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Perioperative analgesia utilizes nerve blocks via peripheral or spinal local
anesthetic delivery. A preoperative pain assessment may identify a
history of uncontrolled postsurgical pain, analgesic intolerance or
contraindication, risks and benefits of regional anesthesia, and presence
of preoperative pain or anxiety.
Multimodal analgesia is a strategy that utilizes a combination of different
analgesic modalities to achieve better postoperative pain management
and a subsequent reduction in adverse effects. The additive and
synergistic effects between different classes of analgesics allow for a
reduction in the doses of individual medications while achieving similar
Low back pain is a very common chronic pain condition. It is complex,
often involving physical and emotional factors. Patients may have
musculoskeletal, neuropathic, and/or central pain that needs to be
assessed, as well as comorbidities.
Chronic pain management requires multimodal therapies, both
pharmacologic and nonpharmacologic. Many factors affect analgesic
selection, including comorbidities, available routes of administration, and
Neuropathic pain may be caused by injury to peripheral nerves or to the
central nervous system. Neuropathic pain is treated with analgesic
antidepressants and anticonvulsants. Peripheral or localized nerve pain
may be treated with topical agents.
Elderly patients and patients with multiple comorbidities are at high risk
for adverse effects. Pharmacokinetic and pharmacodynamic drug
interactions must be considered with the use of anticonvulsants and
Central neuropathic pain may present with peripheralsymptoms that are
localized or generalized. Pharmacotherapy provides only modest relief.
Central poststroke pain is commonly multifactorial, including neuropathic
pain and nociceptive pain. Central pain may respond to traditional
neuropathic pain therapies. NSAIDs are ineffective. Comorbidities and
drug interactions must be considered.
Functional pain does not have a clear pathophysiology. Comorbid mental
health issues and psychosocialstressors complicate chronic pain
management. Analgesic antidepressants and anticonvulsants, in
conjunction with cognitive behavioral therapies, are recommended for
management of functional pain syndromes (FPSs).
Opioid therapy requires effective risk assessment to avoid medication
abuse, misuse, and diversion. Monitoring recommendations should
include use of written opioid agreements, urine drug testing, opioid risk
screening tools, and electronic prescription monitoring program records.
Cancer pain may result from one or more causes related to direct tumor
involvement, cancer therapy, and psychological factors. Pain
management involves assessment of the patient to determine the
etiology of pain and development of a care plan to address pain and
Transdermal fentanyl and methadone are potent opioids commonly used
in cancer pain management. Opioid conversion tables for fentanyl and
methadone are different due to differences in pharmacokinetics.
Supplemental doses of short-acting opioids are recommended for
Opioid adverse effects including sedation, constipation, nausea, vomiting,
itching, and respiratory depression should be addressed in the pain
management plan. Complementary and alternative medicine therapies
are widely used by patients in the management of cancer pain, dyspnea,
and nausea and vomiting. Neuraxial opioid administration may be
appropriate for patients with intolerable pain who cannot tolerate
Pain is defined as “an unpleasant sensory and emotional experience associated with
actual or potential tissue damage or described in terms of such damage.”
to experience pain is critical for survival because it informs the body of real or
potential injury (e.g., touching a hot stove). The body is then able to respond to the
threat and protect itself from further injury (e.g., refraining from touching or removing
the hand from the hot stove). Pain is a hallmark of many acute and chronic conditions.
More than 80% of patients who undergo surgical procedures experience acute pain,
75% of which report the severity as moderate, severe, or extreme.
affects more than 25% of Americans over the age of 20 years.
that pain is a natural part of growing older, and up to 60% of people believe that pain
is just something you have to live with.
5 However, nearly all cases of chronic pain
begin as acute pain stemming from surgery, trauma, or illness.
Medicine in 2011 estimated that $635 billion is spent annually on treatment of
chronic pain conditions alone.
