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.

Cultural Influences. 

Another barrier to accurate pain assessment is cultural influences on pain and pain reporting.⁸⁵ Cultural influences are compounded when the patient speaks a language other than that of the health team members. To facilitate communication, the use of a pain intensity scale in the patient’s language is vital. The 0 to 10 numeric pain scales have been translated into many different languages.²⁴

Although this chapter does not address specific cultural groups and their typical responses to pain, a few generalizations can be made. First, when assessing a patient from a cultural group different from your own, do not assume the patient will have a specific response to pain or exhibit a particular behavior because of his or her culture. Patients have individual responses to pain. The health care practitioner may wrongfully assign or expect behaviors that a patient will not exhibit. A second consideration that is commonly overlooked is the role of pain in the life of the patient. The nurse must communicate with the patient or the family to ascertain what that role is.

Some cultures believe that God’s test or punishment takes the form of pain. Persons with these cultural backgrounds do not necessarily believe that the pain should be relieved. Other cultures perceive pain as being associated with an imbalance in life. Persons from these cultures believe they need to manipulate the environment to restore balance to control pain.⁸⁵

The complexities and intricacies of cultural beliefs require more extensive discussion than is possible here. It is important for the nurse to support, whenever possible, the special beliefs and needs of the patient and his family to provide the most therapeutic environment for healing to occur.

Opioid Analgesics

The opioids most commonly used and recommended as first-line analgesics are the agonists. These opioids bind to mu (µ) receptors (transmission process; see Fig. 9-7), which appear to be responsible for pain relief. Additional pharmacologic information is presented in Table 9-3. In the SCCM guidelines, opioids should be used as first line therapy for treatment of non-neuropathic pain.¹⁷

Preventing and Treating Respiratory Depression

Respiratory depression is the most life-threatening opioid side effect. The risk of respiratory depression increases when other medications with CNS depressant effects (e.g., benzodiazepines, antiemetics, neuroleptics, antihistamines) are concomitantly administered to the patient. While no universal definition of respiratory depression exists, it is usually described in terms of decreased respiratory rate (fewer than 8 or 10 breaths/min), decreased Spo₂ levels, or elevated ETCO2 levels.⁹⁴ A change in the patient’s level of consciousness or an increase in sedation normally precedes respiratory depression.

New Sedative with Analgesic Properties: Dexmedetomidine

Dexmedetomidine (Precedex) is a short-acting alpha 2 agonist that is indicated for the short-term sedation (<24 hours) of mechanically ventilated patients in the critical care unit.¹⁰⁶ Its mechanism of action is unique and differs from those of other commonly used sedatives in critical care. Indeed, compared to midazolam (Versed) or lorazepam (Ativan)—whose hypnotic effects act mainly on the limbic system and/or the cortex—the effect of dexmedetomidine is located in the locus ceruleus section of the brainstem. As a result, patients receiving dexmedetomidine IV infusions are calm and sleepy, yet they remain easily arousable.¹⁰⁷ For this reason, dexmedetomidine is ideal for mild to moderate sedation, often referred to as conscious sedation. Refer to the Sedation and Delirium Management chapter for details on dosage and administration.

Dexmedetomidine also possesses an analgesic property. The analgesic effects of dexmedetomidine are principally due to spinal antinociception via binding to non-noradrenergic receptors (heteroreceptors) located on the dorsal horn neurons of the spinal cord.¹⁰⁵ Recently, dexmedetomidine was found to decrease postoperative opioid requirements in both adults and children.^109,110 These results suggest that dexmedetomidine could be of interest with respect to improving postoperative pain in critical care.

While dexmedetomidine is increasing in popularity for short-term sedation in the critical care unit, it is not without adverse effect. Indeed, inhibition of noradrenergic receptors in the brainstem and the spinal cord often causes hypotension and bradycardia.¹⁰⁷ Less common adverse effects include decreased salivation, decreased secretion, and decreased bowel motility in the gastrointestinal tract; contraction of vascular and other smooth muscle; inhibition of renin release, increased glomerular filtration, and increased secretion of sodium and water in the kidney; decreased intraocular pressure; and decreased insulin release from the pancreas.¹⁰⁸

Nonopioid Analgesics

In the SCCM guidelines, the use of nonopioids in combination with an opioid is recommended to reduce opioid requirements and opioid related side effects.¹⁷ This strategy provides greater analgesic effect through action at the peripheral and central levels. Pharmacologic information is presented in Table 9-3.

