Pain Management

Chapter 51


Pain Management



In the United States it is estimated that approximately 76 million people suffer from some type of pain, including acute, chronic, and/or postsurgical.1 Even though advances have been instituted to help practitioners recognize and treat pain, the incidence of unrelieved pain continues to be a major concern. In 1992 the Agency for Healthcare Research and Quality (AHRQ) devised the first clinical practice guidelines (CPGs) for pain management. Subsequently, other groups including the American Pain Society (APS), American Society of Anesthesiologists (ASA), and the American Academy of Pain Management (APM) have instituted CPGs for management of acute and chronic pain. In addition to these associations, others have developed CPGs specific to patient populations (e.g., elderly and pediatrics) and to types of pain (e.g., cancer pain, postoperative pain, and chronic noncancer pain) in an effort to improve pain management. Even though there are CPGs, pain management remains inadequate. Several professional and regulatory groups have proposed standards, responsibilities, and outcome measures to improve pain management. The Joint Commission (TJC) developed pain management standards that were implemented in 2001. TJC clearly outlined the responsibilities of hospitals, home-care agencies, nursing homes, behavioral facilities, and out-patient clinics seeking accreditation (Box 51-1). The implementation of these standards is a momentous step in the improvement of pain management.



BOX 51-1   The Joint Commission Pain Management Standards


The Joint Commission pain management standards require organizations to:



From Berry PH, Dahl JL. The new JCAHO standards: implications for pain management nurses. Pain Manag Nurs. 2000;1(1):3-12.


As providers of anesthesia care in the United States, certified registered nurse anesthetists (CRNAs) are integral to the research and management of acute and chronic pain. It is their professional and ethical responsibility to participate in the assessment, management, and treatment of pain based on each patient’s unique needs in a holistic and multidisciplinary manner.2 Only recently have CRNAs been recognized as experts in the area of pain management, and their knowledge and skills are essential in pursuing effective pain management modalities.



Pain



Definition


Pain remains a very complex and multidimensional experience. It was defined by the International Association for the Study of Pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”3 The inherent context of this definition is that pain is a physiologic, emotional, and a behavioral experience.4 Commonly used pain terminology is listed in Box 51-2.



BOX 51-2   Pain Terminology




Classification of pain is primarily based on longevity (acute versus chronic) and/or the underlying pathophysiology (nociceptive or non-nociceptive).5 Nociceptive pain is associated with the stimulation of specific nociceptors and can be either somatic or visceral. Somatic pain refers to pain that has an identifiable locus as a result of tissue damage causing the release of chemicals from injured cells that mediate pain. Somatic pain is well localized, sharp in nature, and generally hurts at the point or area of stimulus. Conversely, visceral pain is diffuse, can be referred to another area, and is often described as “dull,” “cramping,” “squeezing,” or vague in nature. Visceral pain is often associated with the distention of an organ capsule or the obstruction of a hollow viscus. It is also often accompanied with autonomic reflexes such as nausea, vomiting, and diarrhea.6 In contrast, non-nociceptive pain can be categorized as being neuropathic or idiopathic. Neuropathic pain is caused by damage to peripheral or central neural structures resulting in abnormal processing of painful stimuli. It is a dysfunction of the central nervous system (CNS) that allows for spontaneous excitation in chronic pain states. Neuropathic pain is often described as “burning,” “tingling,” or “shocklike.”7 Idiopathic pain or psychogenic pain is also associated with chronic pain states and is used to describe pain that has no apparent cause. Neither nociceptive nor neuropathic mechanisms can be identified as a cause for pain, and psychological symptoms are commonly present. Patients in chronic pain states often exhibit more than one type of pain along with a psychological component. Therefore, psychological, cultural, and environmental factors should be addressed when assessing patients with chronic pain.6



