In the mid 1980s, patient-controlled analgesia spurred a post-op pain control revolution. Unlike intramuscular injections, PCAs produced more stable blood levels of morphine and enabled patients to self-titrate doses according to their differing and unpredictable individual needs. While vastly superior to IM dosing, real problems remained—including post-op nausea, vomiting, respiratory depression, ileus, sedation and, often still, inadequate analgesia. Ironically, it was the superiority of PCAs that helped us recognize the limitations of opiates. Today, we've moved away from opiate-centered analgesia to a much more effective approach: multimodal analgesia.
Our strategy starts preoperatively with oral administration of both an anti-inflammatory drug and an alpha-2-delta calcium channel blocker. Peripheral nerve blocks (PNBs), which effectively block surgical pain intra- and postoperatively without nausea, vomiting, or sedation, are a critical element of that strategy. Though single-shot PNBs may only afford 12 to 24 hours of pain relief, continuous PNBs make it possible to extend this analgesia for many days. Disposable pumps have made it possible to extend this benefit to ambulatory surgical patients and to send patients home who would otherwise have needed to stay in the hospital for pain control.
Typical Regimen, Shoulder Procedure
Pregabalin 150 mg; Celebrex 400 mg
Interscalene brachial plexus block (0.5% ropivacaine), single-shot
or continuous catheter
Decadron 4 to 8 mg; Low-dose ketamine, 0.3 mg/kg
Continuous interscalene infusion
of 0.2% ropivacaine, if appropriate
Celebrex 200 mg bid, 4-5 days
Vicodin, Percoset, or Tylenol with Codeine, prn
Intraoperatively, we add low-dose intravenous ketamine. By blocking part of the neuraxial amplification of pain, ketamine provides additional analgesia that lasts well beyond the expected action of the drug. We also administer a single, intraoperative dose of dexamethasone to suppress the body's inflammatory response. Even with PNBs, inflammatory changes take place in the peripheral tissue and spinal cord that exacerbate pain. Research shows that single-dose steroids help suppress this response without hindering wound healing or increasing infection risk.
Postoperatively, in conjunction with the PNB, we administer an NSAID or COX-2 antagonist to reduce inflammation. We now also use small doses of the oral anticonvulsant drug pregabalin (Lyrica).
Should patients require more analgesia, we do still employ opioids. PCA or even PRN oral opioids can help relieve the pain allowed by incomplete blockade. PNBs may not always provide complete blockade of the intended nerve, or the surgical wound may be partially innervated by nerve(s) not included in the PNB. In addition, the low concentrations of local anesthetics infused for continuous PNBs (e.g., 0.1 % ropivacaine for femoral nerve blocks and 0.05 % for sciatic blocks in order to avoid motor blockade and enable rapid mobilization and physical therapy) may not provide complete nociceptive blockade. Although we have not eliminated opioids, our overall post-op narcotic use is down by as much as 80 percent. At the same time, patients mobilize and get discharged much earlier.
As far as we're concerned, the era of opioids as a central pain management strategy is over. For better pain control and minimal complications like breakthrough pain, PONV and sedation, our new mantra is multimodal analgesia.
Dr. Ben-David is a Clinical Associate Professor of Anesthesiology with the University of Pittsburgh Medical Center- Shadyside, Pittsburgh, Pa.