One view explain that pain is a sense similar to vision or hearing, a component of the sensory that warns us of impending damage, gives accurate information to the brain about injuries, and helps us to heal. The inclusion of pain in The Senses: a Comprehensive Reference, alongside vision, hearing, or olfaction shows that this view is persuasive. But there has always been an alternative interpretation of pain. Pain is seen as a trigger of emotional states, a behavioral drive, and a highly effective learning tool. Aristotle, who was the originator of this view, made it very clear: there are only five senses – vision, hearing, touch, taste, and smell. Pain and pleasure are not senses but passions of the soul.
For purposes of definition, acute pain can be described as lasting from seconds to 6 months. However, the 6-month time frame has been criticized (Brook) as inaccurate since many acute injuries heal within a few weeks and most heal by 6 weeks. Usually of recent onset and commonly associated with a specific injury, acute pain indicates that damage or injury has occurred. Pain is significant in that it draws attention to its existence and teaches the person to avoid similar potentially painful situations. If no lasting damage occurs and no systemic disease exists, acute pain usually decreases along with healing.
In a situation where healing is expected in 3 weeks and the patient continues to suffer pain, it should be considered chronic and treated with interventions used for chronic pain. Waiting for the full 6-month time frame in this example could cause needless suffering. Unrelieved acute pain can affect the pulmonary, cardiovascular, gastrointestinal, endocrine, and immune systems. The stress response (neuroendocrine response to stress) that occurs with trauma also occurs with other causes of severe pain. The stress response generally consists of increased metabolic rate and cardiac output, impaired insulin response, increased production of cortisol, and increased retention of fluids.
Chronic (nonmalignant) Pain
Chronic pain is constant or intermittent pain that persists beyond the expected healing time and that can seldom be attributed to a specific cause or injury. Chronic pain may be defined as pain that lasts for 6 months or longer, although 6 months is an arbitrary period for differentiating between acute and chronic pain. An episode of pain may assume the characteristics of chronic pain before 6 months have elapsed, or some types of pain may remain primarily acute in nature for longer than 6 months.
Suppression of the immune function associated with chronic pain may promote tumor growth. Also, chronic pain often results in depression and disability. Although health care providers express concern about the large quantities of opioid medications required to relieve chronic pain in some patients, it is safe to use large doses of these medications to control progressive chronic pain.
Pain associated with cancer may be acute or chronic. Pain resulting from cancer is so ubiquitous that after fear of dying, it is the second most common fear of newly diagnosed cancer patients (Lema).
Pain in the patient suffering from cancer can be directly associated with the cancer (eg, bony infiltration with tumor cells or nerve compression), a result of cancer treatment (eg, surgery or radiation), or not associated with the cancer (eg, trauma). Most pain associated with cancer, however, is a direct result of tumor involvement.
Pathophysiology of Pain
The sensory experience of pain depends on the interaction between the nervous system and the environment. The processing of noxious stimuli and the resulting perception of pain involve the peripheral and central nervous systems.
Peripheral Nervous System
A number of algogenic (pain-causing) substances that affect the sensitivity of nociceptors are released into the extracellular tissue as a result of tissue damage. Histamine, bradykinin, acetylcholine, serotonin, and substance P are chemicals that increase the transmission of pain. The transmission of pain is also referred to as nociception. Prostaglandins are chemical substances thought to increase the sensitivity of pain receptors by enhancing the painprovoking effect of bradykinin. These chemical mediators also cause vasodilation and increased vascular permeability, resulting in redness, warmth, and swelling of the injured area.
Once nociception is initiated, the nociceptive action potentials are transmitted by the peripheral nervous system (Porth, 2002). The first-order neurons travel from the periphery (skin, cornea, visceral organs) to the spinal cord via the dorsal horn. There are two main types of fibers involved in the transmission of nociception. Smaller, myelinated Ad (A delta) fibers transmit nociception rapidly, which produces the initial “fast pain.” Type C fibers are larger, unmyelinated fibers that transmit what is called second pain. This type of pain has dull, aching, or burning qualities that last longer than the initial fast pain. The type and concentration of nerve fibers to transmit pain vary by tissue type.
The same noxious stimulus produces hyperalgesia, and the person reports greater pain than was felt at the first stimulus. For this reason, it is important to treat patients with analgesic agents when they first feel the pain. Patients require less medication and experience more effective pain relief if analgesia is administered before the patient becomes sensitized to the pain. Chemicals that reduce or inhibit the transmission or perception of pain include endorphins and enkephalins. These morphinelike neurotransmitters are endogenous (produced by the body). Endorphins and enkephalins are found in heavy concentrations in the central nervous system, particularly the spinal and medullary dorsal horn, the periaqueductal gray matter, hypothalamus, and amygdala.
Central Nervous System
After tissue injury occurs, nociception (the neurologic transmission of pain impulses) to the spinal cord via the Ad and C fibers continues. The fibers enter the dorsal horn, which is divided into laminae based on cell type. The laminae II cell type is commonly referred to as the substantia gelatinosa. In the substantia gelatinosa are projections that relay nociception to other parts of the spinal cord.
