Take Test
Abstract
PURPOSE: To provide the wound care practitioner with an overview of research and knowledge about the causes, mechanisms, contributing factors, and management of acute wound pain.
TARGET AUDIENCE: This continuing education activity is intended for physicians and nurses with an interest in skin and wound care.
OBJECTIVES: After reading this article and taking this test, the reader should be able to:
1. Describe the causes of acute wound pain.
2. Discuss research findings related to the physiology of wound pain.
3. Identify current concepts in the management of acute wound pain.
INTRODUCTION
Acute wounds that occur as a result of surgery or trauma are associated with moderate to severe pain.1-3 Recent evidence suggests that unrelieved pain can interfere with the wound-healing process. For example, women with higher pain intensity scores experienced delays in wound healing after elective gastric bypass surgery.4 In addition, unrelieved postoperative pain and hyperalgesia may be risk factors for the development of chronic postsurgical pain.5,6
Despite the large numbers of patients who undergo surgery or experience traumatic injuries, the majority of the literature on wound pain is focused on chronic wounds. Therefore, this article will discuss the causes of acute wound pain, the mechanisms of and the factors that contribute to acute wound pain, and the management of acute wound pain.
CAUSES OF ACUTE WOUND PAIN
Acute wounds heal in a timely manner7 and most commonly are a result of surgical or traumatic origin. Acute wound pain (ie, pain at the site or around an acute wound) can occur spontaneously or result from an activity or procedure. The World Union of Wound Healing Societies categorized the causes of wound pain as background, incident, procedural, and operative.8
Definitions and research findings on the causes of wound pain are summarized in Table 1. Not surprisingly, Table 1 shows that level of pain depends on the causes of pain. In both acute and chronic wounds, background pain (ie, pain at rest) ranges from mild to moderate. Incident pain (eg, pain while coughing), procedural pain (eg, pain during dressing removal), and operative pain (eg, wound debridement) are worse than pain at rest.
 | Table 1. DEFINITIONS AND RESEARCH FINDINGS ON THE CAUSES OF PAIN ASSOCIATED WITH ACUTE WOUNDS |
MECHANISMS OF WOUND PAIN
Mechanisms that underlie the development of acute wound pain have been identified in experimental and clinical models of surgical wounds. Although many studies have attempted to determine the mechanisms involved in wound pain, these mechanisms remain poorly understood.9 Apparently, more than 1 mechanism is involved in wound pain. For example, incisional pain may involve nociceptive, inflammatory, and neuropathic pain.10 However, a recent review11 suggests that the ischemic pain mechanism may be responsible for incisional pain. The following sections of this article will summarize the 3 major types of pain, the concepts of peripheral and central sensitizations in relationship to acute wound pain, and factors that can contribute to acute wound pain.
Nociceptive pain. As illustrated in Figure 1, nociceptive pain occurs immediately after exposure to a noxious stimulus (eg, thermal, mechanical, chemical), and it is necessary to prevent further tissue damage.12 Nociceptive pain is mediated through the peripheral (ie, A-delta [A-[delta]] and C fibers) and central nervous systems through the processes of transduction, transmission, modulation, and perception.
