Porth's Essentials of Pathophysiology, 4e

866

Nervous System

U N I T 1 0

TABLE 35-1 Characteristics of Acute and Chronic Pain Characteristic Acute Pain

Chronic Pain

Onset

Recent

Continuous or intermittent

Duration

Short (<6 mo)

6 mo or more

Autonomic responses

Consistent with sympathetic fight-or-flight response Increased heart rate Increased stroke volume Increased blood pressure Increased pupillary dilation Increased muscle tension Decreased gut motility Decreased salivary flow (dry mouth)

Absence of autonomic responses

Psychological component

Associated anxiety

Increased irritability Associated depression Somatic preoccupation Withdrawal from outside interests Decreased strength of relationships

Other types of response

Decreased sleep Decreased libido Appetite changes

Traditionally, the distinction between acute and chronic pain has relied on a single continuum of time with some interval (e.g., 6 months) since the onset of pain used to designate the onset of acute pain or the tran- sition when acute pain became chronic. 16 A more recent conceptualization includes both time and pathophysio- logic dimensions. Some conditions such as osteoarthritis exhibit dimensions of both acute and chronic pain. Acute Pain. Acute pain is generally of short duration and remits when the underlying pathologic process has resolved. 17 Besides alerting the person to the existence of actual or impending tissue damage, acute pain typi- cally prompts a search for professional help. The pain’s location, radiation, intensity, and duration, as well as those factors that aggravate or relieve it, provide essen- tial diagnostic clues. Acute pain is elicited by surgery or trauma to body tissues and activation of nociceptive stimuli at the site of tissue damage. 16,18 This may induce an early wave of hyperexcitability of neurons within the CNS. The devel- opment of an inflammatory reaction to the tissue injury, with sensitization of peripheral receptors, often results in a second wave of longer-acting afferent input and a new increase in central hyperexcitability. 18,19 The result- ing hyperalgesia can lead to increased postoperative and post-traumatic pain, usually about the second or third day, and in some cases an increased likelihood of developing chronic pain. A number of chronic pain syn- dromes, including whiplash injury and phantom pain, develop after trauma and surgery. 18 Because acute pain is self-limited, in that it resolves as the injured tissues heal, long-term therapy usually is not needed. However, pain from acute illness, trauma, surgery, or medical procedures should be aggressively

managed and preemptive analgesia provided before the pain becomes severe. The use of preemptive and multi- modal therapy (two or more analgesics with differing anal- gesic mechanisms) not only allows the person to be more comfortable and active, but also helps to prevent periph- eral sensitization of pain receptors and hyperexcitability of central pain centers. 19 Usually, less medication is needed when the drug is given before the pain becomes severe and the pain pathways become sensitized. Interventions that alleviate acute pain also relieve the anxiety and musculo- skeletal spasms, as well increasing mobility and respira- tory movements such as deep breathing and coughing. Chronic Pain. Chronic pain is pain that persists longer than might be reasonably expected after an inciting event and is sustained by factors that are both pathologically and physically remote from the originating cause. 17,20,21 Chronic pain is highly variable. It may be unrelenting and extremely severe, as in metastatic bone pain. It can be rel- atively continuous with or without periods of escalation, as with some forms of back pain. Some conditions with recurring episodes of acute pain are particularly problem- atic because they have characteristics of both acute and chronic pain, as in sickle cell crisis or migraine headaches. The biologic factors that contribute to chronic pain include peripheral mechanisms, peripheral–central mech- anisms, and central mechanisms. 20 Peripheral mecha- nisms result from persistent stimulation of nociceptors, termed peripheral sensitization . Inflammatory media- tors released from injured tissues increase the sensitiv- ity of the C fibers and lead to increased duration of pain associated with chronic musculoskeletal, visceral, and vascular disorders. Peripheral–central mechanisms involve abnormal function of the peripheral and central portions of the somatosensory system. 21 They typically