval A lock-out interval is the period of time that the PCA device is unable to deliver further demand doses after activation of the demand button. This is usually set in a range of 5 to 10 minutes. Setting a lock-out interval allows the patient to appreciate the effects of the delivered opioid dose prior to administration of another dose. The lock-out serves as an integral safety feature of PCA in that it prevents rapid stacking of doses on top of one another, as might otherwise occur if dosing was achieved every time a patient attempted to activate the device. This significantly limits the potential for inadvertent drug overdosage that could result from robust attempts to achieve rapid analgesia by repeatedly activating the demand button. When assessing the patient’s pattern of analgesic use, caregivers should observe the frequency of demands the patient is attempting to obtain in addition to the actual opioid consumption. This will typically appear as ‘‘demands’’ or ‘‘attempts’’ when reviewing the PCA device history feature. If the number of ‘‘demands’’ or ‘‘attempts’’ appears high compared with the actual number of doses delivered, the patient may need to be reeducated about how PCA works, with a reminder about the lock-out interval. If both ‘‘demands’’ or ‘‘attempts’’ and actual number of opioid doses administered appear frequent, the demand dose may need to be increased to allow for enhanced analgesia.
Continuous (Basal) Infusion A continuous (basal) infusion can be added to PCA if desired. This will be delivered regardless of patient demands. Few studies indicate a distinct advantage to the use of continuous infusions, although some believe analgesia may be better maintained with the use of basal infusions, particularly when patients are not able to activate the demand feature such as during periods of sleep. Total opioid consumption may be increased in the presence of basal infusions. There is some concern that use of continuous infusions increases the likelihood of PCA-related adverse events, with particular concern for the possibility of respiratory depression. The primary indication for use of basal opioid infusions is as a substitution for chronic baseline opioids when opioid-tolerant patients are unable to continue their regular pain medications.
One- or 4 -Hour Maximum Dose Limits can be placed on the total opioid delivered in a specified time interval. Most commonly, a 4-hour maximum dose is selected when such restrictions in dosing are desired. Setting a dose limit may be of particular importance when meperidine is employed in PCA. Owing to the potential for accumulation of normeperidine, as previously described, doses of meperidine should not exceed 600 mg in 24 hours. If dosing limits are not set, it might be fairly easy to exceed such a total daily dose with the typical dosing parameters selected for this agent when initiating PCA. Setting a 1- or 4-hour dosing limit may also provide some protection against overdosage in the event of other programming errors. However, 1- or 4-hour limits can also result in inadequate analgesia in patients requiring large amounts of opioid because restrictive limits may cause them to be ‘‘locked-out’’ from further doses for extended periods and can cause such individuals to be dissatisfied with their analgesic therapy (Table 10–1).
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Table 10^1. Current Therapy: Patient-Controlled Analgesia Setup Parameter
Setting Range
Loading dose*
Morphine 5–10 mg Meperidine 100–150 mg Fentanyl 50–100 mcg Hydromorphone 0.5–1.0 mg Morphine 1.0–1.5 mg Meperidine 10–15 mg Fentanyl 10–15 mcg Hydromorphone 0.1–0.2 mg 5–10 min 2–3 times the selected demand dose This setting is not routinely used by many pain practitioners, but if a continuous infusion is desired, typical initial doses are Morphine 1 mg/hr Meperidine 10 mg/hr Fentanyl 10 mcg/hr Hydromorphone 0.1 mg/hr Setting a 4-hour dosing limit is optional with most agents, but a limit of 100 mg every 4 hr is advisable for meperidine (total daily doses should not exceed 600 mg)
Demand dose*
Lock-out interval Bolus dose Continuous dose
1- or 4-hr maximum dose limit
*These parameters reflect average ranges for opioid-naı¨ve patients. Opioid-tolerant patients may require larger doses, and frail or elderly patients may require smaller doses.