 | Figure 1. NOCICEPTIVE PAIN MECHANISMAbbreviations: A[delta] = A-delta fibers; C = C fibers. |
Transduction converts a peripheral noxious stimulus into electrical activity. The electrical signal is transmitted from the peripheral nervous system to the central nervous system initiated by neurotransmitters found in the spinal cord, brain stem and thalamus, and cerebral cortex.12,13
Modulation refers to the facilitation or inhibition of pain impulses sent to the brain. Modulation occurs directly at the level of the spinal cord and through descending pathways from the midbrain periaqueductal gray region, pons, and medulla to the dorsal horn.12,14,15 In addition to these areas, the thalamus and cortex are involved in pain modulation.16 Finally, perception refers to the interpretation of the nociceptive signal as pain.10
Inflammatory pain. Inflammatory pain arises when tissue damage occurs due to surgery, trauma, or other inflammatory conditions.12 This pain usually resolves when the condition that provokes the inflammation is controlled.17 Inflammation is characterized by redness (rubor), heat (calor), and swelling (tumor).14
Inflammatory pain follows the same pathways and processes as nociceptive pain but is associated with peripheral sensitization and central sensitization.12 According to Meyer et al,18 "sensitization is characterized by a decrease in threshold, an augmented response to suprathreshold stimuli,and ongoing spontaneous activity." As illustrated in Figure 2, peripheral sensitization occurs when tissue damage induces the release of chemical mediators from different cells and/or tissue-damaged sites that activate or sensitize the nociceptors.12,14,18,19 As a consequence of nociceptor sensitization, the process of transduction is altered, and the conduction of the electrical impulse increases.20 In addition, the activation threshold of nociceptors decreases, which results in allodynia (ie, pain caused by a stimulus that normally is not noxious).14,21 These physiological processes result in primary hyperalgesia, a condition in which the site of injury or inflammation has increased sensitivity to pain.12,18
 | Figure 2. PERIPHERAL AND CENTRAL SENSITIZATION MECHANISMSAbbreviations: [up arrow] = increase; A[delta] = A-delta fibers; C = C fibers; NMDA = |
As part of inflammatory pain, central sensitization can occur. In this process, dorsal horn neurons are activated through the release of neurotransmitters from primary afferent nociceptors.12,19 These neurotransmitters stimulate dorsal horn neurons to become hyperresponsive to noxious stimuli, leading to an increase in pain transmission.12N-methyl-D-aspartate (NMDA)-type glutamate receptors participate in the hyperresponsiveness of second-order neurons.14 With central sensitization, secondary hyperalgesia and allodynia occur in uninjured areas surrounding the site of injury.18
Neuropathic pain. Neuropathic pain is caused by lesions in the peripheral or central nervous systems.17 Similar to inflammatory pain, both peripheral and central sensitizations occur, which are characterized by primary and secondary hyperalgesias, respectively.12 Neuropathic pain can occur spontaneously or be provoked by an external stimulus.12 However, unlike inflammatory pain, temporary or permanent changes can occur within the peripheral and central nervous systems, and this can result in chronic pain.6,17
Role of peripheral and central sensitizations in acute wound pain. Although it remains a topic of debate, recent studies suggest that both peripheral and central sensitizations contribute to the symptoms of primary and secondary hyperalgesias associated with incisional pain.10,11 Sensitization can contribute to increases in the severity of wound pain owing to augmentation of noxious inputs.22 Both primary and secondary hyperalgesias were demonstrated in a rat model of incisional pain (plantar aspect of the foot)23 and in human experimental models (small incision through the skin, fascia, and muscle).24 In addition, secondary hyperalgesia was found in the area surrounding an incision in patients who underwent nephrectomy25 and abdominal hysterectomy.26
The mechanisms that underlie the development and maintenance of peripheral and central sensitizations (ie, primary and secondary hyperalgesias) are not well understood. Kawamata et al24 established that secondary hyperalgesia is mediated by peripheral sensitization. After an incision is performed, A-[delta] and C fibers are sensitized and generate spontaneous activities that amplify the responses of dorsal horn neurons.27 Silent nociceptors, which normally do not respond to noxious stimuli, can become activated and contribute to the development of both primary and secondary hyperalgesias.24,28 Finally, an innocuous stimulus can be transformed to evoke allodynia through an increase in the responses of nociceptors, sensitization of silent nociceptors, and an increase in the receptive field of A-[delta] and C fibers.29 Although the specific mechanisms remain unclear, both peripheral and central mechanisms may contribute to the maintenance of secondary hyperalgesia.24 A comparison of the type of pain, characteristic of pain, and clinical symptoms among the 4 causes of wound pain is presented in Table 2.