Nociception continues from the spinal cord to the reticular formation, thalamus, limbic system, and cerebral cortex. Here nociception is localized and its characteristics become apparent to the person, including the intensity. The involvement of the reticular formation, limbic, and reticular activating systems is responsible for the individual variations in the perception of noxious stimuli. Individuals may report the same stimulus differently based on their anxiety, past experiences, and expectations. This is a result of the conscious perception of pain.
The interconnections between the descending neuronal system and the ascending sensory tract are called inhibitory interneuronal fibers. These fibers contain enkephalin and are primarily activated through the activity of non-nociceptor peripheral fibers (fibers that normally do not transmit painful or noxious stimuli) in the same receptor field as the pain receptor, and descending fibers, grouped together in a system called descending control.
The enkephalins and endorphins are thought to inhibit pain impulses by stimulating the inhibitory interneuronal fibers, which in turn reduce the transmission of noxious impulses via the ascending system (Puig & Montes).
The noxious impulses are influenced by a “gating mechanism.” Melzack and Wall proposed that stimulation of the large-diameter fibers inhibits the transmission of pain, thus “closing the gate.” Conversely, when smaller fibers are stimulated, the gate is opened. The gating mechanism is influenced by nerve impulses that descend from the brain.
Factors Influencing the Pain Response
Pain experience is influenced by a number of factors, including; past experiences with pain, anxiety, culture, age, gender, and expectations about pain relief. These factors may increase or decrease the person’s perception of pain, increase or decrease tolerance for pain, and affect the responses to pain.
- Approaches for Using Analgesic Agents
- Local Anesthetic Agents
- Opioid Analgesic Agents
- Nonsteroidal Anti-inflammatory Drugs
- Tricyclic Antidepressant Agents and Anticonvulsant Medications
- Routes of Administration; Parenteral, Oral, Rectal,Transdermal, Transmucosal, Intraspinal and Epidural
Nonpharmacologic Interventions :
- Cutaneous Stimulation and Massage
- Ice and Heat Therapies
- Transcutaneous Electrical Nerve Stimulation
- Relaxation Techniques
- Guided Imagery
Nursing Management of Pain
Nursing Assessment of Pain
The factors to consider in a complete pain assessment are the intensity, timing, location, quality, personal meaning, aggravating and alleviating factors, and pain behaviors. The pain assessment begins by observing the patient carefully, noting the patient’s overall posture and presence or absence of overt pain behaviors and asking the person to describe, in his or her own words, the specifics of the pain. The words used to describe the pain may point toward the etiology.
Instruments for assessing the perception of pain: Pain Intensity Scales
Simple Descriptive Pain Intensity Scale
- 0: No pain
- 1: Mild pain
- 2: Moderate pain
- 3: Severe pain
- 4: Very severe pain
- 5: Worst possible pain
0 – 10 Numeric Pain Intensity Scale
Visual Analog Scale (VAS)
- No pain
- Pain as bad as it could possibly be
Nurses Role in Pain Management:
- Identifying Goals for Pain nursing management
- Establishing the Nurse–Patient Relationship and Teaching
- Providing Physical Care
- Managing Anxiety Related to Pain
• Reports relief that pain is accepted as real
and that he or she will receive assistance in
• Reports lower intensity of pain and discomfort after interventions implemented
• Reports less disruption from pain and discomfort after use of intervention
• Uses pain medication as prescribed
• Identifies effective pain relief strategies
• Demonstrates use of new strategies to relieve pain and reports their effectiveness
• Experiences minimal side effects of analgesia without interruption to treat side effects
• Increases interactions with family and friends
1. Reassure patient that you know pain is real and will assist him or her in dealing with it.
2. Use pain assessment scale to identify intensity of pain.
3. Assess and record pain and its characteristics: location, quality, frequency, and duration.
4. Administer balanced analgesics as prescribed to promote optimal pain relief.
5. Read minister pain assessment scale.
6. Document severity of patient’s pain on chart.
7. Obtain additional prescriptions as needed.
8. Identify and encourage patient to use strategies that have been successful with previous pain.
9. Teach patient additional strategies to relieve pain and discomfort: distraction, relaxation, cutaneous stimulation, etc.
10. Instruct patient and family about potential side effects of analgesics and their prevention and management.
1. Achieves pain relief
a. Rates pain at a lower intensity (on a scale of 0 to 10)
b. Rates pain at a lower intensity for longer periods
2. Patient or family administers prescribed analgesic medications correctly
a. States correct dose of medication
b. Administers correct dose using correct procedure
c. Identifies side effects of medication
d. Describes actions taken to prevent or correct side effects
3. Uses nonpharmacologic pain strategies as recommended
a. Reports practice of nonpharmacologic strategies
b. Describes expected outcomes of nonpharmacologic
4. Reports minimal effects of pain and minimal side effects of
a. Participates in activities important to recovery (eg, drinking
fluids, coughing, ambulating)
b. Participates in activities important to self and to family
(eg, family activities, interpersonal relationships, parenting,
social interaction, recreation, work)
c. Reports adequate sleep and absence of fatigue and