Pain Services

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  Perioperative (acute) pain medicine service: The perioperative pain medicine service is a team of highly specialized members who practice acute pain medicine and regional analgesic interventions for the patient who is about to have surgery, undergoing surgery, and in the process of recovery from surgery, and for trauma-induced pain. The role of the perioperative pain physician is to reduce the pain resulting from surgery and minimize the period of recuperation, and to inhibit the development of chronic (persistent) pain through early intervention. This service is most commonly found in the inpatient setting but crossover to the outpatient setting is expected for continuity of care.

  
  
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  Chronic (persistent) pain medicine service: The chronic pain medicine service is a multidisciplinary team of providers who treat chronic (persistent) pain and cancer pain using diverse treatment modalities including psychological interventions, analgesic medications, and regional analgesic and chronic pain procedural interventions. The patient population served includes the perioperative patient with preoperative chronic/persistent pain issues, the inoperable patient with chronic/persistent pain issues, and patients who have not undergone surgery but have comorbid persistent pain. The role of the inpatient chronic pain physician is to attenuate the patient’s pain, provide rationalized pain medication care, and transition the patient to outpatient pain care. The diagnosis and treatment of chronic pain is most commonly and most successfully performed in the outpatient setting, not in the acute care inpatient setting (also see Chapter 44 ).

Nociception

Nociception involves the recognition and transmission of painful stimuli. Stimuli generated from thermal, mechanical, or chemical tissue damage may activate nociceptors, which are free afferent nerve endings of myelinated Aδ and unmyelinated C fibers. These peripheral afferent nerve endings send axonal projections into the dorsal horn of the spinal cord, where they synapse with second-order afferent neurons. Axonal projections of second-order neurons cross to the contralateral side of the spinal cord, and ascend as afferent sensory pathways (e.g., spinothalamic tract) to the level of the thalamus. Along the way, these neurons divide and send axonal projections to the reticular formation and periaqueductal gray matter. In the thalamus, second-order neurons synapse with third-order neurons, which send axonal projections into the sensory cortex.

Modulation of Nociception

Surgical incision produces tissue injury, with consequent release of histamine and inflammatory mediators, such as peptides (e.g., bradykinin), lipids (e.g., prostaglandins), neurotransmitters (e.g., serotonin), and neurotrophins (e.g., nerve growth factor). The release of inflammatory mediators activates peripheral nociceptors, which initiate transduction and transmission of nociceptive information to the central nervous system (CNS). Noxious stimuli are transduced by peripheral nociceptors and transmitted by Aδ and C nerve fibers from peripheral visceral and somatic sites to the dorsal horn of the spinal cord, where integration of peripheral nociceptive and descending inhibitory modulatory input (i.e., serotonin, norepinephrine, γ-aminobutyric acid [GABA], and enkephalin) or descending facilitatory input (i.e., cholecystokinin, excitatory amino acids, dynorphin) occurs. Further transmission of nociceptive information is determined by complex modulating influences in the spinal cord. Some impulses pass to the ventral and ventrolateral horns to initiate spinal reflex responses. These segmental responses may include increased skeletal muscle tone, inhibition of phrenic nerve function, or even decreased gastrointestinal motility. Other signals are transmitted to higher centers through the spinothalamic and spinoreticular tracts, where they produce cortical responses to ultimately generate the perception of pain.

The question of how the disease of chronic pain develops from the symptom of acute pain remains unanswered. The traditional dichotomy between acute and chronic pain is somewhat arbitrary, as animal and clinical studies demonstrate that acute pain may become chronic pain. The duration of painful or noxious stimuli, type of stimuli, genetic or phenotypic makeup, or other possible factors that lead to the transition from the symptom of acute pain to the disease of chronic pain remain unclear.

Noxious stimuli can produce expression of new genes (the basis for neuronal sensitization) in the dorsal horn of the spinal cord within 1 hour, and these changes are sufficient to alter behavior within the same time frame. Also, the intensity of acute postoperative pain is a significant predictor of chronic postoperative pain. Continuous release of inflammatory mediators in the periphery sensitizes functional nociceptors and activates dormant nociceptors ( Box 40.2 ). Sensitization of peripheral nociceptors results in a decreased threshold for activation, increased discharge rate with activation, and increased rate of spontaneous discharge. Intense noxious input from the periphery may also produce central sensitization and hyperexcitability. Central sensitization is the development of “persistent post-injury changes in the CNS that result in pain hypersensitivity.” Hyperexcitability is the “exaggerated and prolonged responsiveness of neurons to normal afferent input after tissue damage.” Noxious input can trigger the cascade that leads to functional changes in the dorsal horn of the spinal cord and other sequelae. Ultimately, these changes may later cause postoperative pain to be perceived as more painful than would otherwise have been experienced. The neural circuitry in the dorsal horn is extremely complex, and we are just at the beginning of understanding the specific role of the various neurotransmitters and receptors in the process of nociception.

