Acute Pain

Acute pain has a short duration, and it usually corresponds to the healing process (30 days), but should not exceed 6 months. It implies tissue damage that is usually from an identifiable cause. If undertreated, acute pain may bring a prolonged stress response and lead to permanent damage to the patient’s nervous system. In such instance, acute pain can become chronic.8,9

Chronic Pain

Chronic pain persists for more than 6 months after the healing process from the original injury, and it may or may not be associated with an illness.²² It develops when the healing process is incomplete or, as described earlier, when acute pain is poorly managed.²³

Both acute and chronic pain can have a nociceptive or neuropathic origin.¹¹

Nociceptive Pain

Nociceptive pain arises from activation of nociceptors,¹¹ and it can be somatic or visceral. Somatic pain involves superficial tissues, such as the skin, muscles, joints, and bones. Its location is well defined. Visceral pain involves organs such as the heart, stomach, and liver. Its location is diffuse, and it can be referred to a different location in the body.²⁴ Interestingly, not all organs are sensitive to pain and some can be damaged quite extensively without the patient feeling a thing. For instance, many diseases of the liver, the lungs or the kidneys are completely painless and the only symptoms felt are those derived from the abnormal functioning of these organs. On the other hand, relatively minor lesions in viscera such as the stomach, the bladder, or the ureters can produce excruciating pain, as these organs are abundantly innervated by sensory neurons that signal harmful events.²⁵

Neuropathic Pain

Neuropathic pain arises from a lesion or disease affecting the somatosensory system.¹¹ The origin of neuropathic pain may be peripheral or central. Neuralgia and neuropathy are examples related to peripheral neuropathic pain, which implies a damage of the peripheral somatosensory system. Central neuropathic pain involves the central somatosensory cortex and can be experienced by patients after a cerebral stroke. Neuropathic pain can be difficult to manage and frequently requires a multimodal approach (i.e., the combinations of several pharmacologic and/or nonpharmacologic treatments).²⁴

Transduction

Transduction refers to mechanical (e.g., surgical incision), thermal (e.g., burn), or chemical (e.g., toxic substance) stimuli that damage tissues. In critical care, many nociceptive stimuli exist, including the patients’ acute illness or condition, invasive technology used for patients, and multiple interventions that have to be done for them. These stimuli, also called stressors, stimulate the liberation of many chemical substances, such as prostaglandins, bradykinin, serotonin, histamine, glutamate, and substance P. These neurotransmitters stimulate peripheral nociceptive receptors and initiate nociceptive transmission.

Transmission

As a result of transduction, an action potential is produced and is transmitted by nociceptive nerve fibers in the spinal cord that reach higher centers of the brain. This is called transmission, and it represents the second process of nociception. The principal nociceptive fibers are the A-delta (Aδ) and C fibers. Large-diameter, myelinated Aδ fibers that transmit well-localized, sharp pain are involved in “first pain” sensation, which leads to reflex withdrawal. Small-diameter, unmyelinated C fibers transmit diffuse, dull, aching pain, which is referred to as “second pain.”²⁶ These fibers transmit the noxious sensation from the periphery through the dorsal root of the spinal cord. With the liberation of substance P, these fibers then synapse with ascending spinothalamic fibers to the central nervous system (CNS). These spinothalamic fibers are clustered into two specific pathways: neospinothalamic (NS) and paleospinothalamic (PS) pathways. Generally, the Aδ fibers transmit the pain sensation to the brain within the NS pathway, and the C fibers use the PS pathway.²⁷

Through synapsing of nociceptive fibers with motor fibers in the spinal cord, muscle rigidity can appear because of a reflex activity.²⁸ Muscle rigidity can be a behavioral indicator associated with pain. It can contribute to immobility and decrease diaphragmatic excursion. This can lead to hypoventilation and hypoxemia. Hypoxemia can be detected by a pulse oximeter (Spo₂) and by oxygen arterial pressure (Pao₂) monitoring. A ventilated patient’s interaction with the machine (e.g., activation of alarms, fighting the ventilator) also may indicate the presence of pain.²⁹