MONITORING OF THE PATIENT RECEIVING PCA As with any form of medical therapy, patients receiving PCA require appropriate monitoring to ensure efficacy of treatment and to manage any possible adverse effects.14 Assessment of the patient’s pain should be made using such tools as verbal ratings, visual analog pain scales, or the FACES pain rating scale in the pediatric setting. In conjunction with pain assessment, opioid consumption should be quantified and the PCA device history should be reviewed to evaluate how effectively the patient is using it. If it is apparent that the patient is frequently attempting to activate the demand button but the actual number of opioid doses delivered is low, patient reeducation on proper use of the device may be indicated. Conversely, if the patient has been activating the device successfully and complains of inadequate pain control despite a high rate of opioid delivery, adjustment of the demand dose may be appropriate. It is always advisable to assess patients for evidence of easily remediable sources of pain, such as a distended bladder, when contemplating whether dose increases are necessary to enhance pain control. Patients receiving PCA must be observed for evidence of adverse effects related to their pain treatment. Vital signs with attention to respiratory rate should be monitored regularly. Oxygen saturation monitoring is often used in conjunction with PCA, although desaturation is a late indicator of adverse respiratory effects from opioid therapy. Perhaps most valuable as an early clinical indicator of opioid toxicity that could progress to respiratory depression is diminished level of consciousness. For this reason, it is important to assess patients for evidence of sedation while receiving PCA. Sedation scales are used to indicate whether patients are awake, drowsy, sleeping but easily arousable, or difficult to arouse.
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If a patient’s level of consciousness declines while receiving PCA, dose adjustment or termination of opioid administration may be indicated. An emerging means of surveillance for evidence of developing respiratory depression is the use of end-tidal carbon dioxide (ETCO2) monitoring, which is discussed further later in this chapter. Other possible side effects of PCA that should be addressed if present include nausea, pruritus, and constipation. Certain patient populations deserve additional mention with regards to monitoring for adverse effects when receiving PCA. Patients with various underlying organ dysfunctions may be at higher risk of toxicity related to opioid administration. Any patient with severe hepatic or renal disease may have decreased capacity to metabolize or excrete opioids and may, therefore, be susceptible to opioid accumulation with attendant toxic effects. Pulmonary reserve may be compromised in patients with chronic obstructive pulmonary disease when using PCA, and patients with obstructive sleep apnea may exhibit increased sensitivity to the sedative effects of opioids. In addition, significant hypotension can increase sensitivity to opioid effects. This may relate to decreased cerebral perfusion, resulting in increased drug effects. Decreased renal and hepatic blood flow under this circumstance may also contribute to prolongation of opioid effects. Hypotension related to hypovolemia may be exacerbated by opioid administration owing to vasodilatory effects of some opioids as well as diminished sympathetic nervous system outflow resulting from relief of pain. Vigilance should be heightened for the occurrence of adverse effects from opioid therapy in any of these patient populations (Box 10–1).
POTENTIAL SOURCES OF PCA-RELATED ADVERSE EVENTS There are many potential causes of PCA-related adverse events.15,16 Undesired effects can occur from opioid use, particularly in patients with comorbid conditions that have been described previously. Use of concomitant sedatives with PCA can result in oversedation. In addition, human error and mechanical malfunctions of the PCA device can result in adverse events. Operator errors, such as improper device setup and programming, and user-related errors, such as device tampering or PCA by proxy, are potential human errors that can result in adverse events. Mechanical failures related to defective medication syringes, electrical problems that cause inappropriate delivery of medication (either too much or too little), and failure of alarm systems may also result in adverse PCA-related events.
Operator Errors When setting up PCA, prescribing errors such as improper dose selection and lock-out intervals may result in either inadequate analgesia or opioid-related toxicity. Patients who are opioid tolerant may experience poor analgesia if dosing parameters are restrictive, and the opioid-naı¨ve patient may become oversedated or nauseated with overzealous dosing. When the PCA device is programmed, verification of the drug to be used, its concentration, and the dosing parameters should be performed. These settings should be reconfirmed any time changes to the prescription are made, when empty syringes are replaced, and when new personnel take over care of the patient such as at nursing shift change. Aside from programming errors, operator-related problems that may occur with PCA include incorrect loading of the medication cartridge or syringe, failure to clamp or unclamp tubing, failure to turn the machine on after syringe change, and misplacement of the key to the PCA device. Failure to plug the PCA machine into a power source can result in failure of the device once battery power is drained. This may occur when the patient is transported to and from the hospital ward for procedures or physical therapy.