7 Back pain and osteoarthritis (OA) are among the top
5 chronic pain conditions associated with high healthcare costs and the prevalence
continues to rise with the aging U.S. population. A study of Humana insurance
utilization data for Medicare members from 2007 to 2011 found that annual costs
were $327 million for OA and $218 million for back pain.
racial, and socioeconomic disparities that exist with chronic pain. Chronic pain is
reported more often in women than in men, and in non-Hispanic white patients
compared with other races and ethnicities.
4 Chronic pain is also more common in
those whose income is 2 times less than the level of poverty. Pain is more complex
than just physiology. It is a subjective experience, and sometimes the severity of pain
does not appear to equal the extent of tissue damage. A person’s perception of pain is
affected by environmental, emotional, cultural, spiritual, and cognitive factors.
Unrelieved chronic pain affects not only physical well-being but also a person’s
psychological and social well-being and relationships with loved ones. Recent
estimates showed that musculoskeletal-related conditions with low back pain, neck
pain, and knee OA ranked within the top 10 noncommunicable diseases for global
disability-adjusted life years (i.e., years of life lost and years lived in disability).
Factors that increase pain and suffering include sensory factors, cognitive factors,
and emotional factors (Fig. 55-1). All are interrelated and illustrate the complex
Nociception, or the sensation of pain, is composed of four basic processes:
transduction, transmission, modulation, and perception (Fig. 55-2) . Transduction is
the process by which noxious stimuli are translated into electrical signals at
peripheral receptor sites (i.e., free nerve endings located throughout the skin, muscle,
joints, fascia, and viscera). Normal sensory stimuli do not activate the pain signal,
but if the stimulus is powerful enough to surpass the threshold for innocuous
activation, the receptors become nociceptors (i.e., pain receptors). These sensory
receptors target mechanical (crushing or pressure), chemical (endogenous or
exogenous), or thermal (hot or cold) stimuli. Some nociceptors are polymodal,
transducing more than one type of stimuli. One of these types of nociceptors is called
the transient receptor potential (TRP). This family has a large number of members
that are activated by the whole spectrum of thermal stimuli (very hot to very cold), as
well as some mechanical and various chemical stimuli. Other receptors are “silent,”
but are recruited if the stimulus is more intense or prolonged.
Figure 55-1 Factors affecting chronic pain.
Figure 55-2 Pain pathways. 5-HT, serotonin; NE, norepinephrine.
After stimulation of nociceptors, several processes occur. Proinflammatory
mediators, including histamine, substance P, prostaglandins, bradykinins, and
serotonin are released at the site of injury. Immune mediators are also released,
including tumor necrosis factor, nerve growth factors, interleukins, and interferons.
These mediators sensitize the nociceptors, lowering the pain threshold in and around
the injury (peripheral sensitization). The sensitized nociceptors may fire more
frequently and erratically and are stimulated by much weaker stimuli (hyperalgesia).
More frequent firing is correlated with an increase in pain intensity.
Transmission is the propagation of the electrical signal along primary afferent
nerves, through the dorsal horn of the spinal cord to the central nervous system
(CNS). Painful impulses are generated at the nociceptor, with voltage-gated sodium
channels initiating the action potentials. Voltage-gated calcium channels are
responsible for allowing calcium influx to the presynaptic terminal, causing
neurotransmitter release. The message is then transmitted to the spinal cord via two
primary afferent nerve types: myelinated A fibers and unmyelinated C fibers. The Aδ
fibers are responsible for rapidly conducting impulses associated with thermal and
mechanical stimuli. Transmission of signals along Aδ fibers results in sharp or
stabbing sensations that alert the patient to an injury (also called “first pain”). This
produces reflex signals, such as musculoskeletal withdrawal, to prevent further
The smaller, unmyelinated C fibers respond to mechanical, thermal, and chemical
stimuli but conduct impulses at a much slower rate compared with Aδ fibers.