Perception

The pain message is transmitted by the spinothalamic pathways to centers in the brain, where it is perceived. Pain sensation transmitted by the NS pathway reaches the thalamus, and the pain sensation transmitted by the PS pathway reaches brainstem, hypothalamus, and thalamus.²⁷ These parts of the CNS contribute to the initial perception of pain. Projections to the limbic system and the frontal cortex allow expression of the affective component of pain.³⁰ Projections to the sensory cortex located in the parietal lobe allow the patient to describe the sensory characteristics of his or her pain, such as location, intensity, and quality.^30,31 The cognitive component of pain involves many parts of the cerebral cortex and is complex. These three components (affective, sensory, and cognitive) represent the subjective interpretation of pain. Parallel to this subjective process, certain facial expressions and body movements are behavioral indicators of pain occurring as a result of pain fiber projections to the motor cortex in the frontal lobe.

Modulation

Modulation is a process by which noxious stimuli that travel from the nociceptive receptors to the CNS may be enhanced or inhibited. Pain can be modulated by ascending and descending mechanisms. A typical example of ascending pain modulation is rubbing an injury site, thus activating large A-beta (Aβ) fibers in the periphery. Stimulation of these fibers activates inhibitory interneurons in the dorsal horn of the spinal cord, effectively preventing nociceptive signal transmission from the periphery to the higher brain regions. The physiologic basis of this mechanism of pain modulation was elucidated by Melzack and Wall in 1965³² and refers to the Gate Control Theory (GCT). Analgesia may also be produced at the level of the spinal cord and the brainstem (spinothalamic pathway) via the release of endogenous opioids and neurotransmitters. Endogenous opioids are naturally occurring morphine-like pentapeptides found throughout the nervous system and exist in three general classes: beta-endorphins, enkephalins, and dynorphins. These substances block neuronal activity related to nociceptive impulses by binding to opioid mu (µ) receptor sites in the central and peripheral nervous systems.²⁷ In the ascending pain modulation mechanism, endogenous opioids may be produced in the brainstem, and the dorsal horn or exogenous opioids may be introduced by administration of an opioid analgesic. The released or introduced opioids bind to the mu-opioid receptors on nociceptive nerve fibers, blocking the release of substance P. In the descending pain modulation mechanism, the efferent spinothalamic nerve fibers that descend from the brain can inhibit the propagation of the pain signal by triggering the release of endogenous opioids in the brain stem and in the spinal cord. Serotonin and norepinephrine are important inhibitory neurotransmitters that act in the CNS. These substances are also released by the descending fibers of the descending spinothalamic pathway.³³ The use of distraction, relaxation and imagery techniques can facilitate the release of endogenous opioids, and has been shown to reduce the overall pain experience.³⁴

In summary, nociception is an important physiologic mechanism of pain that can integrate many components of pain for its assessment. In transduction, stimuli are sources of pain that trigger the liberation of neurotransmitters. In transmission, diffusion of the action potential along the NS pathway may lead to muscle rigidity—a reflex activity that can be observed as a behavioral indicator associated with pain. Muscle rigidity may also influence respiratory rate and amplitude, and cause decrease in Spo₂ and increase in Pao₂. In perception, the patient’s self-report of affective, sensory, and cognitive information can be obtained, and behavioral responses to pain may also be observed. Finally, in modulation, pain sensation may be attenuated by ascending and descending mechanisms.

