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Showing posts with label Pain and Its Management. Show all posts
Showing posts with label Pain and Its Management. Show all posts

Thursday, September 15, 2011

References of Pain Manegement

2:10 PM  Piscean  1 comment

References
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218. Anand KJS et al. Halothane-morphine compared with high-dose sufentanil for anesthesia and postoperative analgesia in neonatal cardiac surgery. N Engl J Med 1992;326:1.
219. Olkkola KT et al. Kinetics and dynamics of postoperative intravenous morphine in children. Clin Pharmacol Ther 1988;44:128.
220. Gutner LB et al. The effects of potent analgesics upon vestibular function. J Clin Invest 1952; 31:259.
221. Dixon R et al. Levorphanol: pharmacokinetics and steady-state plasma concentrations in patients with pain. Res Commun Chem Pathol Pharmacol 1983;41:3.
222. Forrest WH et al. Dextroamphetamine with morphine for the treatment of postoperative pain. N Engl J Med 1977;296:712.
223. Twycross RG et al. Long-term use of morphine in advanced cancer. Adv Pain Res Ther 1976;1:653.
224. Webb SS et al. Toward the development of a potent, nonsedating, oral analgesic. Psychopharmacol 1978;60:25.
225. Yee JD et al. Dextroamphetamine or methylphenidate as adjuvants to opioid analgesia for adolescents with cancer. J Pain Symptom Manage 1994;9:122.
226. Tong TG et al. Phenytoin-induced methadone withdrawal. Ann Intern Med 1981;94:349.
227. Bernard SA et al. Drug interactions in palliative care. J Clin Oncol 2000;18:1780.
228. Sorkin EM et al. Cimetidine potentiation of narcotic action. Drug Intelligence and Clinical Pharmacy 1983;17:60.
229. Poulsen L et al. The hypoalgesic effect of tramadol in relation to CYP2D6. Clin Pharmacol Ther 1996;60:636.
230. Egberts AC, et al. Serotonin syndrome attributed to tramadol addition to paroxetine therapy. Int Clin Psychopharmacol 1997;12:181.
231. Caufriez A. Menstrual disorders in adolescence: pathophysiology and treatment. Horm Res 1991;36:156.
232. Mackinnon GL et al. Current concepts in the management of primary dysmenorrhea. Can Pharm J 1982;1150:3.
233. Mehlisch DR. Double-blind crossover comparison of ketoprofen, naproxen, and placebo in patients with primary dysmenorrhea. Clin Ther 1990;12:398.
234. Shapiro SS et al. The effect of ibuprofen in the treatment of dysmenorrhea. Curr Ther Res Clin Exp 1981;30:327.
235. Laska E et al. Caffeine as an analgesic adjuvant. JAMA 1984;251:1711.
236. Migliardi J et al. Caffeine as an analgesic adjuvant in tension headache. Clin Pharm Ther 1994;56:576.
237. Harden RN et al. Ketorolac in acute headache management. Headache 1991;31:463.
238. Roberts JE et al. Improved peribulbar anaesthesia with alkalinization and hyaluronidase. Can J Anaesth 1993;40:835.
239. Smith SL et al. The importance of bicarbonate in large volume anesthetic preparations. Revisiting the tumescent formula. J Dermatol Surg Oncol 1992;18:973.
240. Benini F et al. Topical anesthesia during circumcision in newborn infants. JAMA 1993;270:850.
241. Young SS et al. EMLA cream as a topical anesthetic before office phlebotomy in children. South Med J 1996;89:1184.
242. Farrington E. Lidocaine 2.5%/prilocaine 2.5% EMLA cream. Pediatric Nursing 1993;19:484.
243. Gershon RY et al. Intradermal anesthesia and comparison of intravenous catheter gauge. Anesth Analg 1991;73:469.

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Topical Anesthetics and Analgesics

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Topical Anesthetics and Analgesics
73. J.G., a 6-year-old boy, is being treated for osteomyelitis of his foot as a result of a skate boarding accident. Because of the need for long-term antibiotic therapy, he requires occasional IV access replacement. He is very fearful of the procedure because of the associated pain. What can be offered to J.G. to reduce his discomfort?
Insertion of a venous catheter often produces significant discomfort and pain, but there is no reason C.T. has to endure it. Topical lidocaine–prilocaine cream (EMLA) can provide good pain relief during catheter insertion for minor surgical procedures such as circumcision and skin grafts.240,241 The cream must be applied 30 to 60 minutes before the procedure with an occlusive dressing; the anesthetic effect lasts approximately 60 to 120 minutes.242 A smaller-gauge catheter also may reduce the amount of pain associated with the venipuncture.243