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Box 10^1 CURRENT THERAPY: PATIENT MONITORING DURING PCATHERAPY
Box 10^2 CURRENT THERAPY: POTENTIAL SOURCES OF PCA-RELATED MISHAPS
Parameters that should be assessed regularly in patients receiving PCA:
Operator Errors Inappropriate patient selection Selection of inappropriate medication Inappropriate prescribed dosing parameters Insertion of wrong syringe into PCA device PCA pump misprogramming Improper loading of syringe into PCA device Failure to clamp or unclamp PCA tubing Failure to turn on PCA machine after syringe change PCA key displacement Inadequate training of staff regarding PCA and setup Failure to respond to device or monitor alarms
Vital Signs with Particular Attention to Respirations (Breathing Rate/Depth) Normal respiratory rates are in the range of10 ^20 breaths per minute. Visual Analog,Verbal, or FACES Pain Scores Typically, numerical pain scores are scaled 0 ^10 or 0 ^100. Higher scores indicate increased severity of pain. Sedation Scores Sedation usually precedes onset of significant respiratory depression. Assessment of sedation usually involves documenting the patient’s level of consciousness via a numerical rating system such as 1 = Wide awake 2 = Drowsy 3 = Sleeping but arousable 4 = Difficult to arouse 5 = Unable to arouse Opioid Consumption Evaluation of medication use by the patient helps to guide adjustments in therapy. Assessment of opioid consumption allows for more accurate conversion between opioids and routes of administration. This is of particular importance in determining the needs of the opioid-tolerant patient when switching to oral medication. Oxygen Saturation Monitoring of oxygen saturation is not mandatory but may be useful, particularly in individuals at risk of respiratory depression with opioid therapy. Desaturation is a late indicator of respiratory depression, and thus, oxygen saturation monitoring should not be the only means used to assess for this adverse effect of opioid therapy. End-tidal Carbon Dioxide Adequacy of ventilation can be assessed through use of end-tidal carbon dioxide monitoring. This allows for earlier detection of respiratory depression related to opioid therapy. This type of monitoring may not yet be widely available in most institutions. Side Effects Common side effects of opioid therapy include nausea, sedation, pruritus, and constipation. Monitoring for these and any other adverse effects of therapy should be included in patient assessments. Treatment for any untoward effects should be provided as indicated.
Patient Errors User related problems may occur with PCA. Some patients may not understand use of the PCA device or may confuse the demand button for the nurse call button. Patients with arthritic conditions may find it difficult to activate the demand button. Sometimes, well-intentioned friends and family members may deliver PCA by proxy. This can cause opioid toxicity, especially if the proxy continues to activate the device when the patient falls asleep or manifests sedation. There have also been cases of intentional device tampering by patients.
Mechanical Problems Device malfunction may be caused by electrical failure or shortcircuiting. In the case of electrical failure, the patient may suffer uncontrolled pain owing to interruption of drug delivery. Conversely, short-circuiting may cause delivery of medication in the absence of device activation. This could result in clinical opioid overdosage if the malfunction goes unrecognized. Siphoning of medication may occur if a defective or cracked syringe is placed in the PCA device.17 This may also occur with inappropriate syringe seating or if the syringe is placed at a level significantly higher than the patient’s body. Other mechanical problems may relate to alarm malfunctions or defects
Patient Errors Failure to understand PCA therapy or use of device Confusion between PCA button and nurse call button Physical inability to activate demand button PCA by proxy Intentional device tampering Mechanical Problems Electrical failure/battery failure Short circuiting of PCA device Siphoning of medication Alarm malfunctions Tubing defects/lack of antireflux valves Accumulation of drug in tubing dead space Hardware or software failure in PCA machine
in the tubing used to deliver the medication to the patient. Antireflux valves are typically used in the tubing for PCA to prevent medication backflow that could cause large amounts of medication to be bolused to a patient if the tubing becomes obstructed and the obstruction is suddenly relieved (Box 10–2).18,19
NEW OPTIONS FOR PCA PCA has traditionally been delivered via the intravenous route. PCEA and PCRA are other means of PCA that have more recently been developed. In addition, patient-controlled oral, intranasal, and subcutaneous analgesia have been studied with evidence of effectiveness. Currently in development is a transdermal fentanyl iontophoretic delivery system that will serve as an additional option for noninvasive on-demand analgesia.
PCEA PCEA has most extensively been studied and used in the obstetric patient,20 likely because epidural analgesia is very commonly employed in this patient population. This form of analgesia has also been used successfully in postoperative patients, including those having undergone extensive abdominal or spinal surgery. The potential benefits of this form of PCA over conventional intravenous administration include reduction in total opioid consumption with consequent decrease in associated adverse effects. In addition, several studies suggest that use of PCEA compares favorably with use of continuous epidural analgesia, with reduction in total local anesthetic dosing and attendant motor block.