 | Table 2. OVERVIEW OF WOUND PAIN |
Factors that contribute to acute wound pain. Many factors can contribute to the development of both peripheral and central sensitizations and, consequently, wound pain. These factors can be categorized as "wound-direct" and "wound-indirect" (Figure 3).
 | Figure 3. FACTORS THAT CONTRIBUTE TO ACUTE WOUND PAINAbbreviations: # = number; 1° = primary; 2° = secondary. |
Wound-direct factors. Brennan9 suggested that factors associated with the surgical wound contribute to the development of sensitization. Wound-direct factors include acidosis at the wound site, infection, inflammation, size, and location of the wound. Recent findings suggest that acidosis at the site of the wound induces sensitization of nociceptors.30,31 In a rodent model, the development of tissue acidosis after an incision resulted in increased pain behaviors. Rodent pain behaviors decreased when tissue pH levels became normal.31 Kim et al30 suggested that both a decrease in pH levels and an increase in tissue lactate concentration after incision contributed to incisional pain through the induction of ischemia.
Acute wounds are at risk for infection, and wound infection is usually associated with increased pain at the site of the wound. In fact, 1 criterion for diagnosis of an acute wound infection is pain.32 Infection-causing bacteria produce endotoxins and exotoxins, both of which injure tissue33 and may contribute to sensitization. Infection leads to an inflammatory response that releases the inflammatory soup (ie, the several chemical mediators) that induces nociceptor sensitization.
The association between pain and wound size is not well studied. However, in 1 study,2 patients with larger acute wounds reported higher pain intensity scores. It is possible that if the area of the wound is large, more nociceptors are activated and sensitized.
The location of the wound is another factor that is associated with differences in pain intensity. Some wounds are located in areas that involve major peripheral nerves (eg, thorax, breast, groin). These nerves can be damaged during surgical procedures, and this damage can contribute to the development of neuropathic pain as well as hyperalgesia and allodynia.34
Wound-indirect factors. A variety of indirect factors can contribute to pain in acute wounds including repetitive stimuli, cleansing solutions, the primary dressing (ie, dressing applied directly to the wound bed), and the length of time from injury. Repetitive stimulation associated with respiratory movements and coughing, especially following thoracic or abdominal surgery, may contribute to peripheral and central sensitization.24 In addition, wound care that includes removal of the dressing, local care applied to the wound, and reapplication of a dressing may also stimulate or traumatize the wound area and enhance sensitization. Trauma to the wound during local care can be done by mechanical (ie, scrubbing or high-pressure irrigation) or chemical (ie, toxic cleansing solutions) means.35
Numerous solutions are available to clean a wound. However, some solutions (eg, povidone-iodine, acetic acid, hydrogen peroxide, sodium hypochlorite) have antiseptic properties that are toxic to wound cells36,37 and may lead to sensitization of nociceptors. Some of these solutions, as well as other products, are often used as part of the primary dressing. Jurczak et al38 found that the overall ability to manage open surgical or traumatic wound pain was rated significantly (P < .01) better in patients using a hydrofiber with silver dressing than in patients using providone-iodine gauze as the primary dressing. Patients with open wounds from excision of a pilonidal sinus treated with hydrocolloids reported significantly less pain (P = .05) compared with those treated with povidone-iodine gauze.39 In the study by Meaume et al,2 95% of patients reported no pain or less pain during dressing removal when they were treated with a lipidocolloid contact layer dressing compared with wet, dry, or paraffin gauze. The use of wet or dry gauzes and gauzes impregnated in antiseptic solutions (eg, sodium hypochlorite and povidone-iodine) as primary dressings enhance wound pain.40 These dressings often dry out and adhere to the wound bed, traumatizing it when they are removed, thereby sensitizing nociceptors.
