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Anesth Analg 1999;89:3
© 1999 International Anesthesia Research Society


EDITORIALS

Just When We Thought We Understood Patient-Controlled Analgesia...

John C. Rowlingson, MD

Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia

Address correspondence and reprint requests to John C. Rowlingson, MD, Department of Anesthesiology, Box 10010, University of Virginia Health System, Charlottesville, VA 22906- 0010.

Despite a plethora of articles about advances in our understanding of the mechanisms of postoperative pain and our attentive responses in applying therapeutic modalities, clinicians document and patients continue to fear the occurrence of significant levels of postoperative pain (1,2). The obvious reality is that we have not fully matured in thoroughly managing this pervasive problem. Rather, we are still evolving toward identifying the most effective pain management techniques—those that ease pain and allow patients to cooperate with postoperative regimens that are increasingly more ambitious, yet also augment the safety of the patients in those precarious first few days after an operation. Not all operative procedures produce the same amount of pain, and when the patient's unique, personal physical and psychological factors are intermingled, a volatile circumstance results (3,4). It is clear that we must treat postoperative pain (the Agency for Health Care Policy and Research guidelines say it is an obligation), because every body system can be adversely affected, and the co-existent human suffering is unnecessary (3,4). Management of postoperative pain results in earlier mobilization of the patient, increased patient satisfaction, improved outcomes, and both decreased hospital stay and costs (5,6).

Although relatively simple in concept, the use of patient-controlled analgesia (PCA) does require dynamic interaction with both the patient and the machine. First, there must be active assessment of the patient. Slappendel et al. (7), reporting the use of PCA morphine (with a basal rate) in patients after spinal anesthesia for total hip replacement, revealed that the intuitive belief that those with a greater intensity of pain preoperatively will require more analgesia postoperatively is valid (7). Thus, it is essential to elicit the preoperative use of analgesics. Also important to assess is whether the patient has the physical capacity and the cognitive ability to use the control button on the PCA machine and the willingness to do so (8). Not all patients want such control, and their inclusion in a study would obviously dilute the positive results gained with fully cooperative patients. Furthermore, merely attaching the PCA to the IV line to initiate the therapy is not as effective as when the patient's serum level of analgesics has first been titrated to a level of patient comfort with judicious doses of IV medications. Once the therapy has been initiated, the "attempts versus doses delivered" record tabulated by the PCA machine must be reviewed, and changes in doses and/or lockout time must be made based on these data. Finally, the effect of the administered drug on the decrease in pain must be assessed both with the patient at rest and when he/she is active. Even with such interactive efforts, PCA apparently does not change morbidity and mortality, although patient satisfaction is significantly improved (8,9), because the detrimental consequences of the surgical stress response are not largely altered by this technique (3).

In this issue, Stone et al. (10) report a group of patients undergoing total hip replacement under combined regional-general anesthesia and receiving morphine postoperatively using PCA technology. What could be reportable about a treatment so common as PCA morphine? Their particular focus is the prevalence and severity of hypoxemia, as indicated by arterial oxygen saturation (SpO2) data over the first two consecutive postoperative nights, and the apparent benefit of the administration of supplemental oxygen. Respiratory depression with PCA and/or opioids is hardly unknown (1113). At the outset, the authors are to be credited for demonstrating a fundamental principle in the use of PCA—that of providing patients comfort with small IV doses of opioids on arrival in the recovery room before initiating PCA therapy. Furthermore, their patients were oriented to PCA both while in the post anesthesia care unit (when recovered from general anesthesia and not in severe pain) and during a session on the ward before study data were collected. From a scientific point of view, the study, although reporting a very small number of patients, is clinically relevant. It is gender-balanced, and we all treat patients in the fourth to sixth decades of life who are ASA physical status II for hip replacement surgery.