PCRA PCRA has been used for plexus analgesia as well as direct wound infiltration analgesia, as with arthroscopically guided subacromial
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catheter placement after decompressive shoulder surgery.21 PCRA has been used with success in several surgical patient populations, including pediatric patients. Patient satisfaction with this technique appears to be high, and use of elastomeric infusion pumps to deliver the desired local anesthetic allows for continuation of this technique even after patient discharge to home.22 When consideration is made to utilize PCRA at home, however, care must be taken to ensure proper instruction of the patient and caregivers, and a physician must remain readily available to address any potential problems or complications that may arise.
Noninvasive Forms of PCA Several options for noninvasive delivery of PCA have been evaluated with evidence of efficacy. Oral PCA and patient-controlled intranasal analgesia are examples of these options.23,24 Modification of existing systems for intravenous PCA allow for delivery of medication by these alternate routes. When using these alternate delivery modalities, it must be taken into consideration that dose adjustment is necessary because of differences in the bioavailability of opioids when compared with intravenous administration. Once appropriate dose conversions are made, these delivery methods may provide analgesia comparable with that of intravenous PCA. These techniques are particularly useful when intravenous access is unavailable. A transdermal fentanyl PCA delivery system is currently undergoing clinical trials and is anticipated to enter the U.S. market in the near future.25–28 This device is programmed to deliver 40 mcg of fentanyl via iontophoresis (through a low-intensity electrical current) when activated. The fentanyl dose is delivered over 10 minutes, and the device cannot be activated more frequently than in 10-minute intervals. The device is operable for 24 hours after the initial activation and can deliver a maximum of 80 doses. There is no basal fentanyl delivery between device activations, making it purely an on-demand system. Studies have shown use of the PCA fentanyl transdermal system to provide analgesia equivalent to that of intravenous PCA in postoperative patients. This appears to offer a promising alternative to conventional PCA because it eliminates the need for intravenous access to deliver the analgesic and it does not require as much nursing time to implement and maintain.
SMART INFUSION AND MONITORING SYSTEMS FOR PCA Some of the most recent advancements in PCA therapy involve the development of smart systems capable of adapting therapy based upon patient needs and computer-integrated systems that monitor patient ventilation and oxygenation and can terminate infusion of opioids when respiratory parameters fall outside prescribed ranges.29 A PCA device with a computer-integrated handset has been developed that allows patients to select a pain intensity rating on a scale of 1 to 10 prior to delivering an opioid bolus. This device uses an algorithmic approach that calculates a bolus dose based upon pain intensity ratings and adjusts a basal infusion based upon demand frequency. If the patient stops making demands, the infusion is decreased and then discontinued if no further demands are made within a specified time interval. One study performed using this adapted PCA device showed that although opioid consumption was higher when using the adapted PCA compared with conventional PCA, opioid-associated adverse effects were not increased, and patient bolus requests declined as the machine varied its infusion rate based upon the patient usage patterns.30 Similarly, a computer-integrated PCEA device that initiates a basal infusion of a local anesthetic/opioid mixture has been described. With this device, when a patient demands a PCEA bolus, the device initiates a basal infusion at 5 ml/hr of the analgesic mixture. The basal infusion is increased in 5-ml increments to a
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maximum of 15 ml/hr based upon the frequency of demands within the preceding hour. It subsequently will decrease the rate in 5-ml increments if no demands are made over an hour. A study using this device in laboring women showed no significant increase in the total volume of analgesic mixture used with the adapted PCEA device, but did show evidence of increased maternal satisfaction with this mode of analgesia.31 In addition to advances in the sophistication of PCA delivery devices, monitoring capabilities for patients using these devices have also improved. One major enhancement in patient safety for those using PCA is the availability of ETCO2 monitoring. ETCO2 is an indicator of patient ventilatory status. Changes in ventilatory pattern typically occur long before declines in oxygen saturation, which has long been the parameter used to monitor for evidence of respiratory depression. One PCA system currently incorporates the ability to monitor both ventilation and oxygenation and thus allows for early detection of adverse respiratory effects of opioid therapy. The system alerts when respiratory parameters are out of range and does not permit delivery of any additional opioid doses. This system may be especially useful in at-risk patient populations such as those with sleep apnea and those who appear to have large opioid requirements but manifest evidence of sedation even in the presence of ongoing requests for additional analgesia. Perhaps in the future, computer-integrated systems will become available that combine the options for variable infusion based upon patient needs and the ability to monitor for evidence of adverse effects on respiratory function. This combination of features would appear to offer the optimal balance between patient satisfaction and safety.
