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8 PAIN ASSESSMENT visceral organs. Noxious stimuli initiate a painful stimulus G STRUCTURE AND FUNCTION resulting in an inflammatory process, which leads to the release of cytokines and neuropeptides from circulating leukocytes, platelets, vascular endothelial cells, immune DEFINITION cells, and cells from within the peripheral nervous sys- tem. This results in the activation of the primary afferent The International Association for the Study of Pain (IASP) nociceptors (A-delta and C-fibers). Furthermore, the noci- defines pain as “an unpleasant sensory and emotional expe- ceptors themselves release a substance P that enhances rience, which we primarily associate with tissue damage nociception, causing vasodilatation, increased blood flow, or describe in terms of such damage, or both.” Recent and edema with further release of bradykinin, serotonin literature has emphasized the importance of pain and from platelets, and histamine from mast cells. recommended it being the fifth vital sign. Some states in A-delta primary afferent fibers (small-diameter, lightly the United States have passed laws necessitating the adop- myelinated fibers) and C-fibers (unmyelinated, primary tion of an assessment tool and documenting pain assess- afferent fibers) are classified as nociceptors because they ment in patient charts along with temperature, pulse, heart are stimulated by noxious stimuli. A-delta primary afferent rate and blood pressure (see Chapter 7). fibers transmit fast pain to the spinal cord within 0.1 sec- ond, which is felt as pricking, sharp, or electric quality sen- PATHOPHYSIOLOGY sation and usually caused by mechanical or thermal stimuli. C-fibers transmit slow pain within 1 second, which is Several theories attempt to explain the concept of pain. felt as burning, throbbing or aching and is caused by Melzack and Wall in 1965 proposed the gate control model mechanical, thermal or chemical stimuli usually result- emphasizing the importance of the central nervous sys- ing in tissue damage. By the direct excitation of the pri- tem mechanisms of pain; this model has influenced pain mary afferent fibers, the stimulus leads to the activation research and treatment. of the fiber terminals. Pain is explained as a combination of physiologic The is initiated by this inflam- phenomena in addition to a psychosocial aspect that influ- transmission process matory process, resulting in the conduction of an impulse ences the perception of pain. The pathophysiologic phenomenon of pain is sum- in the primary afferent neurons to the dorsal horn of the marized by the processes of transduction, transmission, spinal cord. There, neurotransmitters are released and con- modulation, and perception. centrated in the substantia gelatinosa (which is thought to host the gating mechanism described in the gate control Transduction of pain begins when a mechanical, ther- theory) and bind to specific receptors. The output neurons mal or chemical stimulus results in tissue injury or damage from the dorsal horn cross the anterior white commissure stimulating the nociceptors, which are the primary affer- and ascend the spinal cord in the anterolateral quadrant in ent nerves for receiving painful stimuli. Nociceptors are two ascending pathways (Fig. 8-1): distributed in the body in the skin, subcutaneous tissue, skeletal muscles, and joints. Pain receptors are also located 1. Spinothalamic tract (STT): ascends through the lat- in the peritoneal surfaces, pleural membranes, dura mater, eral edge of the medulla, lateral pons, and midbrain and blood vessel walls rather than in the parenchyma of to the thalamus then to the somatosensory cortex. It 107 108 UNIT III • NURSING ASSESSMENT OF THE ADULT Postcentral • Chronic non-malignant pain: usually associated gyrus with a specific cause or injury and is described as a constant pain that persists more than 6 months • Cancer pain: often due to the compression of peripheral nerves or meninges or from the damage to these structures following surgery, chemotherapy, radiation, or tumor growth and infiltration Ascending pathways Pain is also described as transient pain, tissue injury pain (surgical pain, trauma-related pain, burn pain, iatro- genic pain as a result of an intervention), and chronic neuropathic pain. Also pain is viewed in terms of its inten- sity and location. Thalamus PHYSIOLOGIC RESPONSES TO PAIN A-delta Pain elicits a stress response in the human body triggering C the sympathetic nervous system, resulting in physiologic responses such as the following: Spinal cord • Anxiety, fear, hopelessness, sleeplessness, thoughts of suicide • Focus on pain, reports of pain, cries and moans, Figure 8-1 Pathways for transmitting pain. frowns and facial grimaces • Decrease in cognitive function, mental confu- sion, altered