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Procedural Pain

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Procedural Pain
72. C.T., a 26-year-old woman, injured her left knee during a fall while skiing. After immobilizing her left knee and using ice therapy, most of her swelling has subsided. She is now seen in the outpatient surgical center for an arthroscopic evaluation of her knee. She is very concerned that the lidocaine that is to be used to anesthetize her knee is going to produce pain, because she has had a bad experience with regional lidocaine injections. What can be recommended to reduce the pain associated with lidocaine infiltration?
Lidocaine injection is quite acidic and can produce local irritation and pain during the infiltration procedure before the anesthetic effect takes place. Because this is a common complaint, C.T.'s concerns should be taken seriously. A simple solution is to neutralize the lidocaine injection solution by adding 1 mL of 1 mEq/mL sodium bicarbonate to 9 mL of 1% to 2% lidocaine before injecting C.T.238,239 Because lidocaine is stable over a wide range of pH values, the bicarbonate will not reduce its efficacy of local anesthetic blockade. This technique should not be used with other local anesthetics, however, because they may be subject to rapid degradation by basic agents.

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Headaches

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Headaches
71. M.K., a 32-year-old man, is complaining of severe headaches that occur at least once every 2 weeks. He takes two Excedrin extra-strength tablets (acetaminophen 250 mg, aspirin 250 mg, and caffeine 65 mg) every 2 hours until the headache starts to ease and sometimes requires a cumulative dose of up to 16 tablets. Migraine and vascular headaches have been ruled out in M.K. Would one of the nonsalicylate NSAIDs be more efficacious for M.K.? Are there any other considerations in managing M.K.'s headache? Is caffeine an effective analgesic for headaches?
Headaches are common, afflicting nearly everyone at some time during their life. The incidence of headache is higher in females and increases with age; 10% of headaches develop into chronic disabling conditions. For M.K., who self-medicates chronically with large doses of acetaminophen, the concern is toxicity from the analgesics. Chronic use of both NSAID analgesics and caffeine (either as single agents or in combination) can possibly precipitate withdrawal (“rebound”) headaches on discontinuation. Although NSAIDs are not considered habituating, accumulating evidence indicates that chronic intake of peripheral-acting analgesics can perpetuate the underlying pain syndrome. In the case of M.K., it is important to consider the possibility of caffeine withdrawal headache as well, because he is taking a caffeine-containing combination product. Other dietary sources of caffeine ingestion from coffee, tea, and other foods should be determined as well.
Caffeine is used in analgesic combination products because it has both a CNS stimulant and a vasoconstrictive effect, which may reverse some of the headache symptoms. The value of caffeine, especially in the small quantities found in most pain relievers, has been controversial. A meta-analysis and subsequent study conclude, however, that caffeine does add to the analgesic effect of aspirin and acetaminophen.235,236
Acute headache can be managed with parenteral ketorolac, but it is not a viable alternative for chronic headache management.237 M.K.'s headaches may resolve on gradual withdrawal of NSAID analgesics and caffeine, but this process is slow and requires the clinician's as well as the patient's determination to stay with the treatment plan. (Also see Chapter 53, Headache.)

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Primary Dysmenorrhea

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Primary Dysmenorrhea
70. P.O., a 27-year-old woman, is seen in the primary care clinic because of severe abdominal pain secondary to her menstrual periods. She reports having pain-free menstrual periods only once or twice yearly. She has been diagnosed as having primary dysmenorrhea with no other gynecologic pathology being found. How should P.O.'s menstrual pain be treated?
Primary dysmenorrhea is a common gynecologic disorder affecting 60% to 80% of women at some time in their life.231 Pain usually occurs 2 to 12 hours before the commencement of menstrual flow, but it can occur simultaneously with, or a few hours after, the beginning of menstruation. It reaches maximal intensity at 2 to 24 hours, then decreases over the next few days.232 Primary dysmenorrhea is associated with increases in endometrial and circulatory prostaglandins. Thus, NSAIDs, which alter the production of the prostaglandins, are frequently used to manage primary dysmenorrhea. The dosages required for the treatment of primary dysmenorrhea usually are higher than those used for analgesia, but frequently a single dose is sufficient to terminate the dysmenorrhea pain. On some occasions, frequent, high doses may be required.
The best time to initiate an NSAID remains controversial. Some clinicians recommend beginning drug therapy a few days before the start of menses; others argue that the prostaglandins are not stored and, therefore, prefer to initiate drug therapy only after the start of menses. Pretreatment with an NSAID carries the risk of fetal drug exposure during early pregnancy. Studies comparing pretreatment with dosing at the onset of menses show no difference in the analgesia between either of the regimens.233,234 (Also see Chapter 47, Treatment of Menstrual and Menstrual-Related Disorders.) P.O. should be instructed to take 600 to 800 mg of ibuprofen at the onset of menses or when discomfort begins. Repeat dosages of 400 to 600 mg may be taken every 4 to 6 hours as needed. If this regimen is ineffective, she can take the first dose 1 to 2 days before the first day of menses is expected.