CONCLUSION PCA has been an important option for pain management for several decades. Intravenous PCA is widely used for a variety of painful conditions and has been especially useful in the management of acute postoperative pain. Newer PCA techniques such as PCEA, PCRA, and noninvasive forms of PCA have further expanded the options available for the treatment of pain. PCA should be undertaken with knowledge of the pharmacokinetic properties of the drugs employed and an awareness of patient factors that may increase the potential for adverse events with PCA. Practitioners and patients must be properly educated on use of PCA, and patients must be properly selected for this treatment modality. Advances in PCA technology such as variable-rate infusions that are calculated based upon patient needs for analgesia and improved patient monitoring will further enhance use of these techniques in the future.
REFERENCES 1. McDonald AJ, Cooper MG. Patient-controlled analgesia: an appropriate method of pain control in children. Paediatr Drugs 2001;3:(4)273–284. 2. Lavand’Homme P, De Kock M. Practical guidelines on the postoperative use of patient-controlled analgesia in the elderly. Drugs & Aging 1998;13:(1)9–16. 3. Kluger MT, Owen H. Patients’ expectations of patient-controlled analgesia. Anaesthesia 1990;45:1072–1074. 4. Grass JA. Patient-controlled analgesia. Anesth Analg 2005;101:S44–S61. 5. Lindley C. Overview of current development in patient-controlled analgesia. Support Care Cancer 1994;2:319–326. 6. Jackson D. A study of pain management: patient controlled analgesia versus intramuscular analgesia. J Intravenous Nurs 1989;12(1):42–51. 7. Knudsen WP, Boettcher R, Vollmer WM, Griggs DK. A comparison of patient-controlled and intramuscular morphine in patients after abdominal surgery. Hosp Pharm 1993;28(2):117–118, 120–122, 126, 138. 8. Boldt J, Thaler E, Lehmann A, et al: Pain management in cardiac surgery patients: comparison between standard therapy and patientcontrolled analgesia regimen. J Cardiothoraci Vascular Anesth 1998;12(6):654–658.
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9. Lehmann KA. Recent development in patient-controlled analgesia. J Pain Symptom Manage 2005;29:(5S)S72–S89. 10. Walder B, Schafer M, Henzi I, Tramer MR. Efficacy and Safety of Patient-Controlled Opioids Analgesia for Acute Postperative Pain. Acta Anaesthesiol Scand 2001;45:795–804. 11. Gust R, Pecher S, Gust A, et al. Effect of patient-controlled analgesia on pulmonary complications after coronary artery bypass grafting. Crit Care Med 1999;27(10):2218–2223. 12. Thomas VJ. Rose FD. Patient-controlled analgesia: a new method for old. J Adv Nurs 1993;18:1719–1726. 13. Campbell L, Plummer J. Guidelines for the implementation of patient-controlled analgesia. Dis Manage Health Outcomes 1998;4(1):27–39. 14. Kluger MT, Owen H. Patient-controlled analgesia: can it be made safer? Anaesth Intensive Care 1991;19(3):412–420. 15. Cohen MR, Smetzer J. Patient-Controlled Analgesia Safety Issues. Journal of Pain & Palliative Care Pharmacotherapy 2005;19(1):45–50. 16. Graves DA, Foster TS, Batenhorst RL, et al. Patient-controlled analgesia. Ann Intern Med 1983;99:360–366. 17. Thomas DW, Owen H. Patient-Controlled Analgesia—The Need for Caution. Anaesth 1988;43:770–772. 18. Doyle DJ. Proposed Texonomy for Infusion Pump and Safety Hazards (Abstract). Anesth Analg 2006;102:9. 19. Smythe M. Patient–Controlled Analgesia: A Review. Pharmacotherapy 1992;12:(2)132–143. 20. Halpern SH, Muir H, Breen TW, Campbell DC, Barrett J, Liston R, Blanchard JW. A Multicenter Randomized Controlled Trial Comparing Patient-Controlled Epidural with Intravenous Analgesia for Pain Relief in Labor. Anesth Analg 2004;99:1532–1538. 21. Axelsson K, Nordenson U, Johanzon E, et al. Patient-controlled regional analgesia (PCRA) with ropivacaine after arthroscopic subacromial decompression. Acta Anaesthesiol Scand 2003;47:993–1000.