Anatomy and Physiology


Somatic nociceptive pain is most commonly defined in terms of four processes: transduction, transmission, perception, and modulation. Transduction is the transformation of a noxious stimulus (chemical, mechanical, or thermal) into an action potential. A noxious stimulus is detected by pain receptors, or nociceptors, which are free nerve endings. These peripheral nociceptors that conduct noxious stimuli to the dorsal horn of the spinal cord are categorized according to morphology (diameter, myelination, and conduction velocity). The myelinated A-delta (Aδ) primary afferent neurons conduct action potentials at velocities between 6 and 30 m/sec and elicit fast-sharp pain. They are responsible for the initial mechanical or thermal pain that is felt and alert an individual of tissue damage, thereby resulting in the reflex withdraw mechanism. The smaller nonmyelinated C fibers conduct at velocities significantly slower, between 0.5 and 2 m/sec. Because C fibers respond to mechanical, thermal, and chemical injuries, they are also known as polymodal fibers. Due to their slow conducting velocity, a delayed, slow, second pain is elicited by C fibers.8 Slow pain is commonly described as “dull,” “burning,” “throbbing,” and “aching.”


Consequently, when peripheral tissues (skin, bone, and viscera) receive chemical, thermal, or mechanical stimuli or are traumatized by either surgery or injury, a series of biochemical events take place in peripheral pain transduction. These events include the release of chemical mediators from the inflammatory response and the release of neurotransmitters from nociceptive nerve endings (Figure 51-1). The chemical mediators and neurotransmitters released are extensive, with the more prominent substances listed below:




• Substance P is a peptide found and released from the peripheral afferent nociceptor C fibers and is involved with slow, chronic pain. It acts via the G-protein–linked neurokinin-1 receptor, resulting in vasodilation, extravasation of plasma proteins, degranulation of mast cells, and sensitization of the stimulated sensory nerve.9


• Glutamate is a major excitatory neurotransmitter released in the CNS and from the Aδ and C primary afferent nerve fibers. Its effects are instantaneous, producing initial, fast-sharp pain.8


• Bradykinin is a peptide released during the inflammation process and is notably algesic. It has a direct stimulating effect on peripheral nociceptors via specific bradykinin receptors (B1/B2).


• Histamine is an amine released from mast cell granules, basophils, and platelets via substance P. It reacts with various histamine receptors to produce edema and vasodilation.


• Serotonin (5-hydroxytryptamine [5-HT]) is an amine stored and released from platelets after tissue injury. It reacts with multiple receptor subtypes and exhibits algesic effects on peripheral nociceptors. Like histamine, serotonin can potentiate bradykinin-induced pain.


• Prostaglandins (PGs), along with thromboxanes and leukotrienes, are a metabolite of arachidonic acid. PGs, specifically, are synthesized from cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). They are associated with chronic pain; PGs sensitize peripheral nociceptors, causing hyperalgesia.


• Cytokines are released in response to tissue injury by a variety of immune and nonimmune cells via the inflammatory response. Cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) can lead to the increased production of PGs, thereby exciting and sensitizing nociceptive fibers.10


These chemical mediators and neurotransmitters stimulate the peripheral nociceptors, causing an influx of sodium ions to enter the nerve fiber membranes (depolarization) and a subsequent efflux of potassium ions (repolarization). An action potential results, and a pain impulse is generated.


Transmission is the process by which an action potential is conducted from the periphery to the CNS. There are multiple pathways that carry noxious stimuli to the brain. The spinothalamic (anterolateral) system, which carries pain signals from the trunk and lower extremities, will be discussed here. The primary afferent neurons (Aδ and C fibers) have cell bodies located in the dorsal root ganglia of the spinal cord. Upon entering the dorsal cord, these fibers segregate and ascend or descend several spinal segments in the tract of Lissauer. After leaving the tract of Lissauer, the axons of the primary afferents enter the gray matter of the dorsal horn where they synapse with second-order neurons and terminate primarily in Rexed’s laminae I, II, and V (Figure 51-2). Two types of second-order neurons exist: (1) nociceptive neurons, which receive input solely from primary afferent Aδ and C fibers and (2) wide-dynamic-range (WDR) neurons that receive input from both nociceptive (Aδ and C fibers) and non-nociceptive (A-β) primary afferents. Wide-dynamic-range neurons are therefore activated by a variety of stimulants (innocuous and noxious) (Figure 51-3).




