Principles of Pain Management

Chapter 17 Principles of Pain Management



Stephen D. Coleman, Raymond R. Gaeta


Pain is ubiquitous in daily life, and multiple treatment modalities are available under normal circumstances. However, the wilderness setting presents significant challenges when available treatments are limited to those that are included with medical supplies for travel into remote locations. Many travelers have medical conditions that may restrict or limit the use of certain therapies. Some travelers may suffer chronic pain and are already receiving treatment with medications or implanted devices. The treatment of pain in remote and extreme environments is guided by patient characteristics, type of injury, and available therapies. Optimal treatment reduces the chances of further injury, decreases suffering, and improves the likelihood of successful rescue.


The International Association for the Study of Pain4 defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition indicates that pain is not simply sensory input from tissue damage; rather, it is a complex experience that depends in varying degrees on an emotional component. The emotional component can vary markedly among individuals and circumstances; however, these factors may significantly affect physiology and dramatically alter the impact of pain on an individual patient. For example, fear and anxiety associated with injury in remote areas can exacerbate the situation.


The optimal management of pain often requires a multimodal approach. This approach includes treatment of ongoing tissue damage, which may include interventions locally and systemically, non-narcotic medications, opioid and adjuvant medications, and awareness and management of psychological factors that affect an individual’s perception of pain.



Anatomy and Physiology of Acute Nociceptive Pain


The early understanding of the transmission of sensation was that pain perception followed nerves that were simple conduits to the brain. As a greater understanding of pain has developed, it is clear that nociceptive pain, which is defined as the pain of tissue injury or potential tissue injury, is initiated by nociceptor activation in the periphery and modulated at multiple levels in the nervous system, thereby allowing for multiple targets for therapy. This sequence of events is categorized into four processes:


1 Transduction: Chemical, thermal, or mechanical energy is converted into an electrochemical signal.

2 Transmission: The signal is conducted to the central nervous system via Aδ and C fibers.

3 Modulation: The signal is altered by both positive and negative feedback loops in the spinal cord and the brain.

4 Perception: The signal is finally appreciated as pain.

The skin, the periosteum, and the joint surfaces are abundantly populated with nociceptors that are activated by potential or actual tissue damage. Thinly myelinated Aδ and unmyelinated C fibers terminate in the skin as nociceptors and transmit nociception to the spinal cord. Fast-conducting Aδ fibers respond to mechanical stimuli and transmit sharp sensations. Slow-conducting C fibers respond to chemical, thermal, and mechanical stimuli and transmit burning sensations. Acute injury of the skin results in simultaneous transmission through Aδ and C fibers. Cell bodies of the Aδ and C fibers are located in the dorsal root ganglion, and they project fibers to the posterior horn of the spinal cord. Aδ and C fibers synapse with second-order neurons in the dorsal horn of lamina I to lamina V. These second-order neurons cross to the contralateral side of the spinal cord and ascend in the anterolateral spinal tracts to the thalamic nuclei, brainstem, and midbrain, where they synapse with third-order neurons and project to the cerebral cortex.


The simple stimulation of nociceptors without tissue damage may result in transmission of an action potential to the spinal cord and higher levels of the nervous system, and this may eventually result in a perception. However, if stimulation results in tissue damage, a host of changes can occur; these include the local release of many chemicals near the site of the injury as well as chemical changes at the spinal cord and higher levels of the central nervous system.


Locally released chemicals may be excitatory or inhibitory. Substance P and neurokinin A are excitatory neuropeptides that are released locally during tissue damage that may facilitate nociceptive transmission. Release of calcitonin gene-related peptide and substance P results in tissue edema and erythema by increasing vascular permeability in peripheral vasculature, thereby contributing to inflammation. There are proinflammatory substances released during tissue damage, including bradykinin, which can initiate pain transmission and sensitize nociceptors. Glutamate, nerve growth factor, serotonin, and histamine also potentiate the response of nociceptors. In addition, low pH may reduce the threshold of nociceptors. There are many additional sensitizing chemicals that act locally at the site of tissue injury as well as at the spinal cord level. The opposing system includes release of pain-inhibitory substances such as endogenous opioids, β-endorphins, acetylcholine, γ-aminobutyric acid, and somatostatin; these substances impede nociceptive transmission. Modulating nociceptive input can inhibit or facilitate the transmission of signals.


In addition to local and spinal cord effects of these chemicals, transmission of action potentials to the spinal cord may be modulated by the transmission of signals by other fiber types. A landmark publication by Melzack and Wall3 described the gate control theory, which operates at the spinal cord level. The authors described input from Aβ fibers, which transmit light touch and pressure and have an inhibitory modulation effect on transmission of nociception to the spinal cord. This description of the gate control theory may explain the mechanism for modulating nociception at the spinal cord level when transcutaneous electrical nerve stimulation (TENS) is applied.


