Last week we discussed my favorite block, the popliteal/saphenous block, for which I advocated greater use in podiatric circles. During that discussion I recommended having this block performed before the surgery, ie, pre-incision. As promised, today we’re going to discuss the “why” behind that recommendation.

I’m going to be very clear here and, at the risk of stealing my own thunder, give you the bottom line.

Pre-emptive analgesia appears to be the most appropriate method to reduce postoperative pain. This means peripheral nerve blocks should be performed BEFORE the incision and NOT after. The reason this is so is due to central and peripheral sensitization, which leads to greater postoperative pain.

As much as I try to stay away from significant amounts of basic science, this topic is worth some review. For those of you interested in more detail, I’m gathering most of my discussion from an excellent – if a little long – review by Woolf and Chong¹.

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“Pre-emptive analgesia, performed before the surgery begins, is more effective in reducing post-operative pain.”

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The Science of Pain Response

Consider that there are two general kinds of nerves in the periphery - low threshold fibers and high threshold fibers. Low threshold sensations are mediated by large Aβ fibers, which fire when we come in contact with innocuous, painless stimuli. High threshold nerve fibers, mediated by Aδ and C nerves, are responsible for mediating painful (noxious) stimuli. The responses of both of these nerve types are usually transient and exhibit a stimulus-response relationship.

This leads into classification of pain as physiologic versus clinical. Physiologic pain is determined by high threshold, well localized nociceptor nerves in the periphery. This is what happens during the normal course of life. Clinical pain, though, is caused by other, less common stimuli and leads to hypersensitization.

Clinical pain itself consists of two types, inflammatory and neuropathic. Neuropathic pain is due to damage to the nerves themselves, and we won’t discuss this further here. Inflammatory pain is where we’re going to spend the rest of our time and is due to peripheral tissue damage during surgery. Clinical pain is characterized by a change in sensitivity, with a decreased intensity of stimulus necessary to initiate pain. This sensitivity is where the terms allodynia (nonpainful stimulus causing pain), hyperalgesia (an exaggerated response to painful stimuli), and secondary hyperalgesia (spread of hypersensitivity to uninjured tissue) come in.

There are two primary mechanisms of inflammatory pain, peripheral sensitization and central sensitization. Let’s start with central sensitization. Nociceptive afferent signals (ie, pain coming from the site of injury during the surgery) trigger neurons in the spinal cord to become more excitable. This excitability of the central nervous system (CNS) outlasts the original signal. Now, low threshold nociceptors (usually painless signals) send their regular signal. When that signal hits the now sensitized CNS cells, the patient experiences pain from what was previously an innocuous sensation.

During peripheral sensitization, tissue damage at the site of surgery causes the release of a host of inflammatory mediator chemicals that cause increased sensitivity of the high threshold nociceptor cells in the surgical area. This essentially turns the high threshold pain fibers into low threshold ones that fire more easily during what would have previously been non-noxious stimuli.

How Does This Affect Your Surgery Patient?

Consider where all this fits in with your surgical patients. You perform your foot surgery and do your local block when you’re finished. You then send the patient home. You’ve injured the tissue, which causes what would normally be an innocuous sensation to become a painful one. For example, moving the great toe joint might not normally be excessively painful, but after surgery, simply moving the joint or touching the sutured skin may become painful. The surgery you have performed created inflammatory pain, which sensitized the periphery through local chemical mediators. The spinal cord has also been centrally sensitized. Now, what were previously painless sensations have now become painful ones. Post-incisional anesthesia cannot stop this process from occurring. The horses have already left the barn.

Pre-emptive analgesia, on the other hand (anesthesia prior to injection), creates for us the opportunity to head off this sensitization process before it begins. The basic science has provided a convincing framework for us to utilize preemptive analgesia, and this data should be enough to push surgeons to this method whenever possible. But what does the clinical evidence show? What methods exist to help us create effective preemptive analgesia? Is a single treatment method such as local injection enough or should we combine methods for greater effect? These are the questions we’ll address in Part 2 of our discussion next week.