Transmission of electrical impulses via C fibers results in pain that is dull, aching,
burning, and diffuse (called “second pain”). Prolonged stimulation of C fibers causes
an additive effect on the perceived intensity of second pain, called windup.
At the level of the dorsal horn of the spinal cord, the primary afferents cause
calcium release into the presynaptic terminal. This leads to release of excitatory
amino acids (EAAs) like glutamate into the synapse (Fig. 55-3). C fibers also release
peptides such as substance P, neurokinins, and calcitonin gene-related peptide
(CGRP). The EAAs then stimulate the postsynaptic receptors and the electrical
signals stimulate second-order neurons in the CNS. The postsynaptic α-amino-3-
Usually a magnesium ion holds the channels closed; however, when there is sustained
firing from the primary afferents, the magnesium ion is displaced and the NMDA
receptor is activated. This sensitizes the second-order neurons that will then
discharge at a higher frequency. When sensitization occurs, the firing threshold is
reduced, so even slightly painful stimuli (hyperalgesia) and nonpainful stimuli
(allodynia) cause sustained activation of second-order neurons. NMDA receptor
activation is linked to windup and central sensitization (i.e., decreased thresholds for
response or increased vigor of responses after a sensitizing event) and may
contribute to the maintenance of chronic pain conditions with processes occurring
both at the dorsal horn level and in the supraspinal areas. Central sensitization may
occur with all types of pain when prolonged primary afferent activation causes
plasticity (adaptation) of the pain sensory thresholds in the CNS.
One of the predominant contributors to pain propagation at the synapse and within
the CNS is the glial cell. In the periphery, these are Schwann cells and satellite cells.
In the CNS, these include oligodendrocytes, astrocytes, ependymal cells, and
microglia. Glial cells account for 70% of the CNS and under normal conditions
microglia account for 5% to 20% of glia.
12 The glial cells have historically been seen
as support cells for synaptic homeostasis. This is true; however, they also have an
important role in the synthesis, release, and uptake of neurotransmitters and serve as
a link between the nervous system and the immune system. Nerve damage due to
trauma, infection, drugs, or toxins exposes peripheral nerve proteins, and they are
seen by the immune system as “nonself,” initiating an immune reaction. Glial cells
are activated, causing release of cytokines and inflammatory mediators which
contribute to peripheral sensitization, increasing nociceptor sensitivity, and lowering
of the firing threshold. Continuous nociceptive input results in high levels of
glutamate within synapses. In the setting of chronic pain, glial cells swell (called
gliosis) and an increase in cell surface markers is seen. The more persistent the
stimulus, the more they swell and release inflammatory mediators. This contributes to
the development and maintenance of central sensitization.
receptors may also be activated by medications such as opioids. This is thought to
contribute to opioid tolerance, dependence, addiction, and a phenomenon called
opioid-induced hyperalgesia (OIH).
NK1, neurokinin 1; NMDA, N-methyl-D-aspartate.
Visceral pain is very complex. It follows somatosensory pathways and also its
own systems. Aδ and C fibers have been found in the heart, pleura, abdominal cavity,
gallbladder, and testicles. Additionally, the intestinal tract has its own neuronal
system called the “brain–gut axis” that operates independently and in conjunction
15 Like the somatosensory pathways, peripheral and central
sensitization occurs with chronic visceral pain. Activation of the autonomic nervous
system may also affect visceral sensitivity and the role of emotions in modulating
visceral pain. Visceral pain may be referred to areas of the somatosensory system
(e.g., myocardial ischemia causes left arm pain), leading to a complex presentation of
SUPRASPINAL MODULATION AND THE DESCENDING PATHWAY
Once nociceptive signals reach the CNS (typically at the spinal cord level), they
ascend to the thalamus, primarily via the spinothalamic tract. From the thalamus,
tertiary neurons project to many structures in the brain, including the brainstem,
diencephalon (includes the thalamus), primary and secondary somatosensory
cortices, and frontolimbic area. The somatosensory cortex is where the brain
interprets the qualities of pain such as location, duration, and intensity. Tertiary
neurons also project to the limbic system, which is involved in the affective or
emotional component of pain. Perception is when the sensory (physical) and affective
(psychological) components of the nociceptive message are integrated into the
patient’s overall experience. An individual does not experience pain until the brain
has processed and interpreted the electrical nociceptive signal.