In patients undergoing orthopedic surgery, and in whom thromboprophylaxis is necessary, PCA is a reasonable option for managing postoperative pain. The use of PCA addresses the patient's anxiety about whether there will be undue delay in receiving pain medications and whether they will "receive any/enough pain medicine." The premise that the patient—the one with the pain—should be directly in control of the analgesic administration is a significant feature of PCA that should never be underestimated. When PCA is managed by anesthesiologists, and especially those with the focused attention of an acute pain service, the versatility of the modality is maximized and patient satisfaction is high (14). Stone et al. have aroused our interest about a previously poorly defined clinical circumstance, yet one with potentially significant consequences, and they have recommended a simple solution. As a matter of fact, they introduce the intriguing possibility that data about the number and severity of desaturation events on the first postoperative night while oxygen therapy is provided are predictive of more serious desaturations in terms of their quality and quantity when oxygen is subsequently removed.

Because we are scientists as much as anesthesiologists, we must apply our analytical and critical eye to what we read. First, the lament that the authors did not perform the study they had planned: originally, they were to randomize the application of therapeutic oxygen between the first and second postoperative nights and also to include more patients (10). In such a study, perhaps, there would not have been the mix of patients with spinal anesthesia (and intrathecal fentanyl analgesia) or epidural anesthesia supplemented with general anesthesia. In the present study, the design is also of concern because there were no control groups—a sine qua non of scientific endeavor—who received other common postoperative therapies from which comparative data would be generated. As a substitute, Stone et al. refer to data that document desaturations in patients who receive opioids by other routes. Catley et al. (11) studied patients after they had undergone cholecystectomy or total hip replacement surgery and compared those with IV infusions of opioids with those receiving regional analgesia. The former group manifested more desaturations <80%, but these episodes occurred only while the patients were asleep and were associated with obstructive apnea or paradoxical breathing. Etches (13) documented that the risk of respiratory depression in patients using PCA was similar to that of patients receiving IM or intrathecal opioids. In their patients using PCA morphine after total hip replacement surgery, Slappendel et al. (7) found that over the first 24 h of postoperative monitoring in an intensive care setting, no patient had respiratory depression as measured by transcutaneous oxygen saturation data (7).

In Stone et al.'s work, there is also a profound lack of preoperative data on the individual patient's SpO2 values; therefore, establishing the exact physiologic significance of each sustained decrease in SpO2 can only be guesswork. Episodic hypoxemia in the postoperative period is partly related to sleep disturbance (11). Thus, we must also know more about the sleep habits of these patients to interpret the reported results. Stone et al. cited research about alterations in REM sleep on Postoperative Night 1 (15). Does the fact that there is a rebound of REM sleep on the second and third postoperative nights, which is associated with apnea, episodic hypoxemia, and, potentially, hemodynamic instability, explain some of their findings regardless of the use of PCA? (15). Supplemental oxygen has been recommended to decrease the incidence of tachycardia, improve cerebral function, and decrease wound infection rates, so perhaps the improvement in saturation is no surprise (3,6,12).

Are we to respond only to the number on the oxygen saturation monitor? Is this technology that good? No harm came to patients in this study. Catley et al. (11) did not document any adverse effects in their patients, nor did Slappendel et al. (7) Rosenberg et al. (12) compared the use of 21% or 37% oxygen on Postoperative Night 2 in patients who had undergone total hip replacement surgery (12). They reported no significant difference in the total number of sudden decreases in oxygen saturation or episodes of desaturation to <80%. Boylan et al. (16) reported an equivalent incidence of postoperative apneas, slow respiratory rates, and desaturation events in patients who had undergone abdominal aortic surgery and treatment with epidural bupivacaine-morphine or morphine via PCA. Are these data, then, so telling as to command a clinical response involving the prescription of supplemental oxygen?