Patient-Controlled Analgesia

PCA is a method of medication delivery that uses the intravenous route and an infusion pump. It allows the patient to self-administer small doses of analgesics. Different opioids can be used, but the most extensively used is morphine. This method of medication delivery allows the patient to control the level of pain and sedation and to avoid the peaks and valleys of intermittent dosing by the health care professional. The patient can self-administer a bolus of medication the moment the pain begins, acting preemptively. Nursing management for the patient receiving analgesia medication via a PCA pump is described in the Nursing Interventions Classification (NIC) feature in Box 9-3.

Certain patients are not candidates for PCA. Alterations in the level of consciousness or mentation preclude the patient understanding the use of the equipment. Very elderly patients or patients with kidney failure or liver dysfunction may require careful screening for PCA.

Allowing the patient to self-administer opioid doses does not diminish the role of the critical care nurse in pain management. The nurse advises about necessary changes to the prescription and continues to monitor the effects of the medication and doses. The patient is closely monitored during the first 2 hours of therapy and after every change in the prescription. If the patient’s pain does not respond within the first 2 hours of therapy, a total reassessment of the pain state is essential. The nurse monitors the number of boluses the patient delivers. If the patient is pressing the button to bolus medication more often than the prescription, the dose may be insufficient to maintain pain control. Naloxone must be readily available to reverse adverse opiate respiratory effects. Ideally, the patient undergoing an elective procedure requiring opioid analgesia postoperatively is instructed in the use of PCA during preoperative teaching. This allows the patient to become comfortable with the concept of self-medication before use.

Intraspinal Pain Control

Intraspinal anesthesia uses the concept that the spinal cord is the primary link in nociceptive transmission. The goal is to mimic the body’s endogenous opioid pain modification system by interfering with the transmission of pain and providing an opiate receptor binding agent directly into the spinal cord. The hemodynamic status of the patient changes very little.

Intraspinal anesthesia is particularly appropriate for pain in the thorax, upper abdomen, and lower extremities. The two intraspinal routes are intrathecal and epidural (Fig. 9-8). Regardless of the route, the effects of the opioid agonist used is the same, and assessment parameters are the same as those used for other routes. Nursing management of the patient receiving intraspinal analgesia is described in the Nursing Interventions Classification (NIC) feature in Box 9-4.

Intrathecal Analgesia

Intrathecal (subarachnoid) opioids are placed directly into the cerebral spinal fluid and attach to spinal cord receptor sites. Opioids introduced at this site act quickly at the dorsal horn. The dural sheath is punctured, eliminating the barrier for pathogens between the environment and the cerebral spinal fluid. This creates the risk of serious infections. The intrathecal route is usually reserved for intraoperative use. Single-bolus dosing provides short-term relief for pain that is short lived (the pain of labor and delivery is well managed using this regimen). Side effects of intrathecal pain control include postdural puncture headache and infection.

Epidural Analgesia

Epidural analgesia is commonly used in the critical care unit after major abdominal surgery, nephrectomy, thoracotomy, and major orthopedic procedures. Per the SCCM guidelines, its use should be considered in postoperative abdominal aortic aneurysm patients, and for those with traumatic rib fractures.¹⁷ Certain conditions preclude the use of this pain control method: systemic infection, anticoagulation, and increased intracranial pressure. Epidural delivery of opiates provides longer-lasting pain relief with less dosing of opiates. When delivered into the epidural space, 5 mg of morphine may be effective for 6 to 24 hours, compared with 3 to 4 hours when delivered intravenously. Opioids infused in the epidural space are more unpredictable than those administered intrathecally. The epidural space is filled with fatty tissue and is external to the dura mater. The fatty tissue interferes with uptake, and the dura acts as a barrier to diffusion, making diffusion rate difficult to predict.

The type of medication used determines the rapidity of medication diffusion. Hydrophilic medications (e.g., morphine) are water soluble and penetrate the dura slowly, giving them a longer onset and duration of action. Lipophilic medications (e.g., fentanyl) are lipid soluble; they penetrate the dura rapidly and therefore have a rapid onset of action and a shorter duration of action.