A second tract, called the spinoreticular tract, ascends to the thalamus, but also
branches off at the brainstem to stimulate descending modulation. Modulation
happens throughout the CNS and results in either an increase or a decrease in
transmission. Neurons from the thalamus and brainstem release inhibitory
neurotransmitters, such as norepinephrine (NE), serotonin (5-HT), γ-aminobutyric
acid (GABA), glycine, endorphins, and enkephalins, which inhibit EAA activity in
the ascending pathway. GABA is more active at supraspinal sites, and glycine is
more active at spinal sites. The GABA-A receptor is a binding site for
benzodiazepines and barbiturates, and the GABA-B receptor is a binding site for
baclofen, causing muscle relaxation. Glycine has both pronociceptive and
antinociceptive effects, depending on the receptor. Endogenous opioids (endorphins,
enkephalins) are the most common group of inhibitory peptides, inhibiting EAA
release from the presynaptic terminals and activation of second-order neurons in the
postsynaptic terminals. Opioids also enhance the descending pathway via release of
NE and 5-HT. In fact, activation of most of the supraspinal structures results in
enhancement of NE and 5-HT effects.
Diagnosis and Clinical Presentation
Pain is a symptom and a reactionary response to real or potential bodily harm, but it
is not currently defined as a specific disease state. It also cannot be measured
objectively. It is a symptom that relies on a patient’s subjective report and any
physical findings indicative of underlying pathology. Healthcare teams take on the
task of identifying the cause of the pain using everything from noninvasive imaging
such as magnetic resonance imaging to invasive testing such as electromyelograms
Pain can be classified in many ways. Some conditions are classified as syndromes
because the patient presents with a constellation of symptoms that cannot be
attributed to any definitive diagnosis or disease process (e.g., complex regional pain
syndrome). Often clinicians simply state the location and type of pain (e.g.,
neuropathic pain in bilateral lower extremities). Cancer-related pain, whether from
the disease process itself or the treatment of the disease (e.g., surgery, chemotherapy,
or radiation), presents very much like noncancer pain. One of the most common ways
to classify pain is to describe the time course. Acute pain is caused by an injury or
illness. It alerts an individual to the injury and initiates withdrawal from the noxious
stimulus. It typically has an easily identified cause and location. The course is
predictable, and the pain is expected to diminish in hours, days, or weeks as the
injury heals. It may be associated with an inflammatory response, producing redness
and swelling. Inadequately treated acute pain can evoke physiologic hormonal
responses that alter circulation and tissue metabolism; these can also produce
tachypnea, tachycardia, widening of the pulse pressure, and increased sympathetic
nervous system activity. It can also cause emotional distress.
Chronic pain serves no biologic purpose. It is characterized by persistent pain that
lasts beyond the length of an illness or the healing of an injury. Sometimes there is no
apparent cause. It may be either continuous or recurrent and of sufficient duration and
intensity to adversely affect a patient’s well-being, level of function, and quality of
life. Risk factors for developing chronic pain include individual predisposition (e.g.,
female sex, increasing age, or a genetic predisposition), environmental factors (e.g.,
previous painful experiences or abuse), and psychological factors (e.g., anxiety,
depression, or catastrophizing).
Chronic pain can be further classified based on mechanism, symptoms, or location
of injury. Musculoskeletal or inflammatory pain is described as constant, aching pain,
often mediated by prostaglandins. It is usually caused by injury to the skeletal
muscles or joints. Pain may be localized to the joints (as in rheumatoid arthritis and
osteoarthritis) or more regional (as with myofascial pain or muscle strain).