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PERIOPERATIVE EPIDURAL ANALGESIA Melissa A. Rockford and Martin L. DeRuyter
22. Rawal N, Allvin R, Axellson K, Hallen J, Erkback G, Ohlsson T, Amilon A. Patient-Controlled Regional Analgesia (PCRA) at Home. Anesthesiology 2002;96:(6)1290–1296. 23. Striebel HW, Roemer M, Kopf A, Schwagmeier R. Patient-controlled oral analgesia with morphine. Can J Anaesth 1996;43(7):749–753. 24. Toussaint S, Maidl J, Schwagmeier R, Striebel HW. Patient-controlled intranasal analgesia: effective alternative to intravenous PCA for postoperative pain relief. Can J Anesth 2000;47(4):299–302. 25. Viscusi ER, Reynolds L, Chung F, Atkinson LE, Khanna S. PatientControlled Transdermal Fentanyl Hydrochloride vs Intravenous Morphine Pump for Postoperative pain. JAMA 2004;291(11):1333–1341. 26. Chelly JE, Grass J, Houseman TW, Minkowitz H, Pue A. The Safety and Efficacy of a Fentanyl Patient-Controlled Transdermal System for Acute Postoperative Analgesia: A Multicenter, Placebo-Controlled Trial. Anesth Analg 2004;98:427–433. 27. Koo PJS. Postoperative pain management with a patient-controlled transdermal delivery system for fentanyl. Am J Health Syst Pharm 2005;62:1171–1176. 28. Sinatra R. The fentanyl HCl patient-controlled transdermal system (PCTS): an alternative to intravenous patient-controlled analgesia in the postoperative setting. Clin Pharmacokinet 2005; 44(suppl 1):1–6. 29. Maddox RR, Williams CK, Oglesby H, et al. Clinical experience with patient-controlled analgesia using continuous respiratory monitoring and a smart infusion system. Am J Health Syst Pharm 2006; 63:157-164. 30. Rudolph H, Cade JF, Morley PT, et al. Smart technology improves patient-controlled analgesia: a preliminary report. Anesth Analg 1999;89:1226–1232. 31. Lim Y, Sia AT, Ocampo CE. Comparison of computer integrated patient controlled epidural analgesia vs. conventional patient controlled epidural analgesia for pain relief in labour. Anaesthesia 2006;61:339–344.
adjuvants and modalities of administration have been introduced.2 The focus of this chapter is to review the favorable data supporting the application of epidural analgesia for specific surgeries, recommend dosing schemes, present a troubleshooting algorithm for inadequate analgesia, discuss recent novel approaches, and comment on adverse side effects and the American Society of Regional Anesthesia (ASRA) guidelines for management of epidurals in the setting of perioperative anticoagulation.
ANATOMY INTRODUCTION The first description of epidural analgesia dates back to Leonard J. Corning, a neurologist, who in 1885 inadvertently injected cocaine into the epidural space of a patient. By 1900, epidural analgesia was being used to treat the pain of childbirth, and in 1931, a continuous technique was described. Considered the father of modern epidural anesthesia, A. M. Dogliotti, a 1930’s Italian surgeon, was the first to describe the ‘‘loss of resistance’’ technique. Phillip Bromage published the first textbook on epidural anesthesia in 1978. Bromage introduced the administration of epidural morphine for postoperative analgesia in 1980. The introduction of epidural patientcontrolled analgesia with morphine followed in 1988.1 Administration of medications into the epidural space for postoperative analgesia is a common practice today. Opioids and local anesthetics as single agents or in combination are widely prescribed, and new
Epidural analgesia is produced by placing specific medications within the spinal epidural space. This space extends from the foramen magnum to the sacral hiatus. Lumbar, thoracic, and caudal levels are the most common sites used for postoperative analgesia. The epidural space is bounded anteriorly by the posterior longitudinal ligaments; posteriorly by the ligamentum flavum and vertebral laminae; and laterally by the vertebral pedicles and intervertebral foramina, through which the nerve roots exit the epidural space. The epidural space contains spinal nerve roots, fat, areolar tissue, lymph tissue, and blood vessels including a rich venous plexus. Spread of analgesia occurs in a segmental fashion both cephalad and caudad from the site of injection. Thus, the extent of spread is most affected by site of injection. Other factors that may affect spread include patient age and volume of drug. Patient height, weight, position, parturience, degree of atherosclerosis, speed of injection, and direction of the needle bevel do not seem to affect spread of epidural analgesia to a clinically significant extent.