Short-Term Direct Response

In the presence of a stressor such as pain, the hypothalamus releases corticotropin-releasing factor (CRF), which activates the sympathetic nervous system (SNS). Norepinephrine is then released from the terminals of sympathetic nerves, and epinephrine is released from the adrenal cortex. This mechanism constitutes the short-term direct stress response. The effects of these stress hormones allow observation of physiologic responses associated with activation of SNS. For instance, increased blood pressure, increased heart rate, and increased respiratory rate are common signs of acute pain.15,29,36 Moreover, pupil dilation can be observed.³⁷

If pain persists over time or injuries are located in the bladder or the intestines, the parasympathetic nervous system (PNS) may be dominant. The blood pressure and heart rate may decrease rather than increase. The absence of pain-related indicators related to the activation of the SNS does not necessarily imply an absence of pain sensation.³⁸

Midterm Indirect Response

At midterm, the CRF released from the hypothalamus stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH) and the posterior pituitary to release vasopressin, the antidiuretic hormone. ACTH activates the adrenal cortex to release aldosterone and cortisol. Vasopressin and aldosterone increase sodium and water retention. This increases intravascular volume and decreases diuresis and increases blood pressure and cardiac preload. Cortisol also may contribute to systemic responses such as infection and hyperglycemia.

At midterm, pain may be associated with decreased diuresis, increased blood pressure, increased central venous pressure (CVP), and increased pulmonary artery capillary occlusion pressure (PAOP). However, changes in these parameters are not specific to pain, and their associations with pain are not supported by empirical data.

Long-Term Indirect Response

Long term, the stress hormones, specifically cortisol, influence the immune system in two ways: immunosuppression and release of cytokines.³⁹ Cytokines may prolong by retroactivation the release of cortisol, which may exacerbate tissue damage, contributing to the chronic pain process.²³

In summary, the biologic stress response allows observation of fluctuations in physiologic signs that represent a source of stress and may be associated with acute pain. The short-term signs are mainly related to SNS activation. Other signs, such as decreased diuresis and increased CVP and PAOP, relate to the midterm indirect stress response. The immune system is involved in the long-term indirect response of stress. No acute pain indicators have been associated with this process. All the indicators identified within the biologic stress response are not specific to pain because they can be attributed to other distress conditions, homeostatic changes, and medications.¹⁶

P: Provocative and Palliative or Aggravating Factors

The P in the mnemonic indicates what provokes or causes the patient’s pain, what he or she was doing when the pain appeared, and what makes the pain worse or better. For instance, deep breathing intensifying chest pain in the case of pericarditis is an illustration of an aggravating factor. Moderating factors that reduce/alleviate the pain or discomfort are also important findings and may include resting to diminish burning chest pain due to angina. Knowledge of any intensifying or alleviating conditions can contribute to the patient’s plan of care throughout the continuum of care.

Q: Quality

The Q in the mnemonic refers to the quality of the pain or the pain sensation that the patient is experiencing. For instance, the patient may describe the pain as dull, aching, sharp, burning, or stabbing. This information provides the nurse with data regarding the type of pain the patient is experiencing (e.g., somatic or visceral). The differentiation between types of pain may contribute to the determination of cause and management. A patient who has had open-heart surgery may complain of chest pain that is shooting or burning.⁴ This information can lead the nurse to investigate for cutaneous or bone injuries as a result of a sternotomy. Another patient may describe a sharp thoracic pain that may lead the nurse to consider visceral pain as a result of pulmonary embolism. A verbal description of pain is important because it provides a baseline account, allowing the critical care nurse to monitor changes in the type of pain, which may indicate a change in the underlying pathology.

R: Region or Location, Radiation

R usually is easy for the patient to identify, although visceral pain is more difficult for the patient to localize.²⁴ If the patient has difficulty naming the location or is mechanically ventilated, ask the patient to point to the location on himself or herself or on a simple anatomic drawing.⁴⁴

S: Severity and Other Symptoms

S, the severity or intensity of pain, is a measurement that has undergone much investigation. Many pain intensity scales are available, including the descriptive and numeric pain rating scales that are often used in the critical care environment (Fig. 9-5). Many critical care units use a specific pain intensity scale. The use of a single tool provides consistency of assessment and documentation. Employment of a pain intensity scale is useful in the critical care environment. Asking the patient to grade his or her pain on a scale of 0 to 10 is a consistent method and aids the nurse in objectifying the subjective nature of the patient’s pain. However, the patient’s tool preference should be considered.