At the level of the spinal cord, nociception and the autonomic nervous system are under descending inhibitory control from supraspinal levels. A familiar example of descending inhibitory control is found in our normal disregard for the sounds of our heartbeat and respirations. Normally these signals are suppressed, but they are easily called into consciousness by cortical mechanisms. Similarly, the nociceptive system is also under descending inhibition from supraspinal systems, allowing us to ignore our pain at times during stressful situations. Serotonin and norepinephrine appear to be the primary neurotransmitters that regulate descending inhibitory control; however, others (e.g., α2 agonists, cannabinoids) may be involved.


Thus the perception of pain involves not simply the transmission of signals from peripheral sensors to the brain. It is in fact a complex system that is initiated by stimulating peripheral nociceptors in the presence of a milieu of local mediators that facilitate or inhibit signal transmission. As transmission of the signal moves centrally, modulating influences exert their influence before the perception of the sensation occurs.



Pain Measurement


The experience of pain is completely subjective. Various scales have been introduced that attempt to quantify the level of pain; these include numeric scales (e.g., 0 to 10, with 10 being the worst pain), categoric scales (i.e., none, mild, moderate, or severe), and even face scales (i.e., smile, neutral, or frown). The visual analog scale appears to be more objective because the patient makes a mark along a 100-mm horizontal line that can then be measured to give a pain score of 73 mm, for example. The usefulness of any scale is best determined when making repeated measures for the same patient with the use of the same scale, especially in an acute setting. A baseline value establishes a set point from which higher pain scores should be interpreted as “worse” and lower pain scores interpreted as “better.” Infrequent measures (e.g., for a patient with a chronic condition) are somewhat less reliable. Interpatient reliability is even more problematic, because different people may experience the same injury differently.



Types of Pain


The nomenclature of acute pain versus chronic pain is familiar to many, and relies on time as a determining factor; however, it adds little else to the understanding and treatment of pain. Understanding the mechanisms of pain allows pain to be treated on a continuum, with recognition that unmitigated acute pain can become chronic on the basis of physiologic changes that may occur within the nervous system rather than just with the passage of time. With this approach, the rationale for preemptive strategies and aggressive acute strategies comes into clearer view. Coexistence of acute and chronic pain in the same patient is thus treated in an integrated model.


With an understanding of the common mechanisms of pain disorders, a rational approach to initial therapy can be developed with the use of three general categories that are based on pathophysiology. Pain may be considered nociceptive, inflammatory, or neuropathic, or it may be a combination of two or all three types with certain forms of injury (Figure 17-1). The categories and initial therapies are as follows:


1 Nociceptive. Acute pain that is initiated by tissue injury in the form of a laceration, fractured bone, or crush injury is a type of nociceptive pain. It is a consequence of activating specific nociceptors within the skin, muscle, periosteum, joints, and probably the viscera. These receptors are likely the distal terminals of Aδ and C fibers; they may respond to specific stimuli, including chemical, thermal, and mechanical insults, or they may respond to more than one of these stimuli, in which case they are called polymodal receptors. Polymodal receptors represent the majority of nociceptors. The primary medications directed toward treating nociceptive pain are opioids. Opioids have their primary effects on the opioid receptors µ, δ, and κ. Their analgesic effect is produced in the periphery, at the dorsal horn of the spinal cord, and at supraspinal sites.

2 Inflammatory. Inflammatory pain is mediated by elaborating prostaglandins via the cyclooxygenase pathway. Sensitization of peripheral nociceptors is also mediated via this mechanism, which leads to hyperalgesia around the wound. Nociceptive pain and inflammatory pain generally coexist, because the pain stimulus provokes them both. Immune-mediated inflammation with or without tissue injury also falls into this category. Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids are particularly effective for treating inflammation as well as mild to moderate pain. Peripherally decreased production of prostaglandins, including prostaglandin E2 (PGE-2), is the likely mechanism for decreased pain and inflammation. In addition to their peripheral actions, NSAIDs also appear to act on the dorsal horn of the spinal cord. Prostaglandin 2 at the level of the spinal cord is thought to cause release of glutamate both presynaptically and postsynaptically. Glutamate may augment pain states and hyperalgesia. Inhibition of glutamate release at the spinal cord by reduction of PGE-2 as a consequence of NSAID administration involves a centrally acting mechanism in addition to the well-known peripheral mechanism.