Second-order neurons then cross the midline of the spinal cord through the anterior commissure and ascend in the anterolateral pathway of the spinothalamic tract to the thalamus. In the lateral thalamus and the intralaminar nuclei, second-order neurons synapse with third-order neurons, which then send projections to the cerebral cortex. Perception of pain occurs once the signal is recognized by various areas of the brain, including the amygdala, somatosensory areas of the cortex, the hypothalamus, and the anterior cingulate cortex.


Modulation of pain transmission involves altering neural afferent activity along the pain pathway; it can suppress or enhance pain signals. Suppression of pain impulses occur through local inhibitory interneurons and descending efferent pathways. The descending efferent modulatory pathways from the brain are considered the body’s “analgesia system” or pain control system.8 It is proposed that the descending dorsolateral efferent pathway is activated via a noxious stimulus. Descending axons from the cerebral cortex, hypothalamus, thalamus, periaqueductal gray area (PAG), nucleus raphe magnus (NRM), and locus coeruleus (LC) via the dorsolateral funiculus (DLF) synapse with and suppress pain transmission to the brainstem and the spinal cord dorsal horn. Several neurotransmitters and their receptors play critical roles in the inhibitory modulation of pain, including the inhibitory endogenous opioids (enkephalin/dynorphin). Action potentials arrive at the substantia gelatinosa via the DLF and activate enkephalin-releasing neurons. Enkephalin then binds to the opiate receptors on presynaptic first-order or postsynaptic second-order afferent fibers, which decrease substance P release, thereby suppressing ascending pain transmission. Other inhibitory neurotransmitters released via the descending pathway include glycine, norepinephrine, serotonin, and gamma-aminobutyric acid (GABA) (Table 51-1). Pharmacotherapies for pain control are aimed at many of these neurotransmitters and their receptors.



Pain modulation is enhanced in the presence of “central sensitization.” Central sensitization refers to the neural plasticity that occurs in the CNS. When tissue or neural injury exists, repetitive stimulation and activation of nerves results in changes in neurotransmitter levels and signaling in the CNS. For example, the repetitive firing of dorsal horn nociceptors causes activation of lower non-nociceptive threshold mechanoreceptors (A-β afferents) to trigger a pain response. There are also other factors involved in central sensitization, including the inflammatory response and an increase in receptive field size.11 Central sensitization is associated with chronic pain states and is addressed in more detail later in this chapter.



Acute Pain


Acute pain is caused by noxious stimulation due to traumatic injury (chemical, thermal, or mechanical), surgery, or acute illness. Generally, the intensity of acute pain diminishes over the course of healing; however, social, cultural, and personality factors may affect this. Its duration is usually self-limited and resolves within 1 to 14 days. Acute pain is responsive to pharmacotherapy and treatment of the precipitating cause. Unfortunately, poorly controlled acute pain may lead to chronic pain states. Therefore, optimal pain management is crucial in expediting the healing process and for the prevention of chronic pain.


It is well documented that acute pain causes adverse physiologic consequences involving multiple organ systems, which can contribute to morbidity and mortality in surgical patients. Neuroendocrine responses that are triggered primarily by the sympathetic nervous system (SNS) in response to surgical stress and pain initiate these effects. Factors such as the extent of the surgical field, the number of pain receptors involved in the area, bleeding, infection, anxiety, and presence of coexisting diseases may accelerate the endocrine stress response.


