CHAPTER 47 Analgesic Use for Effective Pain Control *

Fear of pain is a significant reason why many people avoid seeking dental care. No matter how successful or how effectively performed, most dental surgical procedures produce tissue trauma and release potent mediators of inflammation and pain. In the past, postoperative pain was thought to be inevitable and harmless. We now know that unrelieved pain after surgery or trauma has negative physical and psychological consequences. Acute pain is often associated with a reactive anxiety and an increase in sympathetic nervous system activity, resulting in tachycardia, hypertension, diaphoresis, mydriasis, and pallor. A patient with severe tooth or jaw pain may avoid eating or drinking and may become malnourished and dehydrated. Severe chest, abdominal, or back pain may lead to shallow breathing and cough suppression in an attempt to “splint” the injured site, followed by retained pulmonary secretions and pneumonia.¹⁹^,³⁷ Unrelieved pain may also delay the return of normal gastric and bowel function in a postoperative patient.⁴¹ If managed aggressively, pain is preventable or controllable in most cases.

Undertreatment of pain is a significant medical problem. Numerous clinical surveys have shown that postoperative pain is often inadequately treated because of undermedication, leaving patients to suffer needlessly.¹⁴^,³¹ Recognition of the widespread inadequacy of pain management and the detrimental effects of untreated pain has led to corrective efforts in numerous health care disciplines involved with pain management. These efforts culminated in 1992, when the Agency for Health Care Policy and Research, a division of the U.S. Public Health Service, published its Clinical Practice Guideline for Acute Pain Management: Operative or Medical Procedures and Trauma.² This guideline represents the efforts of a multidisciplinary panel of expert clinicians and researchers. It provides an excellent framework for the care of patients with acute pain and includes a section on pain control specifically for dental surgery.

PAIN CLASSIFICATION

Successful treatment of painful conditions with analgesics requires a basic understanding of the relevant pathophysiology. Painful conditions can be divided into two basic categories—nociceptive pain and neuropathic pain—based on the condition’s underlying pathophysiologic features. Nociceptive pain is a result of mechanical, thermal, or chemical activation of nociceptive afferent receptors and can be classified as either somatic or visceral in origin. Somatic nociception involves pathologic conditions of the skin, muscles, fascia, and bones and is well localized. Examples include the pain associated with traumatic injuries and pain after the completion of oral surgery procedures. In both conditions, inflammatory mediators sensitize or activate nociceptive receptors, resulting in transduction of the noxious stimulus into electrical and biochemical signals between neurons. The electrical signals are conducted to the brain for interpretation. Visceral nociceptive pain is poorly localized, may be referred to superficial somatic regions, and involves pathologic conditions in deep, visceral tissues. An example is angina resulting from myocardial ischemia, which can be referred to the jaw, neck, or arm.

Neuropathic pain is thought to be a result of aberrant somatosensory activity either in the peripheral nervous system or the central nervous system (CNS) (see Chapter 23). It is frequently characterized by paroxysmal shooting or electrical shock–like pains, often on a background of burning or constricting sensation. Examples of neuropathic pain encountered in the orofacial region include trigeminal neuralgia, burning mouth syndrome, and postherpetic neuralgia. Orofacial pain of neuropathic origin generally requires more sophisticated diagnostic testing and management; this sort of care is frequently available at specialized clinical practices.

Pain may also be characterized as acute or chronic based on its temporal and other characteristics. Acute pain frequently has a known cause, has identifiable tissue damage, responds to conventional analgesic therapy such as nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids, usually subsides as healing occurs, and has a predictable end point. Acute pain is associated with anxiety and the physiologic “flight or fight” responses of increased pulse, blood pressure, and respiratory rate. In contrast, chronic pain is of greater than 3 to 6 months’ duration, and patients with chronic pain do not usually manifest the physiologic arousal seen with acute pain because the body has adapted to the pain state. These patients may exhibit, however, reactive depression and decreased function. Often, despite numerous diagnostic tests, the area where the pain seems to emanate appears normal or adequately healed, if there was an initial injury. The psychological aspects of the chronic pain syndrome can become so entwined with the patient’s presentation of pain that these aspects must now also be adequately addressed to increase the likelihood of a successful treatment outcome.

PAIN ASSESSMENT

Successful assessment and control of pain depend partly on establishing effective communication between the dentist and the patient. Patients should be informed that pain relief is an important part of their health care. Because pain is a subjective phenomenon, the care provider must accept that the patient’s self-report is the most accurate and reliable indicator of the existence and intensity of pain and any resultant distress.² This orientation is reflected in a commonly cited definition of pain: Pain is whatever the person experiencing it says it is and exists whenever he or she says it does.²⁷ Self-report measurement tools such as adjective or numerical rating scales or visual analogue scales can assist the patient in quantifying and characterizing the pain (Figure 47-1).

FIGURE 47-1 Pain intensity scales. A 10-cm baseline is recommended for the visual analog scale and for the other scales if used for graphic rating (i.e., linear measurement of patient responses).