Neuropathic pain is described as tingling, sharp, shooting, stabbing, burning, or other
uncomfortable feelings (dysesthesias) such as the sensation that there are bugs
crawling on the skin. Neuropathic pain may be constant (as in diabetic peripheral
neuropathy) or intermittent (as in trigeminal neuralgia). It is typically caused by
injury within the nervous system or a nervous system response to persistent pain
stimulus from outside the nervous system. Visceral pain can have a vague
presentation, because the enteric and autonomic nervous systems are involved.
Patients may report nausea or generalized abdominal discomfort (as in
endometriosis, hepatitis, or pancreatitis). Some people report pain in the absence of
physiologic tissue damage; however, their perception of the pain is very real. This is
c a l l e d dysfunctional pain. Conditions such as irritable bowel syndrome,
fibromyalgia, interstitial cystitis, and some abdominal or pelvic pain fall into this
category. In these conditions, pain appears to be generated by an imbalance in
pronociceptive signals and antinociceptive signals in the CNS. Patients with
dysfunctional pain syndromes are heavily influenced by factors that augment or
diminish the CNS pathways (including stress, anxiety, depression, or illness).
Pain is very subjective and difficult to measure in quantitative terms. It is essential to
obtain a thorough history and examination, both physical and psychological. When
obtaining a pain history, clinicians should gather details about the pattern, duration,
location, and character of the pain and should additionally determine what makes the
pain worse and what makes it better, what medications and nonpharmacologic
therapies have been tried in the past, and the result of those therapies (positive or
negative outcome) (Table 55-1).
Pain intensity should be measured using an appropriate pain scale according to the
patient’s ability to communicate (Table 55-2, Fig. 55-4).
scales tend to be more accurate in the acute pain setting and not as helpful for chronic
pain because they only capture a “snapshot” of what the patient is feeling. Chronic
pain symptoms wax and wane over time, so more useful tools are multidimensional
pain scales that evaluate function, including sleep, appetite, performance of activities
of daily living, work, and social interactions. Examples of multidimensional tools
include the McGill Pain Questionnaire and the Brief Pain Inventory.
the most useful aspect of patient assessment is the information provided by the patient
on how pain impacts day-to-day life, such as the number of hours they spend on their
hobbies, or how well they can perform activities of daily living. Some of the most
difficult patients to assess are young children and patients with cognitive, visual, or
hearing impairment. These patients may have difficulty describing and
communicating their pain and discomfort. There are multiple assessment tools that
are designed and tested in these special populations to increase the accuracy of pain
assessment. In addition to physical and functional assessments, psychological
evaluations help to identify those patients who may need more psychiatric or
psychological therapy to help them cope with their chronic pain. Because controlled
substances are used to treat chronic pain, some clinicians advocate for substance
abuse screening (see Case 55-7, Question 4).
History of present illness (HPI)
Current medications, including allergies
Clinician observations of patient behavior (grimacing, withdrawing, guarding)
Treatment of pain is based on guidelines whenever possible. However, the number of
treatment guidelines for pain management is limited. More commonly, clinicians
choose a therapy based on the type of pain (e.g., neuropathic, musculoskeletal,
visceral, and central). For all types of pain, multimodal therapy including
pharmacologic, physical rehabilitation, and cognitive behavioral therapy should be
combined. Interventional therapies should be considered if possible.
A treatment plan must always include evaluation of the following factors: age,
comorbidities (such as renal and liver disease), route of administration (the oral
route may not be suitable), concurrent medications (for duplication or drug–drug
interactions), laboratory abnormalities, and financial resources.
adjunctive therapies as well. Pharmacotherapy for chronic pain is more complex.