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Codeine Interactions With CYP2D6 Inhibitors

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Codeine Interactions With CYP2D6 Inhibitors
Tramadol and SSRI
69. T.R. is a 42-year-old man who suffered a right tibial fracture requiring pinning and external fixation. He is now able to ambulate with crutches. Before discharge from the hospital, four acetaminophen 500 mg with hydrocodone 5-mg tablets throughout the day provided good pain control. At the time of discharge, T.R.'s pain regimen was changed to acetaminophen 325 mg with codeine 60 mg, two tablets orally every 3 to 4 hours, owing to his pharmacy benefit limitations. T.R. calls your office because the acetaminophen with codeine is not controlling his pain even when he takes two tablets every 3 hours. T.R. also is taking oral paroxetine 20 mg every morning for his chronic depression. His physician is considering switching his medication to tramadol or acetaminophen with oxycodone. What changes in T.R.'s therapy can be recommended to provide better pain control?
Codeine is metabolized to morphine in the liver by CYP2D6 isoenzymes. Concurrent administration of codeine with agents that inhibit the CYP2D6 system, such as paroxetine, fluoxetine, amiodarone, and ritonavir, may reduce the conversion of codeine to morphine and influence drug response.229 In addition, this isoenzyme shows genetic polymorphism and individuals may demonstrate ultrarapid, extensive, or poor metabolism. Recognition of these potential drug interactions is important because concurrent administration of CYP2D6 inhibitors may make some patients appear to be poor metabolizers and less responsive to codeine, which, in fact, may not be true.
Oxycodone, hydrocodone, and tramadol are also substrates for the CYP2D6 isoenzyme. Although a potential interaction exists between oxycodone and paroxetine, little evidence at this time indicates that oxycodone requires conversion to an active metabolite via the 2D6 pathway to be an effective analgesic. However, tramadol is partially metabolized by CYP2D6 and has an active metabolite. Concurrent administration with a CYP2D6 inhibitor could potentially reduce analgesic activity.229
Coadministration of tramadol and paroxetine could potentially cause more serious problems in this patient. Tramadol has SSRI-like activity because it decreases the synaptic reuptake of norepinephrine and serotonin. Coadministration with SSRI agents, such as paroxetine, fluoxetine, fluvoxamine, and citalopram, can put the patient at risk for serotonin syndrome.230 Signs and symptoms associated with serotonin syndrome include diaphoresis, chest pain, tachycardia, hypertension, confusion, psychosis, agitation, and tremor. Neurotoxicity can be severe and may progress to seizures or coma. Therefore, tramadol is not a good choice for this patient.
Similarly, tramadol can interact with the antimigraine agents known as “triptans,” because their mode of action includes enhancing serotonin activity centrally. Therefore, combinations of tramadol, SSRI, or triptans are relatively contraindicated and require close and judicious monitoring.
It would be reasonable to consider either acetaminophen with oxycodone or hydrocodone for pain control in this patient, especially because he has experienced good pain control with the hydrocodone preparation in the past.

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Cimetidine and Methadone

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Cimetidine and Methadone
68. One week later, B.D.'s wife calls and says that he is very drowsy and that his speech has started to slur. On further questioning, his wife notes that B.D. restarted oral cimetidine 400 mg TID for symptoms of gastritis. She confirms that B.D. has been taking oral methadone 20 mg every 6 hours. What may explain B.D.'s symptoms of apparent opioid toxicity?
Cimetidine (Tagamet) inhibits CYP3A4 isoenzymes, thereby decreasing the metabolism of methadone and potentially subjecting patients to toxic levels. B.D. also could be reaching serum methadone steady-state levels at this time. He should be instructed to withhold the methadone until his mental status returns to baseline; then, the dose of methadone needs to be decreased to 10 mg every 6 hours. When adding cimetidine to existing methadone therapy, methadone doses need to be decreased; the doses should be increased again if cimetidine is subsequently withdrawn.228
Similar precautions need to be instituted for other CYP3A4 inhibitors, such as antiretroviral agents, ketoconazole or fluconazole, erythromycin, and other agents.