These tools are reliable, valid, and easy for the patient and the dentist or assistant to use. They may be administered by showing a diagram to the patient and asking the patient to indicate the appropriate rating. Some tools may also be used by simply asking the patient for a verbal response (e.g., “On a scale of 0 to 10, with 0 as no pain and 10 as the worst pain possible, how would you rate your pain?”). Patients who may have difficulty communicating require particular attention. This group includes patients who are cognitively impaired; psychologically or severely emotionally disturbed patients; young children; very old patients; and patients whose language, level of education, or cultural background differs significantly from that of the health care team.

Assessment of the patient’s pain is a crucial part of the initial evaluation to estimate analgesic requirements. To determine the adequacy of the chosen analgesic regimen, the clinician must also assess pain intensity and pain relief at the peak of the analgesic effect and at regular intervals after the initiation of analgesic treatment.⁹

MISCONCEPTIONS REGARDING PAIN AND ANALGESICS

A significant barrier to the effective use of analgesics in managing pain involves several misconceptions regarding pain and analgesia held by patients and health care providers.

• Misconception 1: Patients who are in pain always have observable signs. Although many patients in acute pain exhibit evidence of anxiety, distress, or decreased function, many do not. Such overt pain behaviors also may not be seen at all in patients attempting to adapt to, and cope with, persistent pain. Expecting patients to display these pain behaviors and making the decision to dispense analgesics contingent on the display of these behaviors only serve to reinforce pain behaviors that may interfere with recovery. To treat the pain effectively, the clinician first must believe the patient’s complaint of pain irrespective of the patient’s physical presentation.

• Misconception 2: Obvious pathology, test results, and the type of surgery determine the existence and the intensity of pain. Although the ability to identify a pathologic process underlying a patient’s pain complaint is a key element in planning and initiating definitive treatment, failure to identify the source of a patient’s pain does not mean that it does not exist. Patients with chronic neuropathic pain frequently present such diagnostic challenges. As medical and diagnostic technology progresses, clinicians are better able to understand the mechanisms underlying disease processes that might have gone undiagnosed, or misdiagnosed, in the past. Failure to identify an organic source for a patient’s pain does not mean that the pain does not exist.

• Misconception 3: Patients should wait as long as possible before taking a pain medication because this period of abstinence teaches them to have a better tolerance for pain. Pain that is untreated often escalates in severity and disability. Without treatment, sensory input from injured tissue reaches spinal cord neurons and causes subsequent responses to be enhanced. Pain receptors in the periphery also become more sensitive after injury. Studies have shown long-lasting changes in cells within the spinal cord pain pathways after brief painful stimuli.⁷ These physiologic studies confirm long-standing clinical impressions that established pain is more difficult to suppress.^2,^7,¹⁵ Aggressive pain prevention and control that occurs before, during, and after a painful event such as dental surgery can yield short-term and long-term benefits. Patients should be encouraged to use analgesics before pain becomes severe and difficult to control.

CHOICE OF ANALGESIC REGIMEN

Pharmacologic control of pain can be directed at any of three nociceptive processes: (1) initiation of impulses, (2) propagation of the impulses, and (3) perception of painful stimuli. NSAIDs are thought to act primarily at the site of initiation of nociceptive impulses. Although separating their anti-inflammatory effects from their analgesic effects is difficult, nonopioid drugs, such as salicylates, other NSAIDs, and cyclooxygenase (COX)-2 inhibitors, work predominantly in the periphery by preventing the synthesis and release of inflammatory mediators that sensitize nociceptive receptors to other algesic mediators, such as bradykinin, and to physical forces. More recent studies suggest that NSAIDs may also have central effects.⁶^,²⁴ Acetaminophen has been shown to have analgesic and antipyretic properties, but it lacks significant anti-inflammatory effects. Acetaminophen seems to exert its effects in the CNS and in the periphery.^1,^28,³⁹

Local anesthetics can be administered topically or parenterally to block the propagation of nerve impulses originating from nociceptive stimuli at a peripheral site so that they do not reach the spinal cord or brain. Administration of long-acting local anesthetics can have significant value in delaying the onset of pain after oral surgery procedures and decreasing the overall level of discomfort in the immediate recovery period. The systemic use of local anesthetics also has some use in the management of chronic pain.

Opioids decrease the perception of pain in the CNS. Opioid analgesics act in the CNS at receptors in the spinal cord, rostroventral medulla, and periaqueductal gray matter. These anatomic loci are considered important to the perception of pain (see Chapter 20). Laboratory studies have also identified and characterized opioid receptors in peripheral tissue. This finding has led to clinical studies that have identified opioids as contributors to antinociceptive responses in the peripheral nervous system.²²^,²⁹ Likewise, there has been a search for drugs that reduce the incidence of opioid peripheral side effects, most notably constipation, in patients taking these drugs for various types of pain.⁴