The length of time from injury is another factor that contributes to sensitization and wound pain. Wounds are more painful during the inflammatory phase of healing than during the active repair phases.40,41 Mechanisms that may contribute to increased pain include inflammation, wound hypoxia, and exposed nerve endings.40 Patients with acute wounds reported severe pain when the wound had less time from injury (P < .001).2 Patients who underwent a hysterectomy were evaluated preoperatively and at different postoperative times for pain intensity using a 0- to 100-mm visual analog scale. Pain intensity at rest was significantly higher at 4 hours (42 mm), 6 hours (22 mm), and the first day (21 mm), decreasing gradually to 0 mm by the fourth postoperative day.42 Their pain intensity during coughing gradually decreased (88 mm at 4 hours, 85 mm at 8 hours, 51 mm at the first day, and 45 mm at the fourth day), but was still significantly higher up to the eighth day (33 mm) when compared with preoperative pain intensity (0 mm).
PAIN MANAGEMENT FOR ACUTE WOUNDS
Pain management for acute wounds should focus on the use of strategies that will attenuate modifiable factors that contribute to wound pain, such as infection, repetitive stimuli, cleansing solutions, and primary dressing (Table 3). These strategies involve both pharmacological and nonpharmacological interventions that need to be individualized. Pharmacological treatments will vary based on the different types, causes, and severity of the pain. Whereas moderate to severe nociceptive pain is usually managed with opioids (eg, morphine, fentanyl, oxycodone with acetaminophen), inflammatory pain responds better to nonsteroidal anti-inflammatory drugs (NSAIDs). However, clinicians need to exercise caution with the use of NSAIDs, specifically selective cyclooxygenase-2 inhibitors, which may increase the risk for cardiovascular events in some patients.43 Neuropathic pain is treated with coanalgesics, such as antidepressants and anticonvulsants. Nonetheless, because acute wound pain may involve multiple mechanisms, the use of a combination of analgesics is recommended.10
 | Table 3. STRATEGIES DIRECTED AT ATTENUATING MODIFIABLE WOUND FACTORS |
Ketamine, another pharmacological agent, has been a focus of study to prevent or treat central sensitization (ie, decrease secondary hyperalgesia) in the postoperative period.25,44 Ketamine is an NMDA noncompetitive receptor antagonist that has antihyperalgesic and analgesic properties at subanesthetic doses (ie, small doses). In several clinical trials,45-47 small doses of ketamine in combination with opioids decreased postoperative pain. Although ketamine has been associated with psychomimetic adverse effects,48 in a systematic review49 of randomized, double-blind clinical trials of perioperative pain management, the incidence of central nervous system adverse effects did not differ between patients who received an opioid with a small dose of ketamine compared with patients who received only an opioid.
It is imperative to consider the causes of wound pain to provide adequate pain management. Because background pain can be continuous, the administration of analgesics "around the clock" is recommended, instead of "as needed," to maintain a steady analgesic level.50 In addition to an analgesic given to decrease background pain, it is necessary to administer rescue doses for incident pain. In terms of procedural and operative pain, it is critical to know the pharmacokinetics (ie, time to peak analgesic effect, duration of analgesia) of the various analgesics to determine the correct time to administer the agents to prevent pain.
CONCLUSION
Acute wound pain is common in patients with surgical and traumatic wounds. The principal causes of acute wound pain are background, incident, and procedural pain. Different mechanisms underlie acute wound pain including nociceptive, inflammatory, neuropathic, and ischemic. Wound pain can be a consequence of 1 or all of these mechanisms.
Research has advanced the wound care practitioner's knowledge of pain mechanisms. Nevertheless, there are still gaps in the research that require further attention. For example, clinical studies could target wound-direct and wound-indirect factors and could contribute to the understanding of the perception of pain, as well as to the development of clinical symptoms, such as hyperalgesia and allodynia. Furthermore, research could investigate the best pharmacological therapies to treat background, incident, and procedural wound pain. Acute wound pain is not only distressing; it can also develop into chronic pain if ineffectively treated.
Pain research can contribute to a better understanding of the mechanisms involved in different clinical situations that evoke wound pain, as well as promote the development of new pharmacological therapies to improve a patient's pain experience. The translation of these research findings into clinical practice can contribute to the improvement of wound pain assessment and management, eventually achieving better patient outcomes.
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