temperament, high somatization, transmits location, quality, and intensity of acute pain and dilated pupils and threatening events. • Increased heart rate, peripheral, systemic, and 2. Spinoreticular tract (SRT): ascends to the reticular for- coronary vascular resistance, blood pressure mation, the pontine, medullary areas, and medial tha- • Increased respiratory rate and sputum retention lamic nuclei. It transmits pain information from the resulting in infection and atelactasis brainstem to the limbic area through noradrenergic • Decreased gastric and intestinal motility bundles. • Decreased urinary output resulting in urinary Modulation of pain is a difficult phenomenon. Mod- retention, fluid overload, depression of all ulation inhibits the pain message and involves the body’s immune responses own endogenous neurotransmitters (endorphins, enkeph- • Increased antidiuretic hormone, epinephrine, alins, and serotonin) in the course of processing the norepinephrine, aldosterone, glucagons, pain stimuli. decreased insulin, testosterone The process of pain perception is still poorly under- • Hyperglycemia, glucose intolerance, insulin stood. Studies have shown that the emotional status resistance, protein catabolism (depression and anxiety) affects directly the level of pain • Muscle spasm resulting in impaired muscle perceived and thus reported by patients. The hypothal- function and immobility, perspiration amus and limbic system are responsible for the emotional aspect of the pain perception while the frontal cortex is responsible for the rational interpretation and response G HEALTH ASSESSMENT to pain. CLASSIFICATION COLLECTING SUBJECTIVE DATA: Pain has many different classifications. Common cate- THE NURSING HEALTH HISTORY gories of pain include acute, chronic non-malignant, and There are few objective findings on which the assess- cancer pain. ment of pain can rely. Pain is a subjective phenomenon • Acute pain: usually associated with an injury with and thus the main assessment lies in the client’s report- a recent onset and duration of less than 6 months ing. The client’s description of pain is quoted. The exact and usually less than a month words used to describe the experienced of pain are used CHAPTER 8 • PAIN ASSESSMENT 109 to help in the diagnosis and management. Pain, its onset, pain on the physical, psychosocial, and spiritual aspects duration, causes, alleviating and aggravating factors are are questioned. Past experience with pain in addition to assessed. Then the quality, intensity and the effects of past and current therapies are explored. GG® HISTORY OF PRESENT HEALTH CONCERN Review JCAHO standards (Display 8-1) and tips for col- Following JCAHO standards and tips for collecting sub- lecting subjective data (Display 8-2) before assessing the jective data will enhance evaluation of the client’s per- client’s subjective experience of pain. sonal experience of pain. Use the COLDSPA mnemonic as a guideline for informa- tion to collect. In addition, the following questions help C • O • L • D • S • P • A elicit important information. C HARACTER: Describe the sign or symptom. How does it feel, look, sound, smell, and so forth? O NSET: When did it begin? L OCATION: Where is it? Does it radiate? D URATION: How long does it last? Does it recur? S EVERITY: How bad is it? P ATTERN: What makes it better? What makes it worse? A SSOCIATED F ACTORS: What other symptoms occur with it? DISPLAY 8-1 JCAHO STANDARDS FOR PAIN MANAGEMENT • Recognize patients’ rights to appropriate assessment and management of pain. • Screen for pain and assess the nature and intensity of pain in all patients. • Record assessment results in a way that allows regular reassessment and follow-up. • Determine and ensure that staff is competent in assessing and managing pain. Address pain assessment and management when orienting new clinical staff. • Establish policies and procedures that support appropriate prescribing of pain medications. • Ensure that pain doesn’t interfere with a patient’s participation in rehabilitation. • Educate patients and their families about effective pain management. • Address patient needs for symptom management in the discharge planning process. • Establish a way to collect facility-wide data to monitor the appropriateness and effectiveness of the pain management plan. Joint Commission on Accreditation of Healthcare Organizations. [Retrieved from: http/www.jcaho.com] DISPLAY 8-2 TIPS FOR COLLECTING SUBJECTIVE DATA • Maintain a quiet and calm environment that is comfortable for the patient being interviewed. • Maintain the client’s privacy and ensure confidentiality. • Ask the questions in an open-ended format. • Listen carefully to the client’s verbal descriptions and quote the terms used. • Watch for the client’s
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