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Important Drug Interactions

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Important Drug Interactions
Phenytoin and Methadone
67. B.D., a 32-year-old man, has an 18-year history of chronic pain in the right hip as a result of a motor vehicle accident. He has a long problem list that includes grand mal seizures and gastric ulcer disease. In the past, he has been treated with a variety of opioid analgesics on an as needed schedule, which resulted in escalating drug requirements and a complex regimen of multiple-ingredient drugs (e.g., Percocet, Tylenol #3, Vicodin). B.D.'s attending physician prescribed methadone 10 mg every 6 hours several weeks ago. This switch was initially very successful, but B.D. now presents with symptoms suggestive of opioid withdrawal and poor pain control despite good compliance to his methadone regimen. A note in his chart indicates that B.D. saw a neurologist recently who started him on phenytoin therapy. What important drug–drug interactions might explain this rather complex case?
Phenytoin (Dilantin) induces cytochrome P450 (CYP) 3A4 isoenzymes that are responsible for the clearance of methadone, and can thereby decrease serum concentrations of methadone and precipitate symptoms of withdrawal.226,227 The methadone dose should be increased to 20 mg every 6 hours, and a note should be made in the chart that the doses will need to be reduced if the phenytoin is discontinued for any reason. After his dose has been increased, B.D. should be watched closely for the next several days for drug-induced drowsiness because the long half-life of methadone can produce accumulation.

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Use of Central Nervous System Stimulants

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Use of Central Nervous System Stimulants
66. D.H., a 34-year-old man, is diagnosed with acquired immunodeficiency syndrome (AIDS) and Kaposi's sarcoma. He was discharged from the hospital with a prescription for oral morphine solution, 30 mg every 3 hours. He has been relatively pain free for about a month, but now returns to the clinic complaining of excessive morning sedation. He cannot reduce his morphine dose because the pain makes him too uncomfortable. What therapeutic intervention can be used to alleviate D.H.'s problem of excessive morning sedation?
Limited clinical data suggest that a morning dose of methylphenidate (Ritalin) or dextroamphetamine (Dexedrine) could both relieve opioid-induced drowsiness and potentiate analgesia.222 Less sleepiness has been associated with these combinations than with opioid analgesics alone, and a 10-mg dose of amphetamine combined with the opioid analgesic improved pain tolerance more than the analgesic alone.223,224 Although these studies involved only single doses, these agents should cause sufficient CNS stimulation to obviate morning drowsiness. D.H. should try a morning dextroamphetamine dose of 5 to 20 mg. A somewhat smaller dose may be added around noon if he desires increased alertness in the late afternoon and early evening hours. Another alternative would be to switch D.H. to an opioid analgesic that is less sedating. Drugs such as hydromorphone, levorphanol, methadone, and fentanyl often produce the desired clinical response in a patient such as D.H.225

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Morphine-Induced Nausea and Vomiting

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Morphine-Induced Nausea and Vomiting
65. J.J., a 48-year-old woman, has advanced inoperable cervical cancer. The physician has ordered 30 mg of oral morphine solution every 4 hours for pain, but she has vomited after each dose despite apparently adequate doses of prochlorperazine. What can be done to relieve pain in J.J. who vomits after oral morphine?
Morphine and its derivatives induce nausea and vomiting by stimulating the chemoreceptor trigger zone (CTZ). Although the CTZ is stimulated initially, subsequent doses of morphine generally suppress the vomiting center. Because the incidence of nausea (40%) and vomiting (15%) increases in ambulatory patients, a vestibular component also is likely to be involved. If the vomiting is vestibular in origin, instructing J.J. to lie quietly, with as little head motion as possible for an hour or two, often will help. The nausea usually persists for 48 to 72 hours.220
Levorphanol (Levo-Dromoran) may cause less nausea and vomiting than other potent opioid analgesics at equianalgesic doses and might be an alternative to morphine if the aforementioned recommendations are ineffective in modifying J.J.'s nausea and vomiting. An equipotent dose of levorphanol for J.J., according to Table 8-3, would be 4 mg. The reported duration of action of levorphanol is 6 hours, longer than that of morphine.221
Adjunctive drugs such as droperidol, prochlorperazine, hydroxyzine, scopolamine, and diphenhydramine have been used successfully to control opioid-induced nausea and vomiting. Patients who are extremely sensitive to this opioid-induced effect have to be placed on concurrent or scheduled antiemetics; transdermal scopolamine can be used for this purpose. Although much more costly, agents such as ondansetron may also be useful in patients who have contraindications to the use of phenothiazines or butyrophenones.