The S in the mnemonic also refers to other symptoms accompanying the patient’s pain experience, such as shortness of breath, nausea, and fatigue. Anxiety and fear are common emotions associated with pain.

T: Timing

The T in the mnemonic refers to documenting the onset, duration, and frequency of pain. This information can help to determine whether the origin of the pain is acute or chronic. Duration of pain can indicate the severity of the problem. For instance, chest pain of less than 15 minutes’ duration may be angina, and pain lasting more than 15 minutes may indicate a myocardial infarction.

U: Understanding

The U in the mnemonic is the patient’s perception of the problem or cognitive experience of pain. Patients with known cardiac problems can tell the nurse whether their pain is the same as they had during myocardial infarction. Patients with a cerebral hemorrhage often describe experiencing the worst headache they have ever had.

Because of the patient’s change in communication, lack of concentration due to sedation therapies, and the life-or-death immediacy of most actions in the critical care environment, pain assessment is often reduced to minimal information. Begin by asking, “Do you have pain?” The use of a simple yes or no question allows the patient to answer verbally or to indicate his or her response by nodding the head or by other signs. It is easier for mechanically ventilated patients to communicate with nurses in this way because they cannot express themselves verbally. Pain intensity and location also are necessary for the initial assessment of pain.

Behavioral Pain Scale

The BPS shown in Table 9-1 was tested mostly in nonverbal mechanically ventilated patients with altered levels of consciousness.^46,53–56 Its validity was supported with significantly higher BPS scores during nociceptive procedures (e.g., turning, endotracheal suctioning, peripheral venous cannulation) compared with rest or nonnociceptive procedures (e.g., arterial catheter dressing change, compression stocking applications, eye care). The authors of the BPS determined a cut-off score greater than 5 for the presence of pain. A positive association was found between nurses’ BPS ratings and conscious sedated patients’ self-report of pain intensity during turning.⁵⁴ Good interrater reliability of BPS scores between several raters including nurses was reached. The BPS can be used quickly (2 to 5 minutes), and most clinicians were satisfied with its ease of use.⁴⁶ However, some expressed concerns about the lack of conceptual clarity of certain items.⁴⁹ For instance, scores of 3 (i.e., fighting ventilator) and 4 (i.e., unable to control ventilation) for compliance with the ventilator category may be ambiguous. Similarly, movements with upper limbs category may be confused with muscle tension.

Critical-Care Pain Observation Tool

The CPOT shown in Table 9-2 was tested in verbal and nonverbal, critically ill adult patients.^15,29,47,57 Content validity was supported by critical care unit expert clinicians, including nurses and physicians.⁵⁸ Validity of the CPOT was supported with significantly higher CPOT scores during a nociceptive procedure (e.g., turning with or without other care) compared with rest or a nonnociceptive procedure (e.g., taking blood pressure). Positive associations were found between the CPOT scores and the patient’s self-report of pain.^15,29,47 A cut-off score greater than 2 was established with the CPOT in postoperative critical care unit adults.⁵⁹ Similarly to the BPS, good interrater reliability of CPOT scores was achieved with critical care nurses.^15,47 Feasibility and clinical utility of the CPOT were positively evaluated by critical care nurses.⁶⁰ Nurses agreed that the CPOT was quick enough to be used in the critical care unit, simple to understand, easy to complete, and helpful for nursing practice. An online teaching video to learn how to use the CPOT at the bedside is available (see Table 9-2).

