Chronic Pain Management - Clinical Tree

Introduction

Surgeons, and especially trauma surgeons, are often confronted with chronic pain situations that develop subsequent to skeletal trauma. In addition to having a good professional working relationship with a pain specialist, surgeons need to have an in-depth and up-to-date working knowledge of at least three chronic pain topics to apply appropriate preventative measures, correct and timely diagnosis, and appropriate referral. For that reason, this chapter extensively deals with the important topics of the chronification of pain, complex regional pain syndrome (CRPS; formerly known as reflex sympathetic dystrophy), and neuromodulation as a treatment modality of the latter and other chronic pain conditions. For the purpose of this chapter, neuromodulation refers to spinal cord stimulation (SCS) and dorsal root ganglion (DRG) stimulation. Although peripheral nerve neuromodulation is slowly entering our body of knowledge in the literature, it has not reached maturity and thus will not be discussed at this early stage. All other chronic pain topics are not discussed because they fall outside the scope of this chapter and the practice of orthopaedic surgeons.

Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” by the International Association for the Study of Pain (IASP). If pain persists beyond an arbitrary time period of 3 to 6 months after an initiating event (in this case, trauma and surgery), it is defined as “chronic.” Although acute pain is usually valued as “a life-saving warning sign,” the biologic and physiologic function of chronic or persistent pain is still under debate. It is generally regarded as a pathologic and not a physiologic condition.

Chronification of Pain After Trauma

Incidence of Chronic Pain After Trauma

Unintentional injuries are still the most common cause of death in those aged 1 to 44 years in developed countries. This fact has a significant impact not only on the patients and families involved but also on society at large, which is affected by the associated costs such as medical care and costs related to premature death as expressed in calculations of “years of potential life lost.”

Combined efforts from regulatory agencies, industries such as the automobile industry, and the medical profession have led to a decrease in the unintentional death rate. Unfortunately, improved survival does not come without a price, as reflected by increased healthcare utilization and disability costs.

When we home in on the details, we realize that most injuries are associated with musculoskeletal trauma. More than 70% of patients suffering a major trauma have to undergo at least one surgical intervention to address an orthopaedic injury. Balogh et al. reported that 83% of patients with a pelvic or lower extremity injury did not return to their preinjury functional level 2 years after trauma. Of those 83%, 35% were not able to return to work, and 30% complained about severe pain, and a study conducted in the Netherlands by Ringburg et al. detected that up to 68% of patients reported pain as an outcome 1 year after severe injury. Major orthopaedic surgeries such as hip joint replacements are associated with chronic pain in 28.1% of patients 18 months after surgery.

These observations are confirmed by other researchers. Steel et al. provide additional data, especially about the long-term consequences after major trauma. They analyzed the functional and psychological long-term outcomes of 620 patients 10 or more years after multiple blunt force trauma with or without traumatic brain injury (TBI). An average of 33% of patients reported pain at follow-up 10 or more years after trauma. This percentage of pain is similar to observations seen 2 or 5 years after major trauma.

Acknowledging that there remain limitations in the literature, we can still draw important conclusions about the incidence of chronic pain after trauma:

More than one-third of patients report chronic pain after trauma, not accounting for the time passed since the trauma.
Patient-centered outcome measures such as pain and disability should be the focus of future studies.

Etiology of Chronic Pain After Trauma

First, we have to mention that most studies discussed in this chapter are not related to skeletal trauma surgery specifically, but we do think that the findings and concepts based on these studies can be transferred to skeletal trauma surgery.

To make the subject even more complicated, chronic pain after skeletal trauma is a multifactorial disease process, and we do not have a simple answer as to why pain persists. The studies discussed in the section “ Incidence of Chronic Pain After Trauma ” give us some important insights about not only the incidence but also the etiology of chronic pain after trauma.