It is fascinating that there was poor correlation with desaturation events and ASA physical status, age, obesity, and PCA dosing. Still, this is a small study. Are we certain of how reliably sicker and more elderly patients interact with PCA (or how compliant any patient is with keeping the nasal cannula in place), especially at night when residual medication effects can team up with unfamiliar surroundings to create disorientation and confusion? Is anyone concerned that SpO2 data in this study are derived from a toe on the operative extremity? Can we really expect the mixture of various levels of pain with the well known consequences of parenteral morphine to be so different on Postoperative Day 2 than on Postoperative Day 1, such that we really learn much by withdrawing supplemental oxygen from all patients on the second night? In relation to this latter point, an interesting finding in Stone et al.'s study is the data that suggest a predictive function from observing the nadirs reached during Postoperative Night 1 with supplemental oxygen provided. Those patients with decreases <95% had a high rate of disturbing desaturations the next night without oxygen. However, to further their model, are the authors recommending not only supplemental oxygen therapy, but also continuous postoperative electrocardigram monitoring in patients receiving such therapy? How else can one determine the stability of the heart rate, in their study, a determinant of the severity of a desaturation event.

This study may not be perfect science, and we can quibble over whether 27 of 32 patients being ASA physical status II–III really represents patients who are "healthy and fit," yet it notifies us of an important patient care issue and one that seems easy to manage. As I ponder why we have not dealt more routinely with this important phenomenon before, other questions arise. Are we so satisfied with, so complacent about, common therapies, such as PCA and morphine, that we have lost our obligation to be objective? Are we to be concerned that patients use PCA for its sedative side effects to aid sleep and thereby amplify their risk for hypoxemia? Can we establish any criteria from this article to permit clinicians to discriminate among patients who need such therapy and those who do not? Is giving oxygen to patients using PCA necessary? What are the cost implications of the additional oxygen therapy? Choinere et al. (17) have recently taken the stand that PCA therapy alone adds expense compared with the administration of IM opioids and that, because the outcomes were the same (in their patients after hysterectomy), the routine use of PCA should be more carefully considered. Will the "need" for supplemental oxygen, as advocated by Stone et al., lead to restricted use of PCA because of the added cost and/or effort involved in setting it up and monitoring its use?

What a pity it would be to lessen the use of this relatively simple workhorse in the armamentarium of acute pain management. Stone et al. provoke the query: can we refine the application of PCA to make it safer? No advantage was taken, in this study, of the general concept to provide patients with a program of pain management options. Each modality applied singularly might not effectively treat pain, or it may be used to excess such that undesirable side effects occur. Conventional wisdom holds (and Stone et al. validate) that one cannot treat all pain with single modality therapy, e.g., only opioids for acute pain, especially as we strive to maximize pain control and uphold patient safety. Thus, perhaps the addition of ketamine to morphine PCA, as suggested by Javery et al. (18), merits more consideration. In most cases of total hip replacement, patients would also be given a nonsteroidal antiinflammatory drug (if not regional analgesia). These drugs have some opioid-sparing effects. What impact would the use of nonsteroidal antiinflammatory drugs have had on Stone et al.'s data? Contrarily, what would have happened if they had used basal rates?

Stone et al. recommend using supplemental oxygen in patients receiving ordinary postoperative pain management with PCA. This seemingly simple suggestion leads to a cascade of questions. It is no surprise that more of their patients had more severe pain on Postoperative Night 1 and used more morphine. Those who received supplemental oxygen generally had mean SpO2 readings that were 5% higher than those recorded on Postoperative Night 2, when breathing room resulted in more hypoxemia. (We are to be encouraged that they also document that our nursing colleagues monitor this situation and apply supplemental oxygen at the first signs of desaturation, clearly benefiting patient care). This article may herald that it is time to take a fresh and more critical look at some of our ordinary therapies for pain management. We do need the authors to complete their original study. We may then have to consider obtaining continuous SpO2 data for selected patients preoperatively to forecast the need for oxygen postoperatively (and to be able to more accurately assess the clinical significance of Stone et al.'s findings). We need to restudy the safety of and clinical protocols for the use of PCA and stay involved in its use to exploit its advantages (14). As for the current article, we should not seize too heavily on the science, but rather appreciate the lessons it can teach us and the energy it fosters for further study. It challenges the validity of the patient being "in charge" of the degree of analgesia and the side-effects with PCA. Because there are interplaying factors beyond the patient's control, Stone et al. implicitly reinforce the critical need to have well established patient monitoring systems for all postoperative patients, no matter what analgesic technique is being used. Stone et al.'s article stands along the path of our evolution toward establishing safer and more effective programs for the management of postoperative pain.