3 Neuropathic. Neuropathic pain results from injury to the nervous system (e.g., peripheral nerve, spinal cord) that may occur as an acute injury of the nerve. Neuropathic pain may be the result of an isolated injury to the nervous system, or it may be the result of an injury that causes nociceptive or inflammatory pain. At the dorsal horn of the spinal cord, after peripheral nerve injury, release of cytokines and growth factors results in upregulation of nociceptive neurons. Although this is considered a broad category, various mechanisms are responsible for maintaining neuropathic pain, which results in multiple agents that are used to treat it. Antidepressants, anticonvulsants, antiarrhythmics, and local anesthetics are considered first-line agents for treatment of neuropathic pain, and are given empirically. Gabapentin, which is commonly prescribed, was developed for treatment of epileptic seizures and designed to bind to γ-aminobutyric acid receptors. However, its analgesic effect is thought to be related to actions at the α2-δ subunit of L-type calcium channels that block the influx of calcium.

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FIGURE 17-1 Categories of pain.



Pretravel Preparation


Optimally a pretravel evaluation should assess the individual’s suitability for the wilderness experience and include an assessment of chronic medical conditions. A thorough history and physical examination should include the individual’s use of medications as well as any allergies and intolerances. Determining the use of chronic pain medications is important, because there are common and potential side effects to these medications. Some medications may cause cognitive impairment and psychomotor changes that may increase an individual’s risk for injury. Use of opioids may be associated with side effects including cognitive changes, constipation, and tolerance as well as withdrawal if the medication dose is significantly reduced or terminated abruptly. Termination of adjuvant medications—including antidepressants (e.g., desipramine, duloxetine), benzodiazepines (e.g., lorazepam, alprazolam), and anticonvulsants (e.g., carbamazepine, gabapentin)—can also cause withdrawal-type syndromes.


Individuals who are receiving chronic opioids or adjuvants for chronic pain may not have a predictable response to acutely administered analgesic medications for acute injuries. As management of chronic pain has become more complex and as more sophisticated implanted devices have become available, it has become more likely that individuals with chronic pain will be traveling in the wilderness. These devices include spinal cord stimulators, peripheral nerve stimulators, cortical and deep brain stimulators, and implanted intrathecal infusion devices. If an individual has one of these devices, it will be important for him or her to understand how to operate the device and to have contingency plans in case the device fails. For example, individuals with implanted pumps that deliver intrathecal medication require periodic refills of the reservoir, typically every 1 to 3 months. Persons who use these devices and persons with allergies should wear identification bracelets. Device manufacturers have a worldwide network of support that is accessible by telephone or e-mail, but this may not be practical in the wilderness, so written instructions should be available. Having the device information (i.e., the name of the manufacturer and the model number) and contact information for local health care providers and manufacturers will facilitate resolving difficulties when civilization is reached.


When medications are transported internationally and specifically by air carrier, the Travel Security Administration in the United States may require specific handling of medications. Because regulations change periodically, one should check for updates before traveling. Medications should be properly labeled with appropriate prescription and patient identification information.



Treatment Modalities


After injury, the patient should be assessed with regard to mechanism and severity of injury. Treatment modalities are available for management of acute pain; these include local, regional, and systemic techniques. Local physical modalities (e.g., cold, heat), local anesthetics, and topical medications may be effective. Regionally, nerve blocks of the extremities or other body parts may provide excellent analgesia or even anesthesia for many hours. Systemically, medications include opioids, NSAIDs, and antineuropathics for treatment of acute pain. Preparation of a pain first-aid kit for excursions into the outdoors allows for the greatest number of options for treatment of various maladies (Box 17-1).



BOX 17-1 Pain Management First-Aid Kit*



Basics



Esmarch bandage, 3 × 36 inches

Hot and cold packs


Oral Medications



Acetylsalicylic acid, 500 mg

Acetaminophen, 500 mg

Carisoprodol (Soma), 350 mg, or metaxalone (Skelaxin), 500 mg

Diazepam (Valium), 5 mg

Hydrocodone, 5 mg


Injectable Medications



Naloxone, two 0.4-mg ampules

Ketamine, 50 mg/mL, 5 to 10 mL

Lidocaine, 1%, 30 mL

Procaine, 1%, 30 mL

Midazolam (Versed), 5 mg/mL, 5-mL vial

Morphine, 5 mg/mL, 5-mL vial

Meperidine (Demerol), 50 mg/mL, 5-mL vial


Topical Therapies



Capsaicin ointment, 2-g tube

Lidocaine ointment, 5%, 30 to 50 g

Lidocaine patches, 5%

Diclofenac, 1% gel, 100 g

Diclofenac, 1.3% patch (Flector Patch)


Additional Supplies



Intravenous cannula, 20 gauge, three

Intravenous cannula, 18 gauge, three

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Sep 7, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Principles of Pain Management

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