First-line agents for the treatment of neuropathic pain consist of antidepressants,
preferably serotonin and norepinephrine reuptake inhibitors (SNRIs), including
tricyclic antidepressants (TCAs). These agents enhance the descending inhibitory
pain pathway. Anticonvulsants (e.g., sodium-channel blockers, calcium-channel
blockers, or GABA agonists) are also considered first-line therapy for many common
types of neuropathic pain. They inhibit activation of sodium and calcium channels,
block release of EAAs such as glutamate, or block the postsynaptic receptors. Some
anticonvulsants also enhance the inhibitory effects of GABA. If the pain is localized,
topical agents may be useful (e.g., capsaicin or local anesthetics). Addition of an
opioid may be considered if the former agents fail to provide adequate analgesia.
Combination therapy has been shown to be more effective in some cases (TCA–
anticonvulsant or opioid–anticonvulsant combinations).
interventional therapies may be helpful for short-term relief.
Chronic musculoskeletal pain usually responds to acetaminophen, salicylates, or
NSAIDs, in addition to nonpharmacologic therapies such as heat and ice or physical
rehabilitation modalities. Localized pain may be amenable to topical therapies
(NSAIDs, capsaicin), and trigger points (i.e., taut muscle bands) may be amenable to
injections. SNRIs may also be considered for this indication.
Visceral pain is complex, and there are no clear treatment guidelines. Because it
travels the somatosensory pathways, antidepressants that enhance inhibitory
modulation are most commonly used. Additionally, anticonvulsants that reduce
central sensitization and hyperalgesia may be helpful.
Trials of any pharmacologic therapy must be monitored for both efficacy and
toxicity. Patients must have realistic expectations for any medication trial. Even the
most effective analgesics are expected to achieve only about 30% to 50%
improvement in chronic pain. This is why multimodal therapy is essential. NSAID
therapy should be accompanied by monitoring for dyspepsia, peptic ulcers, and
gastrointestinal (GI) bleeding, elevated blood pressure, and declining renal function,
at a minimum. Antidepressants do not usually require laboratory monitoring but are
known to cause dry mouth, constipation, urinary retention, and drowsiness. Some of
the anticonvulsants require laboratory monitoring for liver toxicity, electrolyte
imbalance, or bone marrow abnormalities. All anticonvulsants may cause
drowsiness, dizziness, and cognitive dysfunction, with short-term memory loss and
word-finding difficulty. Opioids require laboratory monitoring for long-term adverse
effects such as osteoporosis, hypogonadism, and end-organ impairment, and patients
must be routinely screened for sleep apnea, constipation, drowsiness, nausea, and
vomiting. Drug interactions, both pharmacokinetic (e.g., hepatic enzyme interactions)
and pharmacodynamic (e.g., additive sedation), are common with many of these
agents, particularly when used in combination.
Pain Assessment Tools for Adults
Administration Advantages Disadvantages
Visual analog scale (VAS) Verbal, visual Reliable; sensitive to acute
Verbal, visual Reliable; good validity;
Faces pain scale (FPS) Visual Reliable; good validity;
Brief pain inventory (BPI) Verbal, written Reliable; intensity and
It is estimated that 25 million inpatient surgeries and 35 million ambulatory surgeries
are performed annually in the United States.
25 Greater than 80% of surgical patients
experience postoperative pain and of those patients, up to 40% experience “severe”
2 The mismanagement of postoperative pain, whether undertreatment or
overtreatment, is associated with negative physiologic consequences such as
persistent postoperative pain, impaired rehabilitation, increased hospital length of
continuum to effectively manage pain.
Pain management during the perioperative period can be divided into three phases:
pre-, intra-, and postoperative analgesia. Preoperative analgesia is treatment started
1 to 2 hours before surgery, with medications used to decrease peripheral
sensitization. Intraoperative analgesia prevents the establishment of central
sensitization caused by incisional injury and includes only the intraoperative time
period. Postoperative analgesia is aimed at proactively reducing acute pain and
preventing central sensitization, thereby avoiding subsequent development of chronic
Prevalence of Chronic Postsurgical Pain
Type of Surgery Incidence of Chronic Pain (%) Clinical Presentation
Limb amputation 30–85 Phantom limb pain
Mastectomy >50 Scar pain, phantom breast pain,
shoulder or arm pain, chest wall
Thoracotomy 30–50 Scar pain, chest wall pain
Coronary artery bypass surgery 30–55 Sternal pain, postsaphenectomy
Inguinal hernia repair 20–60 Scar pain, ilioinguinal nerve pain,
Source: Cregg R et al. Persistent postsurgical pain. Curr Opin Support Palliat Care. 2013;7:144–152.