Key receptors (e.g., N -methyl- d -aspartate [NMDA]) may play a significant role in the development of chronic pain after an acute injury. Neurotransmitters or second messenger effectors (e.g., substance P, protein kinase C-γ) may also play important roles in spinal cord sensitization and chronic pain ( Box 40.3 ). Our understanding of the neurobiology of nociception includes the dynamic integration and modulation of nociceptive transmission at several levels. Still, the specific roles of various receptors, neurotransmitters, and molecular structures in the process of nociception are not fully understood.

Preemptive and Preventive Analgesia

The development of central or peripheral sensitization after traumatic injury or surgical incision can result in amplification of postoperative pain. Therefore, preventing the establishment of altered central processing by analgesic treatment may, in the short term, reduce postprocedural or traumatic pain and accelerate recovery. In the long term, the benefits may include a reduction in chronic pain and improvement in the patient’s quality of recovery and life satisfaction. Although the concept of preemptive analgesia in decreasing postinjury pain is valid, clinical trials are difficult to objectively conduct, which partly accounts for inconsistent conclusions.

The precise definition of preemptive analgesia is one of the major controversies in perioperative pain medicine, and this lack of precision contributes to the confusion regarding its clinical relevance. Preemptive analgesia can be defined as an analgesic intervention initiated before the noxious stimulus develops in order to block peripheral and central pain transmission. Preventive analgesia can be functionally defined as an attempt to block pain transmission prior to the injury (incision), during the noxious insult (surgery itself), and after the injury and throughout the recovery period. Unfortunately, the concept of preventive analgesia has not been examined in a rigorous fashion. Confining the definition of preemptive analgesia to only the immediate preoperative or early intraoperative (incisional) period may not be clinically relevant or appropriate because the inflammatory response may last well into the postoperative period and continue to maintain peripheral sensitization. However, preventive analgesia is a clinically relevant phenomenon. Katz and McCartney described an analgesic benefit of preventive analgesia but no such benefit with the preemptive strategy. Maximal clinical benefit is observed when there is complete blockade of noxious stimuli, with extension of this blockade into the postoperative period. Central sensitization and persistent pain after surgical incision are predominantly maintained by the incoming barrage of sensitized peripheral pain fibers throughout the perioperative period, extending into the postsurgical recovery period. By avoiding central sensitization and its prolongation by peripheral input, preventive analgesia along with intensive multimodal analgesic interventions could, theoretically, reduce acute postprocedure pain/hyperalgesia and, therefore, chronic pain after surgery.

Opioid-Induced Hyperalgesia

Short-term administration of opioids in the perioperative setting may unfortunately lead to opioid-induced hyperalgesia (OIH), a paradoxical increase in the patient’s pain severity and decrease in pain tolerance. This has been demonstrated in humans who received intraoperative opioid infusion for operative analgesia as well as in human and animal experimental models. Although the clinical impact of OIH has not been fully elucidated, the possibility of it contributing to acute postoperative pain should be considered. OIH has also been implicated as a risk for the development of CPSP and the pronociceptive process involves the activation of the NMDA receptor.

Multimodal Approach to Perioperative Recovery

A multimodal approach to analgesia is a broad definition that may include a combination of interventional analgesic techniques (epidural catheter or peripheral nerve catheter analgesia) and a combination of systemic pharmacologic therapies (nonsteroidal antiinflammatory drugs [NSAIDs], α-adrenergic agonists, NMDA receptor antagonists, membrane stabilizers, and opioid administration) (also see Chapter 9, Chapter 17 ). Postprocedural or posttraumatic pain is best managed through this multimodal approach. For instance, basic perioperative therapy, such as including a single dose of the membrane stabilizer, gabapentin, can attenuate postoperative pain and decrease opioid dosage with minimal side effects in various types of surgeries.

The principles of a multimodal strategy include a sufficient improvement of the patient’s pain to instill a sense of control over the pain, enable early mobilization, allow early enteral nutrition, and attenuate the perioperative stress response. The secondary goal of this approach is to maximize the benefit (analgesia) while minimizing the risk (i.e., side effects of the medication being used). These goals are often achieved through regional anesthetic techniques (also see Chapter 17, Chapter 18 ) and a combination of analgesic drugs (also see Chapter 9, Chapter 10 ). Epidural anesthesia and analgesia form an integral part of the multimodal strategy because of the superior analgesia and physiologic benefits conferred by epidural analgesia. A multimodal approach involving a combination of neuraxial analgesia and systemic analgesics during recovery from radical prostatectomy resulted in a reduction of opioid use, lower pain scores, and decreased length of hospital stay. Patients undergoing major abdominal or thoracic procedures and managed with a multimodal strategy have a reduction in hormonal and metabolic stress, preservation of total-body protein, shorter times to tracheal extubation, lower pain scores, earlier return of bowel function, and earlier attainment of criteria for discharge from the intensive care unit. Integrating the most recent data and techniques for surgery, anesthesiology, and pain treatment, the multimodal approach is an extension of clinical pathways or fast track protocols by revamping traditional care programs into effective postoperative rehabilitation pathways. This approach may potentially decrease perioperative morbidity, decrease the length of hospital stay, and improve patient satisfaction without compromising safety. However, the widespread implementation of these programs requires multidisciplinary collaboration, changes in the traditional principles of postoperative care, additional resources, and expansion of the traditional acute pain service, all of which may be challenging in the current medical economic climate.