Pathophysiology of Chronic Pain After Trauma

Tissue destruction and inflammation due to trauma or surgery activate “nociceptors” on neurons, which transduce this stimulus into an electrical impulse. Neuropathic pain due to a peripheral nerve or spinal cord injury itself causes an inflammatory response, which also activates the signal pathways. Some receptors and their neurons react to only one specific stimulus (e.g., mechanical stimulation from pressure), whereas polymodal neurons react to more than one stimulus. The neurons, primary afferent Aδ and C fibers, transmit the electrical impulse to the dorsal horn of the spinal cord. Their cell bodies are located in the dorsal root ganglion. Upon entering the spinal cord, these primary afferent neurons connect with secondary neurons in laminae 1 and 2 in the dorsal horn. These secondary neurons cross the midline and continue to transmit the stimulus, mainly through the spinothalamic and spinoreticular pathways, to various “pain signal-processing centers” in the central nervous system, such as the brainstem, periaqueductal gray, midbrain, thalamus, and several other subcortical and cortical centers, such as the limbic system. It is important to point out that these “higher centers” not only play a role in pain processing and intensity, but they also attach an emotional component to it, such as anxiety or depression. These neuroanatomical and functional connections between pain and emotional centers explain why pain and psychological disorders frequently present together. Pain signal pathways—nicknamed “the grid” or hardware—are designed to protect us from potentially dangerous situations. On the other hand, it is also clear that the hardware can be challenged in several ways so that the short-term alarm pain stimulus becomes chronic. The wide-dynamic-range neurons are involved in this process. These neurons comprise the majority of cells in the posterior horn of the spinal cord and receive signals from various somatosensory cells entering the spinal cord. Although most neurons produce the same action potential to a stimulus, including a repeated stimulus, wide-dynamic-range neurons increase their output with repeated stimulation from peripheral nerve fibers. This phenomenon is referred to as wind-up, which involves N -methyl- d -aspartate (NMDA) receptors. The reaction of the wide-dynamic-range neurons and repeated stimulation of the somatosensory system modulates the stimulus, leading to molecular changes that are referred to as neuroplasticity. This process is not confined to the spinal cord itself; it also affects higher brain centers and the cortex. In addition, we assume that cell systems not primarily involved in the processing of pain signals are becoming involved to further promote pathologic neuroplastic changes. Depending on where the changes or neuroplasticity occurs, we can distinguish among peripheral sensitization, central sensitization, or a combination of both. The changes associated with the sensitization process are thought to be responsible for the development of chronic pain and, once established, are difficult to reverse. These changes cannot be dismissed as existing only in the patient's imagination—they can be identified using technologies such as functional magnetic resonance imaging just as fractures can be identified by radiography. Based on this progress in understanding chronic pain and the neural pathways involved, it becomes clear that therapies focusing on these pathways are becoming crucial in the treatment of chronic pain, including spinal cord and DRG stimulation. Refer to the section “Neuromodulation for Chronic Pain After Trauma” for more details about these fascinating technologies.

Risk Factors and Mitigation Strategies for Chronic Pain After Trauma

Demographic and Social Factors

Gender is an independent predictor of worse outcomes in severely injured patients, with a prevalence of 80% in females versus 60% in males 1 year after trauma. This finding is supported by several studies identifying female gender as a higher risk factor for chronic pain than male gender. Younger age is associated with a worse long-term outcome after trauma and surgical procedures in general. Regarding the environment, social support was, for example, associated with less phantom limb pain after amputation at 2 years, whereas increased spousal support in the same patient population was associated with more phantom limb pain. This can be explained by a model of operant conditioning in which the spouse takes over social functions for the amputee, therefore reinforcing the pain behavior. Disability caused by the injury is another factor associated with unfavorable outcomes after trauma.

Traumatic Brain and Spinal Cord Injury

Several researchers describe an increased risk of chronic pain after trauma in patients who sustained TBI or a spinal cord injury. Steel et al. and Lippert-Gruner et al. found that TBI is associated with significantly less favorable outcomes after trauma and that persistent pain is present in up to 50% of the studied patient population. Unfortunately, few long-term follow-up studies provide a detailed description of the reported pain, except that some studies examining the impact of TBI on pain identify headaches as the pain complaint. These studies fail to report what type of pain the patients suffering TBI experience. Spinal injuries, especially if associated with a persistent neurologic deficit such as paraplegia, are associated with the worst functional outcomes, as confirmed by long- and short-term follow-up studies.

Traumatic Amputation

Traumatic amputation was associated with the worst long-term outcome in several studies. Pain in the missing body part, known as phantom limb pain, is reported in most patients who undergo an amputation, ranging from 50% to 80%. The level of preamputation pain does influence the occurrence of phantom limb pain in the immediate postamputation period but not beyond 2 years after amputation. Various interventions, including mirror therapy, have been attempted to prevent phantom limb pain, with limited or no positive effects. Surgical techniques and the type of nerve dissection have shown variable outcomes regarding chronic pain. Similar results are observed regarding anesthetic technique and phantom limb pain. One study applying an epidural infusion of local anesthetic to provide a dense motor block days before a scheduled amputation demonstrated improved outcomes, but this result could not be repeated in additional studies. Most studies evaluating phantom limb pain generally have severe limitations. For example, the surgical technique, including the nerve dissections, are rarely detailed. That said, severe preexisting or postoperative pain is associated with a higher incidence of phantom limb pain; thus interventions to limit these events should be employed. Of course, if the amputation is the result of the initial trauma, pain mitigation strategies and a preventive approach are obviously not employable.

