Since beginning my career as a CRNA, on a daily basis I use the pharmacology and physiology I  learned to administer narcotic medications in a monitored and 'controlled' situation. This has given me the opportunity to see almost immediate cause and effect of the medications and increased my confidence level in administering high dose narcotics to those with tolerance and physical dependence. I have cared for patients with myriad non-narcotic, narcotic, alcohol, and ilicit drug use histories. Some are in agonizing pain and are opioid naive for fear of side effects or addiction.

After a couple of years I really began to notice that most nurses (and myself for the record) had received limited education in nursing programs on treating pain. Up until this realization, I had assumed (and we all know what that means) that some people just did not care. Let me digress and give you an example:

     It is 1993, in a level 2 facility in Meridian, MS. I was a SNA (student nursing assistant) on the night shift. The call bell had rang, and it was a patient requesting pain medication.  Her prn medication was Demerol (meperidine) q 4 hours. I alerted the LPN to the patient's request. The LPN was preparing to go out on a smoke break. Angry that the patient had requested medication, she stated "I'll teach her to ask for more Demerol". The nurse drew up the meperidine, and placed an 18g needle onto the syringe and proceeded to the patients room to administer the IM meperidine.

We have all taken care of 'clock watchers' but there are two important pieces of information about meperidine missing here that I know I was never taught, and other nurses I worked with in a parituclar ICU did not know until 1996, and here is how we found out:

     In 1996, a patient was legally drunk, and decided to climb a ladder to clean out his gutters.  Well, he fell and fractured multiple ribs. He was placed in the ICU for monitoring and high-dose meperidine PCA.  the settings and lockouts allowed the patient to utilize a 600mg meperidine PCA syringe every four hours. 12 hours into this gentlemans stay he became combative, delusional, and punched a nurse. Multiple doses of Ativan (for presumed early DTs) had no effect. It was decided by the physician to heavily sedate and intubate the patient to avoid further hypoventilation and pneumonia. Anesthesia was consulted for pain management. We (ICU physcian and staff) had caused this entire scenario in our treatment of the patients pain because we lacked the following knowledge:

Meperidine is a narcotic analgesic with a half-life of only 3 hours. This information would indicate that meperidine should be administed every 3 hours prn. However, meperidine has an active metabolite, normeperidine, with a half-life of 6 hours and has limited excretion by the kidneys. If meperidine is adminstered q 3 hours, there is an unavoidable buildup of the active metabolite leading to CNS irritation causing agitation and even seizures.

So, in the first scenario, q 4 hour prn meperidine is not adequate in the patient having ongoing pain (as opposed to treatment for breakthrough pain only). This is why the patient was on the call bell as soon as they could have medication...they had been in pain for almost an hour already, with their pain escalating as the meperidine levels in their blood continued to decrease. In the second scenario, this is a prime example of why meperidine is not a good medication for ongoing acute pain.  Meperidine is not as potent as morphine and carries the risk of toxic side effects in high doses and repetitive dosing.

These are a couple of caveats in managing pain that I learned along the way in my early nursing career. Both scenarios could have been handled differently, in that requests for alternative medication orders that would allow adequate dosing and appropriate intervals. Something else I have learned about pain management in the last few years, is that many physicians admit they aren't given much more of an indepth education on pain management--a complex and subjective experience for patients. 

We all need to take a proactive approach in broadening our understanding of pain and pain management. We owe it to ourselves and our patients. 
 

The following case study is provided to give insight into the complicated task of managing acute on chronic pain. It is not intended to replace institutional standards of care, so refer to your institutional policy and procedure guidelines. Consult your hospital pharmacist or specific product prescribing and conversion guidelines for assistance. When developing a plan of care for this patient population collaboration between anesthesia, the surgeon, pharmacy and pain management teams are highly recommended.

A 62 year-old, 110Kg patient Mr. "A"*  presents for total knee replacement. The patient has a history of chronic back pain, for which he takes Opana ER 120mg BID and hydromorphone 4mg prn every 4 hours for breakthrough pain three to four times a day depending on activity levels.

On the day of surgery the patient was instructed to take his a.m. dose of Opana ER as prescribed. Operative analgesia was obtained with a spinal anesthetic containing bupivicaine 0.75% and 0.3mg of Duramorph. Mr. A was then sedated with a propofol infusion for the duration of the procedure. At the end of the procedure the surgeon injected 100ml of a local anesthetic mixture containing ketorolac 15 mg into the intraarticular and subcutaneous surgical areas. On arrival to the PACU in the late afternoon, Mr. A was awake and alert.

The postoperative plan:
     Resume Mr. A's baseline narcotic requirements using oral agents as soon as possible. Opana ER is not on formulary, so the first priority was converting to an equianalgesic dose of OxyContin. Dosing for Opana ER is one-half the dosing for OxyContin. Therefore to convert to an equianalgesic dose of OxyContin, the 24 hour dose of Opana ER must be doubled. In Mr. A's scenario he takes 240 mg of Opana ER every 24 hours, therefore his OxyContin dose would be 480 mg every 24 hours. Mr. A was given 240mg of Oxycontin as soon as he was able to take oral medication in the PACU to cover his baseline narcotic requirements. 

     To treat surgical pain, in addition to the intrathecal (spinal) duramorph, Mr. A was given a high-dose hydromorphone PCA at 0.5 mg every five minutes with a 4 hour lockout of 3 mg for breakthrough to treat his surgical pain. 

Due to the bi-modal respiratory depression associated with duramorph, the greater bioavailability of OxyContin over Opana ER, and the PCA for breakthrough, Mr. A was considered moderate to high-risk for a respiratory event. He was placed on monitored unit with continuous pulse-oximetry for 24 hours until the bi-modal effect of the duramorph had passed and his oral medication and PCA usage could be further evaluated and adjusted for patient safety and comfort.

When converting to equianalgesic doses, it is important to remember that cross-tolerance across narcotics is not complete. Therefore when initially converting from one narcotic to another it is recommended to start the new medication at 75-80% of the equianalgesic dosage and titrate upward. Mr. A was started on 100% of his dose of OxyContin because he would not be receiving the same breakthrough dosage of hydromorphone AND duramorph is usually not considered adequate when used alone for total joint pain.
 
When managing acute on chronic pain in a chronic opiate user always remember- if they are not receiving their baseline narcotic requirement as a minimum, their pain will not be controlled.

reference: http://www.medscape.com/infosite/opana_er/article-5

* All specific identifiers changed and/or omitted for privacy