The activation of the sympathetic nervous system in response to the stress of pain from surgery or trauma results in many cardiovascular responses. The increased release of catecholamines from the SNS and adrenal glands, along with cortisol, produces an increased heart rate, increased vascular resistance (peripheral, systemic, and coronary), increased myocardial contractility, and increased arterial blood pressure. These ultimately increase the myocardial demand and myocardial oxygen consumption. Additionally, in the presence of coexisting cardiovascular disease, atherosclerotic plaque from vascular walls may rupture, thereby decreasing oxygen supply further. This may lead to dysrhythmias, angina, myocardial ischemia, and myocardial infarction. Overall, the incidence of increased myocardial oxygen demand and decreased myocardial oxygen supply can have deleterious effects in those patients with coexisting cardiovascular disease. Therefore, aggressive pain management is essential in reducing the incidence of postoperative cardiac complications.12


The presence of pain can have significant effects on the respiratory system. These effects are most pronounced in those patients having surgery or trauma in the upper abdominal area and thorax. Inadequate pain management causes a measurable decrease in tidal volume because of limited thoracic and abdominal movement. Specifically, there are decreases in vital capacity, inspiratory capacity, and functional residual capacity (FRC), as well as a decreased physical ability to clear the airway, due to unrelieved pain. Additionally, muscle spasm below and above the site of injury caused by the noxious stimuli promotes limited movement of the respiratory muscles. Patients often voluntarily decrease the movement of the thorax and abdomen (splinting) and are reluctant to breathe deeply or cough in an attempt to limit pain, which can lead to atelectasis and pneumonia.13,14 These pulmonary alterations may be aggravated in those patients with preexisting pulmonary dysfunction (e.g., asthma, chronic obstructive pulmonary disease) or in those with decreased FRC (e.g., morbidly obese, elderly). Consequently, those affected by postoperative respiratory compromise due to inadequate pain management also may be at risk for deep venous thrombosis and subsequent pulmonary embolism due to a decrease or delay in mobilization. See Table 51-2 for physiologic consequences of acute pain.



The physiologic effects and the consequences of inadequate pain management have been reported to have an impact in delaying postoperative stay, patient recovery, and an overall increase in healthcare costs.15 It also negatively impacts the patient’s surgical/hospitalization experience, resulting in reduced patient satisfaction.



Acute Pain Assessment


To devise a plan for intraoperative and postoperative surgical pain management, a preoperative pain assessment and discussion with the patient should be conducted. A thorough preoperative assessment should involve a physical and medical history assessment, including laboratory and diagnostic tests that are patient and surgery specific. Inquiries specific to preoperative pain also should be addressed; these are found in Box 51-3. Part of the preoperative pain assessment process also should consist of identifying those at high risk for increased postoperative acute pain. A recent study identified that the most important predictors of acute postoperative pain after elective surgery include: (1) the presence of preoperative pain, (2) patient fear regarding the outcome of his/her surgery, (3) patients who catastrophize pain, and (4) expected pain postoperatively.16 Overall, goals for pain management should be based on patient physical/medical assessment, history, invasiveness of the surgical procedure, an individual’s pain response, and prediction of identifying those who are at high risk for developing increases in acute pain postoperatively. The patient should be informed of the varying modalities for postoperative pain control, and a unique pain management plan should be implemented by both the patient and care providers. Furthermore, realistic expectations for postoperative pain control should be discussed.



BOX 51-3   Preoperative Pain Assessment




OTC, Over-the-counter; TENS, transcutaneous electric nerve stimulation; SCS, spinal cord stimulator; prn, as needed.