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Neonates and Children

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Neonates and Children
63. M.M., a 2-day-old, 3-kg girl, has just had bowel surgery for congenital bowel atresia. How should pain management be approached for M.M.?
Many misconceptions exist about the management of pain in the pediatric population. Historically, infants and children have been undertreated for pain and painful procedures. This is partly because of difficulty in communicating with, and evaluating pain, in children, particularly those who are nonverbal. It was also believed that children did not experience pain in the same way as adults do. Significant advances have been made in the understanding of children's pain perception, and assessment tools designed for different stages of development and communication abilities are available.216,217 Nevertheless, misconceptions still exist, ranging from the amount of pain a child should experience after a painful procedure to the fear of addiction. Inadequately treated pain can interfere with the healing process, increase heart and respiratory rates, reduce oxygen saturation, and induce hyperglycemia and metabolic acidosis. Increased morbidity and mortality associated with unrelieved pain has been documented in neonates undergoing cardiac surgery.218 The reality is that infants and children experience pain just as adults do and should receive appropriate medication and doses to treat their pain.
64. What would be a rational pain management plan for M.M.?
Because M.M. has had significant GI surgery, severe pain should be anticipated and prevented. Therefore, use of opiates, such as morphine or fentanyl, would be appropriate in this situation. Children appear to mature very early with respect to morphine metabolism. Infants as young as 5 months of age show very similar pharmacokinetic parameters as adults; however, morphine concentrations in patients younger than 2.4 months are five times higher than in older patients because of slower metabolic clearance and a lower central compartment volume of distribution.219 The dosing of morphine in children is similar to adults on a milligram-per-kilogram basis, but children <5 months of age may require less-frequent dosing. The use of opiates in infants and children does not lead to addiction. Critically ill children who are receiving opiates for long periods of time develop tolerance and physical dependence and exhibit signs and symptoms of withdrawal if opiates are weaned too quickly, which however, should not preclude pediatric patients from receiving opiates.
An appropriate initial dosing regimen for M.M. would be fentanyl 1 mcg/kg IV every 4 hours with 1 mcg/kg every 2 hours as needed for breakthrough pain. When using parenteral morphine preparations in infants, close attention should be given to the preparation used and the age of the infant. Parenteral morphine preparations are available with and without preservatives. Infants <3 months of age are more susceptible to respiratory depression caused by an allergic reaction to the sulfites or to CNS irritation induced by benzyl alcohol. Thus, neonates and infants <3 months of age should receive only preservative-free morphine. When choosing a route of administration, attention should be given to the patient's clinical condition. Although oral routes are preferred, they may not be appropriate immediately following surgery. Opiates are frequently administered IM; however, IM administration offers no advantage over IV and causes much more pain and distress. Children receiving repeated IM injections often deny the presence of pain to avoid the injection.217 Therefore, IV administration is the preferred parenteral route in pediatric patients.
Assessment of pain and relief in M.M. is more challenging because she is unable to verbalize specific information. Careful attention to behavioral responses, such as crying characteristics, crying duration, facial expressions, visual tracking, response to stimuli, and body movement, will be most useful in assessing pain and relief in M.M.216,217 Heart rate, respiratory rate, blood pressure, and presence of diaphoresis can provide useful clues to M.M.'s level of pain or comfort and can alert the clinician to potential side effects. Careful monitoring, together with adjustments to the dose and frequency of administration, provides optimal therapy.