TABLE 9-2

CRITICAL CARE PAIN OBSERVATION TOOL (CPOT)

INDICATOR	SCORE		DESCRIPTION
Facial expression	Relaxed, neutral	0	No muscle tension observed
	Tense	1	Presence of frowning, brow lowering, orbit tightening and levator contraction or any other change (e.g., opening eyes or tearing during nociceptive procedures)
	Grimacing	2	All previous facial movements plus eyelid tightly closed (the patient may present with mouth open or biting the endotracheal tube)
Body movements	Absence of movements or normal position	0	Does not move at all (doesn’t necessarily mean absence of pain) or normal position (movements not aimed toward the pain site or not made for the purpose of protection)
	Protection	1	Slow, cautious movements, touching or rubbing the pain site, seeking attention through movements
	Restlessness/Agitation	2	Pulling tube, attempting to sit up, moving limbs/thrashing, not following commands, striking at staff, trying to climb out of bed
Compliance with the ventilator (intubated patients) or Vocalization (nonintubated patients)	Tolerating ventilator or movement	0	Alarms not activated, easy ventilation
	Coughing but tolerating	1	Coughing, alarms may be activated but stop spontaneously
	Fighting ventilator	2	Asynchrony: blocking ventilation, alarms frequently activated
	Talking in normal tone or no sound	0	Talking in normal tone or no sound
	Sighing, moaning	1	Sighing, moaning
	Crying out, sobbing	2	Crying out, sobbing
Muscle tension	Relaxed	0	No resistance to passive movements
	Tense, rigid	1	Resistance to passive movements
	Very tense or rigid	2	Strong resistance to passive movements, incapacity to complete them
TOTAL		___ / 8
1. The patient must be observed at rest for one minute to obtain a baseline value of the CPOT. 1.1. Observation of patient at rest (baseline).     The nurse looks at the patient’s face and body to note any visible reactions for an observation period of one minute. She gives a score for all items except for muscle tension. At the end of the 1-minute period, the nurse holds the patient’s arm in both hands—one at the elbow, and uses the other one to hold the patient’s hand. Then, she performs a passive flexion and extension of the upper limb and feels any resistance the patient may exhibit. If the movements are performed easily, the patient is found to be relaxed with no resistance (score 0). If the movements can still be performed but with more strength, then it is concluded that the patient is showing resistance to movements (score 1). If the nurse cannot complete the movements, strong resistance is felt (score 2). This can be observed in patients who are spastic. 2. Then the patient should be observed during painful procedures (e.g., turning, wound care) to detect any changes in the patient’s behaviors. 2.2. Observation of patient during a painful procedure.     While she’s performing a procedure known to be painful, the nurse looks at the patient’s face to note any reactions such as frowning or grimacing. These reactions may be brief or can last longer. The nurse also looks out for body movements. For instance, she looks for protective movements like the patient trying to reach or touching the pain site (e.g., surgical incision, injury site). In the mechanically ventilated patient, she pays attention to alarms and if they stop spontaneously or require that she intervenes (e.g., reassurance, administering medication). It is important that the nurse auscultates the patient to check for the position of the endotracheal tube and the presence of secretions as these factors may influence this item without being indicative of pain. According to muscle tension, the nurse can feel if the patient is resisting to the movement or not. A score 2 is given when the patient is resisting against the movement and attempts to get on his/her back. 3. The patient should be evaluated before and at the peak effect of an analgesic agent to assess whether the treatment was effective or not in relieving pain. 4. The patient should be attributed the highest score observed during the observation period. 5. The patient should be attributed a score for each behavior included in the CPOT and muscle tension should be evaluated last as it may lead to behavioral reactions not necessarily related to pain, but more to the actual stimulation. According to compliance with the ventilator, the nurse must check that the endotracheal tube is well positioned, and for the presence of secretions which could lead to higher scores for this item.

An online teaching video funded and created by Kaiser Permanente Northern California Nursing Research (KPNCNR) to learn how to use the CPOT at the bedside is available at http://pointers.audiovideoweb.com/stcasx/il83win10115/CPOT2011-WMV.wmv/play.asx.