The dura acts as a physical barrier and causes delay in diffusion of the medication. Compared with the intrathecal route, it allows more medication to be absorbed in the systemic circulation, requiring greater doses for pain relief. Medications delivered epidurally may be administered by bolus or continuous infusion. Epidural analgesia is being used more often in the critical care environment, and it requires careful monitoring.

The nurse must assess the patient for respiratory depression. This phenomenon may occur early in the therapy or as late as 24 hours after initiation. The epidural catheter also puts the patient at risk for infection. The efficiency of this pain control method and the increased mobility of the patient do not diminish the nurse’s responsibility to monitor and evaluate the outcomes of the pain-management protocol in use.

Equianalgesia

When a modification of opioid is considered, the nurse must be aware of equianalgesic dosages. In doing any conversion, the goal is to provide equal analgesic effects with the new agents. This concept is referred to as equianalgesia. Morphine is the standard for the conversion of opioids. Prescribed dosages must take into account the patient’s age and health status.²⁴ The critical care nurse must have access to a chart for easy referral on the unit to administer the correct dosages of opioids to critically ill patients. Because of the variety of agents and routes, the professional pain organizations have developed equianalgesia charts for use by the health care professional. All critical care units need to have an equianalgesic chart posted for easy reference. Box 9-5 presents a guide to using these charts. Table 9-4 provides the equianalgesic dose for different medications used in clinical practice. Table 9-5 presents an equianalgesic chart with PO nonopioid and opioid doses for mild to moderate pain.

Cold Application

Ice therapy was found to be helpful to reduce procedural pain in critically ill patients. In a study with 50 cardiac surgery patients in a critical care unit, a significant decrease in pain intensity was obtained after chest tube removal when ice packets were placed around the site for 10 minutes prior to removal.¹¹⁷ The analgesic property of ice therapy was also studied by Demir and Khorshid¹¹⁸ using a 20-minute application of cold packs before chest tube removal in the critical care unit. Pain intensity was significantly lower after chest tube removal in patients who received the cold packs and a dose of analgesic compared with a placebo and a control group.

Massage

The effect of massage on pain relief was explored in two studies with postoperative cardiac surgery patients after they have been transferred from the critical care unit.119,120 In these two studies with a total of 171 patients, a significant decrease in pain intensity scores was obtained in patients who received a 20-minute massage intervention between postoperative day 2 and day 5 compared to a control group who received standard care and a 20-minute quiet time during the same period. Similar findings were found in the critical care unit. Indeed, in a recent pilot study¹²¹ with 40 postoperative cardiac surgery patients, a decrease in pain intensity scores was observed in patients who were administered two to three 15-minute hand massage sessions during the first 24 hours after surgery compared to a control group who did not receive hand massage but had the nurse holding their hands and reported no change in pain intensity.

Relaxation

Relaxation is a well-documented method for reducing the distress associated with pain. Although not a substitute for pharmacology, relaxation is an excellent adjunct for controlling pain. Relaxation decreases oxygen consumption and muscle tone, and it can decrease heart rate and blood pressure. Relaxation gives the patient a sense of control over the pain and reduces muscle tension and anxiety. Not all patients are interested in relaxation therapy. For those patients, deep-breathing exercises may be helpful. Indeed, in a recent study,³ lower pain scores were found both after chest tube removal in 40 critically ill patients executing deep breathing and receiving an analgesic compared to those who solely received an analgesic. Excellent references for thorough techniques in relaxation therapy are available.²⁴

Guided Imagery

Guided imagery is a technique that uses the imagination to provide control over pain. It can be used to distract or relax. Guiding a patient to a place that is pain free and relaxing takes a considerable time commitment on the part of the nurse. Although this may be difficult in the critical care environment, guiding a patient to a place in his or her imagination that is free from pain may be beneficial.¹²²

Music Therapy

Music therapy is a commonly used intervention for relaxation. Music that is pleasing to the patient may have soothing effects, but its effects on reducing pain are controversial.¹²³ Ideally, the music should be supplied by a small set of headphones. It is important to educate the patient and family regarding the role of music in relaxation and pain control and to provide music of the patient’s choice.

The patient and family may provide information about other sources of distraction for the patient. Determining what distraction therapies the patient normally uses may provide a clue to which one may work during the illness. Some persons are distracted by television; for others, television is a source of increased anxiety. Do not assume that the patient does or does not want to watch television until you determine whether it will be beneficial or harmful to the patient.