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Opiates in Special Age Groups

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Opiates in Special Age Groups
Advanced Age
61. B.V., a 75-year-old woman, is seen in the office for a routine physical examination. She has a history of osteoarthritis in both knees, osteoporotic vertebral disease, and peptic ulcer disease. In addition to estrogen and calcium supplementation, B.V. takes acetaminophen 650 mg every 4 hours during the day for general discomfort and ibuprofen 400 mg every night to “help [her] sleep.” What further information should be assessed before modifying B.V.'s drug therapy?
Chronic pain can have a significant impact on daily functioning and quality of life and should be recognized as a significant problem requiring prompt attention. Chronic pain is common in older adults and may easily go unrecognized and untreated. Painful conditions affecting bones and joints often develop as people age. These conditions provide a chronic source of pain and are often incurable. Approximately one of five older adults takes analgesic medications regularly and more than half of these patients have taken prescription analgesics for >6 months. Prevalence rates for chronic pain among community-dwelling older people have been estimated to be between 25% and 50%.208 Studies of nursing home residents have documented similar rates for chronic nonmalignant pain and also have shown a consistent trend toward undertreatment with analgesics.209,210
Clinical practice guidelines have been developed for the management of chronic pain in older persons.208 All older patients should be assessed for evidence of chronic pain as well as for acute pain that may indicate a new illness or exacerbation of a chronic condition. Older patients may be reluctant to report pain because they may fear the consequences of a diagnostic workup. Older adults may also perceive pain to be synonymous with serious disease or death.208 When providing a history, they may not use the word “pain” to describe how they feel. Instead, they may describe their discomfort as “aching, soreness, burning, or tightness.” Finally, patients with dementia or language deficits may not be able to communicate the presence of pain. In these individuals and others, grimacing or other unusual behavior may provide clues to the presence of pain.
B.V. should receive a comprehensive assessment that includes a complete medical history and physical examination to determine any new underlying causes of pain, sensory deficits, or neurologic abnormalities. Physical function and pain associated with activities of daily living should be assessed as well as her psychosocial function to evaluate her for depression and to understand her social network and support system. A thorough evaluation of current pain should be performed to characterize her pain and to determine the patterns of her analgesic use and their effectiveness. The medication history should be reviewed for potential drug side effects and interactions. B.V.'s use of ibuprofen should be further evaluated, because older patients who use NSAID chronically have a higher frequency of GI bleeding, especially if they have a previous history of this condition.208
62. When asked, B.V. states that her current pain level is a 7 on a 10-point scale, and that it can vary from 4 to 8 during the day. It is usually better after rest and worsens later in the day, especially after physical exertion. Although she takes acetaminophen and ibuprofen regularly, they do not effectively reduce her pain. B.V. realizes that her current medical condition will probably not allow her to be completely pain free and states that a pain level of 3 would be acceptable. Would opiate analgesics be appropriate to control B.V.'s pain?
The use of opioid analgesic for chronic nonmalignant pain is controversial. The usefulness of this class of drugs should not be overlooked, however, and may provide fewer risks than long-term or high-dose NSAID therapy. The doses needed are often much smaller than those needed to treat chronic malignant pain. Older patients often experience greater pain relief from opioid analgesics than do younger patients, probably because both the extent and duration of analgesia are enhanced in this group.211,212 Older patients achieve higher-than-expected plasma opioid levels (compared with younger patients) after IM or IV administration. Physiologic changes associated with aging, such as decreases in lean body mass, renal function, plasma proteins, hepatic blood flow, and hepatic metabolism,213,214 may be responsible for the enhanced activity of opioids in older patients.215
When initiating opioid or adjunct analgesics in older patients, it is important to remember the phrase “start low and go slow.” Because B.V. has underlying conditions that cause continuous pain, time-contingent dosing will be more beneficial. An appropriate initial regimen for B.V. using oxycodone HCl 2.5 mg and acetaminophen 325 mg would be one tablet orally every 6 hours, with one tablet every 4 hours as needed. This would provide continuous analgesic therapy throughout the day and allow B.V. flexibility to take an additional dose before activities that may exacerbate her pain. B.V. should be instructed to discontinue taking ibuprofen and to avoid other products containing acetaminophen. B.V. may also respond to tramadol 25 to 50 mg (i.e., 1/2–1 tablet) every 8 hours for her pain, because it has shown efficacy equivalent to NSAIDs in osteoarthritis pain. This agent can be considered as an alternative to a high-potency analgesic, but still presents a risk of dizziness and drowsiness.
B.V. should be monitored closely for sedation that could affect her concentration and ability to perform her activities of daily living. Because older patients are more sensitive to the constipating side effects of opioids, a bowel regimen consisting of a stimulant laxative and stool softener should be started at the beginning of therapy. Patients also should be encouraged to maintain good fluid intake and to include fruits and vegetables that are high in fiber in their diet. B.V.'s therapy should be adjusted based on careful monitoring for efficacy and side effects.