Nerve Injuries

A trauma-related nerve injury or an unintended nerve injury caused by the required surgery with even small, unavoidable nerves in the surgical field is a risk factor for chronic pain after (surgical) trauma. Nerve injuries, independent of the cause, are most likely the most dominant risk factor for chronic pain after trauma or surgery.

Periarticular Fractures/Combination Injuries and Development of Posttraumatic Arthritis

The progression of certain injuries (e.g., periarticular fractures) further contributes to chronic pain after initial trauma. Reviewing long-term outcomes of periarticular fractures of the lower extremities, Pape and his coworkers found that 69.9% of patients with a periarticular ankle fracture, 36.4% of patients with a periarticular hip fracture, and 34.2% of patients with a periarticular knee fracture developed posttraumatic symptomatic arthritis. The combination of different injuries (e.g., a shaft and an articular fracture or two article fractures of the same extremity) is additionally associated with poor outcomes after trauma in terms of function and pain.

Surgical Factors

Degenerative mechanisms are the most common source of chronic pain, but interestingly, the second most common source of chronic pain is pain after surgery. Of note, these data did not distinguish between trauma-related and elective surgeries. As a general statement, surgeries with a duration of more than 3 hours are associated with worse outcomes, as are surgeries performed at institutions where experience with the particular surgical procedure is limited. Of note, the longer duration of the surgical procedure may simply reflect the complexity of the injury. The surgical trauma adds to the activation of nociceptors already sensitized from the initial tissue injury and inflammation. Institutions with a specialized approach and larger surgical volumes can minimize this risk factor. The risk for chronic pain increases further with a trauma- or surgery-related nerve injury. Thoracotomies, inguinal hernia repair, and amputations (see “ Traumatic Amputation ”) are the most prominent surgical interventions, although admittedly, most surgeries are not related to skeletal trauma. Nerve injuries due to surgical trauma are the most likely mechanism for chronic pain, as in intercostal nerve injury during a thoracotomy. Progress in surgical techniques such as minimally invasive approaches has decreased the incidence of chronic postsurgical pain after these surgeries compared with an open approach. For example, chronic pain after a thoracotomy has been reported in up to 50% of patients, whereas chronic pain after a thoracoscopic approach ranged from less than 33% to less than 5%, depending on the study.

Nonetheless, most surgeries can actually decrease or facilitate a decrease in pain and improve healing (e.g., fracture stabilization and joint replacement surgery). It should be noted that a surgical intervention to resolve pain can lead to additional pain followed by additional surgeries. This cycle can be avoided with careful assessment of the situation and realistic expectations.

Preexisting Conditions

Preexisting diseases ranging from presurgical pain to a history of chronic pain to psychological factors such as a posttraumatic stress disorder are positively correlated with the likelihood of developing chronic pain. Interventions to address each of these factors will likely improve outcomes.

Preexisting CRPS is associated with increased postoperative pain if additional surgeries are indicated on the affected limb.

Presurgical Pain

Presurgical pain is a significant factor in the transition to chronic pain in surgical patients. Interestingly, this observation is not limited to surgical patients. Severe herpes zoster pain is predictive for the severity of postherpetic neuralgia. Postherpetic neuralgia, although not a surgical disease, is one of the few conditions in which older age rather than younger age is associated with increased pain and chronic pain. Returning back to surgical patients, severe pain before limb amputation is correlated directly with postamputation acute and chronic phantom limb pain. It is unclear at this time which factors are responsible for the correlation of presurgical pain with postsurgical and chronic pain. One can speculate that this observation may be a result of changes in the peripheral and central nervous system (neuroplasticity), inadequate analgesia, or preoperative predisposing factors such as hereditary components. Most likely, it is a multifactorial process.

Postsurgical Pain

The intensity of acute postoperative pain is an important risk factor in the development of chronic pain after surgery. This association has been observed in several surgical procedures ranging from thoracotomy to inguinal hernia repair.

Genetic Factors

Variations in the molecular pathways involved in the transmission and processing of pain signals point strongly toward a genetic predisposition for chronic pain. Polymorphisms in sodium channel molecules, opioid receptor subtypes, and various enzyme complexes support this hypothesis.

Rehabilitation

Long-term outcomes after trauma are correlated with not only rehabilitation but also with patient perception of the quality of the rehabilitation. Patients who were less satisfied with their rehabilitation had higher dissatisfaction and disability scores and reported more frequent use of a medical device.

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