Normally, the acute pain trajectory has a rapid decline during the first week after
surgery, and most patients fully recover within a few weeks with no residual pain.
Although there is no single definition of a time frame for chronic pain, chronic
persistent surgical pain (CPSP) is usually regarded as pain of at least 2 months
duration and which all other causes have been excluded.
highest with limb amputation, thoracotomy, mastectomy, hernia repair, and cardiac
28 Risk factors for CPSP include history of chronic pain prior to
surgery, gender, age, surgical site, invasiveness of surgery, unrelieved postoperative
pain, and comorbid anxiety or depression.
29 Genetic factors also account for a
significant degree of inter-individual variation in pain sensitivity and treatment
will be undergoing shoulder arthroplasty in 2 weeks. She also has fibromyalgia and takes
analgesic regimen is effective.
It is paramount that all patients have a thorough preoperative assessment including
review of medical comorbidities, medications, history of chronic pain, and substance
abuse, as well as prior postoperative analgesic regimens and responses.
include evaluating kidney or liver function, pulmonary function, or coagulation status.
Pharmacists should also ask about sleep apnea. The presence of central or
obstructive sleep apnea is associated with a higher risk for perioperative
complications including opioid-induced respiratory depression.
not have a sleep apnea diagnosis, a screening tool called the STOP-BANG
questionnaire can be utilized to assess the risk (Table 55-4).
screening are associated with postoperative critical care admission.
medication review, the pharmacist should consult with the respective state
prescription drug monitoring program to determine what controlled substances the
patient has been filling. It is expected that patients have only one prescriber of
controlled substances so it is helpful to determine whether stated use matches the
prescription history. Keeping with The Joint Commission standards, the pharmacist
should reconcile outpatient medication profiles, contacting dispensing pharmacies if
34 Current and past substance use should be addressed in an open and
nonjudgmental manner. Some hospitals perform urine drug testing to confirm
prescription and/or illicit drug use.
Do you feel tired, fatigued, sleepy during the day?
Has anyone observed you stop breathing during sleep?
Are you being treated for high blood pressure?
Yes to 3 or more item = high risk for OSA
Yes to <3 items = low risk of OSA
Patients always bring their past experiences and current fears to surgery. These
factors affect how they perceive and cope with acute pain after surgery (Table 55-5).
Risk factors for increased pain after surgery in B.B. include female gender, work
injury, and chronic opioid therapy. Functional pain syndromes such as fibromyalgia
are associated with inefficient diffuse noxious inhibitory control (DNIC). This means
that the inhibitory pathway is not effectively blocking pain transmission into the CNS,
and she will likely have an exaggerated pain response to surgery. Her chronic opioid
use could also complicate pain management because she will likely require higher
CASE 55-1, QUESTION 2: What should be done to help B.B. prepare for surgery?
Clinicians should provide the patient and family with individually tailored
education, including information on treatment options for management of
postoperative pain, making sure to document the plan and goals in the medical record
and on paper for the patient to take home.
30 Patient-tailored education has been
shown to reduce postoperative opioid consumption, reduce preoperative anxiety,
reduce requests for sedatives, and reduce length of stay.
30,35 Education should include
changes in analgesics prior to surgery, reporting and assessment of pain and when to
report, multimodal pharmacologic and nonpharmacologic options, as well as
realistic goals for pain control.
Risk Factors for Increased Postoperative Pain
Adverse experience with previous surgery
Preexisting pain (moderate–severe >1 month)
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