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Respiratory Disease and Analgesia

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Respiratory Disease and Analgesia
59. C.T., a 65-year-old man admitted to the hospital with a hip fracture, has a history of chronic obstructive pulmonary disease (COPD). On admission, C.T. has a nonpurulent productive cough and wheezing. His medical history includes several episodes of pneumonia. Morphine sulfate 6 to 10 mg IM every 3 hours is ordered for his severe hip pain. What risks are associated with using morphine in C.T.? Are there better alternative potent analgesics?
Systemic opioids remain the first-line agents in managing pain in patients with COPD. Careful monitoring orders also should be written along with the opioid orders. Morphine and all other opioid analgesics can depress respiration when given in therapeutic doses and should be used cautiously in patients with advanced respiratory disease and decreased respiratory function. Respiratory rate, tidal volume, and sensitivity to hypercapnia or hypoxemia are all decreased by opioid analgesics.200 Although all opioids and agonists produce respiratory depression at therapeutic doses, there appears to be a ceiling effect to the respiratory depression caused by butorphanol (Stadol), nalbuphine (Nubain), and buprenorphine (Buprenex) at higher doses.201,202 Increased doses of these compounds do not further depress respiration and still provide increased analgesia. The antagonist naloxone reverses the respiratory difficulty (and analgesia) produced by nalbuphine and butorphanol. Although respiratory depression caused by buprenorphine is uncommon, naloxone does not reverse buprenorphine's effects predictably.203 Ventilatory support is the only treatment.
Because C.T. is in severe pain, a lower dosage of morphine should be used initially. Opioids do not always depress respiration when dosed correctly and, in some instances, they actually can improve respiratory function in patients who have recently had a thoracotomy. These patients often are afraid to breathe deeply because of the pain elicited by such activity. The analgesic phenothiazine, methotrimeprazine, nerve block, or epidural anesthetics also can be used with fewer respiratory effects than systemic morphine.204,205 Alternatively, morphine PCA should be considered for C.T., because PCA will allow him to self-administer small, frequent doses, thereby reducing the possibility of opioid-induced respiratory depression.
 
60. During his admission, C.T. mentions that he was recently diagnosed with sleep apnea. Would your approach to C.T.'s pain management change?
Patients with sleep apnea must be carefully monitored when receiving pain medications and sedation, especially via the parenteral route.
Sleep apnea generally can be described as prolonged apneic episodes during sleep that can be attributed to relative hypotonia of upper pharyngeal muscles. These muscles play an important role in patency of the airway.
During an apneic episode, arterial oxygen saturation falls and carbon dioxide concentration rises, which stimulates arousal by the autonomic nervous system alerting the patient to breathe. This can occur multiple times during sleep and often is unnoticed by a patient with sleep apnea. In severe disease, patients may experience cardiac dysrhythmias owing to repeated falls in oxygen saturation. Chronic and untreated sleep apnea can lead to pulmonary and systemic hypertension, cor pulmonale, and cardiopulmonary arrest.206 Clinicians must exercise caution when providing pain management to patients with sleep apnea. Opioid administration causes relaxation of upper respiratory tract muscles as well as a decrease in the sensitivity to rising CO2. The ability to maintain an open airway is already compromised in a patient with sleep apnea. As a result, patients with sleep apnea may experience respiratory failure, cardiac arrhythmias, and even death.206
Currently, there are no published guidelines on pain management of patients with sleep apnea. It is prudent that C.T. receive continuous cardiac and oxygen saturation monitoring while being treated with opioids. Continuous positive airway pressure (CPAP) may be used to prevent hypoxic episodes caused by opioids.207 Short acting opioids would be preferred if C.T.'s pain can be adequately controlled with these agents.
Use of buprenorphine, a partial opioid agonist, for severe pain in patients with sleep apnea has been postulated, but published clinical trials are lacking. Concomitant use of an NSAID and acetaminophen is recommended to reduce opioid requirements.206