References

  1. Warfield CA, Kahn CH. Acute pain management : programs in US hospitals and experiences and attitudes among US adults. Anesthesiology 1995;83:1090–4.[Web of Science][Medline]
  2. Rawal N. 10 years of acute pain services : achievements and challenges. Reg Anesth Pain Med 1999;24:68–73.[Web of Science][Medline]
  3. Kehlet H. Modification of responses to surgery by neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and pain management. 2nd ed. Philadelphia:Lippincott-Raven, 1998:129–75.
  4. Acute Pain Management Guidelines Panel.Acute pain management: operative or medical procedures and trauma. Clinical practice guideline. Rockville, MD:Agency for Health Care Policy and Research, Public Health Service, US Dept. of Health and Human Services, 1992.
  5. American Society of Anesthesiologists Task Force on Pain Management.Practice guidelines for acute pain management in the perioperative setting : a report by the ASA Task Force on Pain Management. Anesthesiology 1995;82:1071–81.[Web of Science][Medline]
  6. Sinatra RS. Acute pain management and acute pain services. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia:Lippincott-Raven, 1998:793–836.
  7. Slappendel R, Weber EWG, Bugter MLT, Dirksen R. The intensity of preoperative pain is directly correlated with the amount of morphine needed for postoperative analgesia. Anesth Analg 1999;88:146–8.[Abstract/Free Full Text]
  8. Jamison RN, Taff K, O'Hara JP, et al. Psychosocial and pharmacological predictors of satisfaction with intravenous patient-controlled analgesia. Anesth Analg 1993;77:121–5.[Abstract/Free Full Text]
  9. Ballantyne JC, Carr DB, Chalmers TC, et al. Postoperative patient-controlled analgesia : meta-analyses of initial randomized control trials. J Clin Anesth 1993;5:182–93.[Web of Science][Medline]
  10. Stone JG, Cozine KA, Wald A. Nocturnal oxygenation during patient-controlled analgesia. Analg 1999;89:104–10.[Abstract/Free Full Text]
  11. Catley DM, Thornton C, Jordan C, et al. Pronounced episodic oxygen desaturation in the postoperative period : its association with ventilatory and analgesic regimen. Anesthesiology 1985;63:20–8.[Web of Science][Medline]
  12. Rosenberg J, Pederson MH, Gebhur P, Kehlet H. Effect of oxygen therapy on late postoperative episodic and constant hypoxaemia. Br J Anaesth 1992;68:18–22.[Abstract/Free Full Text]
  13. Etches RC. Respiratory depression associated with patient-controlled analgesia : a review of eight cases. Can J Anaesth 1994;41:125–32.[Web of Science][Medline]
  14. Stacy BR, Rudy TE, Nelhaus D. Management of patient-controlled anesthesia : a comparison of primary surgeons and a dedicated pain service. Anesth Analg 1997;85:130–4.[Abstract]
  15. Knill RL, Moote CA, Skinner MI, Rose EA. Anesthesia with abdominal surgery leads to intense REM sleep during the first postoperative week. Anesthesiology 1990;73:52–61.[Web of Science][Medline]
  16. Boylan JF, Katz J, Kavanagh BP, et al. Epidural bupivacaine-morphine analgesia versus patient-controlled analgesia following abdominal aortic surgery. Anesthesiology 1998;89:585–93.[Web of Science][Medline]
  17. Choiniere M, Rittenhouse BE, Perreault S, et al. Efficacy and costs of patient-controlled analgesia versus regularly administered intramuscular opioid therapy. Anesthesiology 1998;89:1377–88.[Web of Science][Medline]
  18. Javery KB, Ussery TW, Stager HG, Colcough GW. Comparison of morphine and morphine with ketamine for postoperative analgesia. Can J Anaesth 1996;43:212–5.[Web of Science][Medline]
Accepted for publication April 8, 1999.





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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press