Modified from Gélinas C, et al. Validation of the Critical-Care Pain Observation Tool (CPOT) in adult patients. Am J Crit Care. 2006;15:420. Figure of facial expressions a courtesy of Caroline Arbour, RN, BSc, PhD candidate, McGill University, Canada, and redrawn by Elsevier.

Use of Cut-Off Scores

A cut-off score refers to the score on a specific scale associated with the best probability of correctly ruling in or ruling out a patient with a specific condition—in this case pain. The use of a cut-off score with behavioral pain scales can help to identify when pain is highly likely to be present, and guide nurses in determining whether an intervention to alleviate pain is required or not. Also, a cut-off score can help to evaluate the effectiveness of pain-management interventions. It is important to highlight that cut-off scores are established using a criterion (i.e., a gold standard in the field). As mentioned previously, in the case of pain, the patient’s self-report is known as the gold standard criterion.¹¹ For a case example showing how a cut-off score can be used in practice, refer to Box 9-1.

Limitations Related to the Use of Behavioral Pain Scales

Behaviors have been validated for pain assessment in critically ill patients, but they present some limitations. In fact, they are impossible to monitor in patients unable to respond behaviorally to pain such as those suffering from paralysis or under the effects of neuromuscular blocking agents. Also, behavioral responses may be blurred with the administration of high doses of sedative agents.¹⁵ Indeed, minimal behavioral responses to painful procedures were found in unconscious, mechanically ventilated critically ill adults who were more heavily sedated compared with conscious patients.²⁹ Similar results were found in previous studies in which patients who received a higher dose of midazolam obtained a lower score on the BPS.⁵⁶

In addition, behavioral pain scales developed for nonverbal critically ill patients may not be applicable for those with a brain injury and an altered level of consciousness as they were found to exhibit atypical behavioral responses to pain.29,61,62 Instead of frowning and grimacing, brain-injured patients with altered levels of consciousness seemed to react mostly by opening their eyes, showing tears, opening their mouth, and exhibiting repetitive movements of the lower limbs when exposed to pain. Further studies are needed to better understand how brain-injured patients react to painful procedures. Therefore existing behavioral pain scales may be inappropriate for this specific vulnerable group. When selecting a scale, nurses should make sure that is has been tested in a patient population and context in which they plan to use it. Indeed, a scale can only be shown to be valid with a specific group of people and in a given context.⁶³

Physiologic Indicators

When patients cannot react behaviorally to pain, the only possible clues left for the detection of pain are physiologic indicators (i.e., vital signs). Although vital sign values generally increase during painful procedures,15,29,36,46,56 they are not consistently related to the patient’s self-report of pain, nor are they predictive of pain.^15,29 For example, none of the monitored vital signs (heart rate, mean arterial pressure [MAP], respiratory rate, transcutaneous oxygen saturation [Spo₂], and end-tidal CO₂) predicted the presence of pain in critically ill patients.²⁹

In the ASPMN recommendations and the SCCM guidelines, it is stated that vital signs should not be considered as primary indicators of pain because they can be attributed to other distress conditions, homeostatic changes, and medications. Changes in vital signs should instead be considered a cue to begin further assessment of pain or other stressors.16,17 Physiologic measures other than vital signs can support the nurses in detecting the presence of pain in nonverbal critically ill patients especially when behavioral indicators are no longer available.

Cerebral Monitoring and Pain Assessment

Other than vital signs, human brain reactivity has been studied using brain imaging technology such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) in healthy individuals and in patients with clinical pain conditions.⁶⁴ Many regions of the brain are involved in the perception of pain, including the somatosensory cortex, the frontal cortex, and the thalamus. The anatomic connections between these regions suggest that they function in an interactive way in encoding the different aspects of pain (sensory and affective components of pain). For instance, the somatosensory cortex plays a major role in processing the sensory component of pain, whereas the frontal cortex appears to reflect the affective component of pain.²⁶ A closer look into brain activity may elucidate how pain inputs are first received and processed within the cerebral cortex, offering a direct and more precise indicator of pain.