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Liver Disease and Analgesia

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Liver Disease and Analgesia
58. A.A., a 54-year-old man with alcoholic cirrhosis, severe ascites, and mild jaundice, has been hospitalized with severe right upper quadrant abdominal pain. His stools are guaiac positive, and he occasionally has bright red blood present at the rectum secondary to hemorrhoids. He was placed on oral lactulose 30 g QID when the protein content of his diet was increased. Although he has a history of hepatic encephalopathy, he is currently alert and receiving only spironolactone 200 mg/day and prophylactic lactulose. What problems can arise when administering opioid analgesics to patients such as A.A.?
Morphine can induce electroencephalogram (EEG) changes similar to those associated with impending hepatic encephalopathy when administered to patients with hepatic cirrhosis.196 These morphine-induced EEG changes cannot be correlated with alkalosis, hypokalemia, or increased blood ammonia levels, and the mechanism is unknown.
Because most opioid analgesics are significantly metabolized in the liver, their serum levels can accumulate if dosing intervals are not adjusted in patients with decreased hepatic function.197,198 The oral bioavailability of some of the opioids also can be increased because of a decreased hepatic first-pass effect.199 The opioids with the greatest first-pass effect or a high extraction ratio have the greatest variability in bioavailability. For example, oral morphine and meperidine have a higher extraction ratio than methadone and, therefore, are more likely to be absorbed unpredictably in patients with severe liver disease. In these patients, methadone is most likely to be absorbed consistently when administered orally.
It would be reasonable to treat A.A.'s pain with a single, modest dose of parenteral morphine, but subsequent doses should await the reappearance of signs of pain to prevent the possible precipitation of hepatic encephalopathy. Careful monitoring of A.A. is essential to minimize risk while maximizing analgesia. The clinician should remember that any CNS depressant can trigger significant problems in a patient such as A.A. If an oral opioid is to be used, then methadone will be a good choice because of its more consistent bioavailability. Although methadone has a long half-life, it is still safer to use orally than morphine. All opioid analgesics should be given in small, frequent, on-demand doses in patients such as A.A. Time-contingent dosing of opioids should be avoided in patients with liver disease because of the risk of drug accumulation. A.A. can be given methadone 2.5 mg no more often than every 6 hours, as needed, accompanied by close monitoring.

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Colic Pain

1:52 PM  Piscean  No comments

Colic Pain
Biliary Colic
56. B.C., a 42-year-old man, is admitted for severe, intermittent right upper quadrant pain accompanied by nausea, vomiting, and clay-colored stools. The differential diagnosis is biliary colic versus acute pancreatitis. Two doses of meperidine 100 mg IM 3 hours apart fail to ease the pain. What other potent analgesics are preferred in this situation?
Opioid analgesics can induce smooth-muscle spasms in the sphincter of Oddi and thereby increase intrabiliary pressure.184,185 The resulting intraductal back pressure can aggravate pain symptoms and increase the serum concentrations of amylase 5 to 10 times above the control value.186 Although it often is claimed that meperidine is less likely than morphine to cause spasm of the sphincter of Oddi, no clear evidence indicates the superiority of one agent over the other.187 Significant increases in intrabiliary pressures of patients receiving fentanyl (Sublimaze), morphine, meperidine, pentazocine (Talwin), butorphanol (Stadol), and oxycodone are documented.188,189
In one study,190 buprenorphine (Buprenex) did not increase biliary pressure, but further controlled investigations are needed to substantiate this finding. Generally, biliary pressure increases and spasm begins within 5 minutes of parenteral opioid administration. These effects peak within 20 to 60 minutes, and values gradually return to normal over 1 to 2 hours.191,192 Because the reported severity, intensity, and duration of biliary hypertension vary greatly, it is unlikely that any agent presently available has a clear advantage over another.187
Opioid-induced biliary hypertension and sphincter of Oddi spasm can be reversed by parenteral glucagon or naloxone.191,193 It is still unclear whether orally administered naloxone will have similar effects, although orally administered naloxone prevented opioid-induced constipation in one study.194 It is unclear whether B.C. is having more pain because of an adverse drug effect or primary failure of meperidine. Because no consistent way exists to measure intraductal pressure clinically, it is recommended that he be given a longer-acting opioid, such as methadone 5 mg IV every 8 hours for pain.
 
Renal Colic
57. M.J., a 36-year-old woman with a history of urolithiasis, comes to the ED because of severe flank pain along with microscopic hematuria. She is diagnosed with renal colic by the ED physician who wishes to treat her pain with meperidine 100 mg IM, but M.J. does not want to take opioids. What can M.J. be given for her severe pain from her renal colic?
Renal colic is extremely painful, and patients often require parenteral opioid analgesics. No significant clinical difference is seen between any of the opioids for this type of acute analgesic indication. Because M.J. does not want to receive opioids, the choice of analgesics is limited. The parenteral nonsteroidal analgesic ketorolac is likely to be the best alternative.195 It would be appropriate to start M.J. on ketorolac 15 mg IV every 6 hours as an alternative to the opioids for acute analgesia.

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