As discussed earlier, adequate postoperative pain control is essential in the recovery process. Assessing the adequacy of postoperative pain control through vigilance and by using simple assessment tools is vital. Because pain is subjective, the most reliable pain assessment tool is primarily via self-report. Pain assessment scales, which are both clinically valid and used in research, are available and are based on measuring pain intensity. The common pain intensity scales include the visual analog scale (VAS), the numerical rating scale (NRS), and the Wong-Baker FACES scale. Even though these scales are available and are used in the clinical setting, they are not all-inclusive. The NRS, VAS, and Wong-Baker FACES scales assign a numerical value to an individual’s pain, which is subjective and multidimensional. In addition, they do not take into consideration the patient’s age or variations in cognitive level. The NRS is most often used by practitioners in assessing pain by asking the patient “What is your pain level on a scale of 1 to 10, with 10 being the worst pain you have ever experienced and 0 being pain-free?” Although this is a quick tool used to assess pain, it lacks the depth of determining the quality of pain or exacerbating factors that affect pain. Inevitably it is the provider’s responsibility to investigate the patient’s pain, be it surgical or nonsurgical, and intervene with a treatment modality. Key to successful acute pain control is vigilant reassessment and evaluation of the patient’s response to a given treatment and changing treatment modalities, if necessary, in an effort to alleviate pain.



Preemptive Analgesia


Preemptive analgesia is a concept first postulated approximately 100 years ago. It was asserted that by administering analgesics prior to noxious stimulation, a decreased pain response would result. The premise is that peripheral and central sensitization results from noxious stimulation, thereby causing an increase in postoperative pain. Preemptive analgesia in preventing central sensitization remains controversial. For example, in an animal study by Chang et al.,17 preincisional treatment with an N-methyl-d-aspartate (NMDA) antagonist was not found to be more beneficial than postincisional treatment. Likewise, Hariharan et al.18 found in a human study that local anesthesia administered prior to incision with abdominal hysterectomy did not reduce the intensity of postoperative pain. However, in contrast, Arici et al.19 concluded that preemptive intravenous (IV) paracetamol provided “good quality” postoperative analgesia and a reduction in morphine administration postoperatively. Similarly, Persec et al.20 reported that the administration of intrathecal clonidine reduced postoperative pain significantly more than did administration of intrathecal levobupivicaine.


Regardless of the controversies surrounding preemptive analgesia, a multimodal approach to acute and chronic pain management is common practice. Multimodal pain management consists of using a combination of analgesics that work on a variety of receptors with different mechanisms of action, both peripherally and centrally, resulting in additive or synergistic effects in an effort to improve pain control.



Acute Pain Analgesics



Nonsteroidal Antiinflammatory Drugs


Nonsteroidal antiinflammatory drugs (NSAIDs) are best known for their use in the management of mild to moderate postoperative pain and pain related to inflammatory conditions. They are the most common analgesic adjuvants used in multimodal analgesia remedies. When using NSAIDSs and opioids together, a synergistic effect results in analgesia along with an overall decreased dose of opioids and decreased opioid side effects. NSAIDs vary in chemical structure but all possess antiinflammatory, antipyretic, and analgesic properties. They produce their therapeutic effects by inhibiting cyclooxygenase (COX) and thereby preventing conversion of arachidonic acid to prostaglandins. Prostaglandins (primarily PGE1 and PGE2) are responsible for sensitizing and amplifying peripheral nociceptors to the inflammatory mediators (substance P, bradykinin, and serotonin), which are released when tissue is traumatized. Therefore, prostaglandins do not directly produce pain but instead contribute to hyperalgesia. Centrally, prostaglandins mediate pain by enhancing the release of substance P and glutamate in first-order neurons, increasing nociceptive transmission at second-order neurons, as well as inhibiting the release of descending inhibitory neurotransmitters (Figure 51-4).



COX exists in two isoforms: COX-1 and COX-2. COX-1 is constitutive, widespread throughout the body, and necessary for homeostasis. It is responsible for platelet aggregation, gastric mucosal integrity, and renal function. Conversely, COX-2 is an inducible enzyme that in the presence of inflammation releases prostaglandins, thereby mediating pain, fever, and carcinogenesis.21 Until recently, all of the NSAIDs were nonselective in their COX inhibition. As a result, in addition to the analgesia effects from the inhibition of the COX-2 isoform, inhibition of COX-1 was responsible for the detrimental side effects of gastric irritation, renal microvasculature constriction, and platelet inhibition. Presently in the United States, celecoxib is the only COX-2–selective NSAID available. Others have been withdrawn from the market because of cardiovascular side effects. Celecoxib is available orally and is used for treating acute surgical pain, chronic pain syndromes, and cancer pain in conjunction with other analgesic approaches. It is metabolized by the liver extensively via cytochrome P450 (CYP450). A contraindication for celecoxib administration includes known hypersensitivity to sulfonamides because it contains sulfa. In addition, celecoxib should also be avoided in patients with a history of asthma or allergic reaction to aspirin or other NSAIDs, because COX-2 inhibitors can convert arachidonic acid to the precursor of leukotrienes, potentially causing bronchoconstriction and/or anaphylaxis.



Ketorolac

Ketorolac, a nonselective COX inhibiter, is also available for short-term acute postoperative pain, administered either alone or in combination with other analgesic modalities. Ketorolac can be administered orally, intravascularly, intramuscularly, and intranasally. Comparatively, the analgesic potency of ketorolac 30 mg intramuscular (IM) is equivalent to approximately 12 mg of morphine IM.22 Because of the potential adverse effects caused by the inhibition of COX-1, ketorolac should not be administered beyond 5 days.23 Contraindications for administering ketorolac include coagulopathies, renal failure, active peptic ulcer disease, gastrointestinal bleeding, history of asthma, hypersensitivity to NSAIDs, and surgery that involves a high risk for postoperative bleeding. In addition, controversy exists regarding bone healing and ketorolac administration. Ketorolac’s inhibition of COX-1, COX-2, and prostaglandin synthesis interrupts normal prostaglandin effects on osteoblast and osteoclast functioning that promotes bone healing.24,25 However, currently there are no recommendations regarding ketorolac administration and orthopedic procedures.



Acetaminophen

Acetaminophen reduces prostaglandin synthesis by an uncertain mechanism. It has minimal antiinflammatory effects with mainly analgesic and antipyretic properties. It is suitable for acute mild to moderate postoperative pain and fever. Oral acetaminophen is frequently combined with weak opioids (e.g., oxycodone, hydrocodone, codeine) for the treatment of moderate postoperative pain and chronic pain syndromes. Because it lacks the negative effects of typical NSAIDs (e.g., platelet inhibition, gastrointestinal irritation, renal toxicity), acetaminophen is an ideal drug for multimodal analgesia for surgical pain. Acetaminophen is metabolized primarily by the liver and is therefore contraindicated in patients with liver failure. Parenteral acetaminophen (Ofirmev) is also available for the treatment of acute mild to moderate pain and is effective in treating moderate to severe pain with adjunctive opioid analgesics.26 Dosing for adults weighing over 50 kg is 1000 mg every 6 hours or 650 mg every 4 hours infused over 15 minutes to a maximum of 4000 mg/day. Dosing in children over 2 years of age and under 50 kg is 15 mg/kg every 6 hours or 12.5 mg/kg every 4 hours to a maximum of 75 mg/kg/day. Onset of action is approximately 10 minutes with a duration of action of 4 to 6 hours. Adverse effects of IV acetaminophen are rare when dosed accordingly, with more common side effects being nausea, vomiting, headache, and insomnia.27



Opioids


Opioid analgesics remain the drugs of choice for treatment of moderate to severe pain in the early postoperative period. Opioids produce analgesia by binding to and activating G-protein coupled opioid receptors (GPCRs) peripherally and in the CNS. Centrally, opioid receptors are predominantly found in the dorsal horn of the spinal cord, specifically Rexed’s lamina II of the substantia gelatinosa, and supraspinally in the periaquadectal grey (PAG) area, medial thalamus, amygdala, and limbic cortex. Peripherally, they are found on afferent sensory nerve fibers as well as in the gastrointestinal tract, lungs, and joints.28

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May 31, 2016 | Posted by in ANESTHESIA | Comments Off on Pain Management

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