It is estimated that 35% to 80% of people addicted to prescription
opioids report that they were first exposed to opioids for the legitimate treatment of
pain, including postsurgical pain.
6 The use of nonopioid medication can help reduce
CASE 55-2, QUESTION 3: What other nonopioid medications would be helpful in the management of
Recent guidelines on postoperative pain management reviewed studies on
acetaminophen and NSAIDs in conjunction with opioids and found that the
combination of both medications is more effective than either drug alone in reducing
30 Perioperative oral acetaminophen at a dose of 1,000
mg 3 or 4 times/day for 48 hours after surgery in adults with normal liver function is
51 After the initial postoperative period, the dose should be
reduced to 650 mg and administered on an “as-needed” frequency. To reduce the risk
of liver toxicity associated with acetaminophen daily totals exceeding 3,000 mg,
patients who will need opioid therapy should not be prescribed combination
products containing acetaminophen such as oxycodone/acetaminophen or
hydrocodone/acetaminophen. Use of intravenous acetaminophen has generally been
reserved for patients who cannot take oral medications after surgery and cannot use
NSAIDs due to increased risk of gastrointestinal bleeding or renal insufficiency.
Most research indicates that there is no clear difference between intravenous and
oral acetaminophen in reducing postoperative pain.
Compared with acetaminophen, NSAIDs are more efficacious for reducing
postoperative pain due to their anti-inflammatory effects. Most of the oral
nonselective NSAIDs are comparable in efficacy so selection may be influenced by
other factors such as cost, availability for use over the counter, and lower
cardiovascular adverse effects. All NSAIDs are contraindicated for management of
perioperative pain in patients who undergo coronary artery bypass graft surgery
because of an increased risk of cardiovascular events.
Osteoarthritis for more detailed information on NSAIDs.
Intravenous ketorolac is a nonselective NSAID and very effective in reducing
postoperative pain. The recommended ketorolac dose for adult patients <65 years
with normal renal function is 30 mg every 6 hours as needed. For patients over 65
years of age or with mild-to-moderate renal failure, the dose of ketorolac must be
reduced to 15 mg every 6 hours as needed. The maximum duration for ketorolac
administration is limited to 5 days to prevent adverse events related to
gastrointestinal bleeding with prolonged use. It is not recommended to administer
ketorolac to patients who are hypovolemic postoperatively due to excessive blood
loss or dehydration due to the risk for renal injury.
Gabapentin or pregabalin are neuromodulators that are helpful in reducing
postoperative neuropathic pain. The initial dose should be based on the patient’s use
prior to admission. For patients who were not taking gabapentin or pregabalin for
chronic pain prior to surgery, the dose should be titrated up from the lowest dose and
adjusted for renal function (Table 55-8). Patients who were taking gabapentin or
pregabalin for preexisting neuropathic pain prior to surgery should have their dose
and frequency resumed as soon as possible postoperatively to prevent uncontrolled
Pharmacologic Options for Treatment of Neuropathic Pain
a Adverse Effects Monitoring/Comments
Oxcarbazepine 75 mg BID, titrate to max
Lamotrigine 25 mg daily, titrate to max
Lacosamide 50 mg BID, titrate to max
Same as gabapentin Same as gabapentin
Amitriptyline, Nortriptyline 10 mg QHS, titrate to 100
Venlafaxine 37.5 mg daily, titrate to
b Apply QID Rash, burning feeling on
bFood and Drug Administration–approved for treating pain conditions.
every night at bedtime; QID, 4 times a day; TID, 3 times a day.
The use of ketamine is becoming increasingly popular postoperatively in patients
with a history of chronic pain that is poorly responsive to traditional analgesic
medications including opioids. Ketamine is a NMDA receptor antagonist that is
effective in decreasing central sensitization after surgery. There is insufficient
evidence in the literature on the optimal ketamine dose and duration of use
postoperatively. Doses for postoperative intravenous ketamine bolus dosing or
continuous infusion range from 0.1 to 0.5 mg/kg.
postoperative ketamine is hallucinations which can be mitigated by keeping the dose
low. Ketamine is contraindicated in patients with uncontrolled hypertension.
Intravenous lidocaine has been evaluated as part of multimodal analgesia in
patients who underwent open or laparoscopic abdominal procedures. Studies
showed that perioperative or intraoperative intravenous lidocaine infusions were
associated with shorter duration of ileus and better quality of analgesia compared to
In trials, lidocaine was typically administered as an intravenous bolus
(100–150 mg or 1.5–2.0 mg/kg) followed by an infusion of 2 to 3 mg/kg/hour through
53,54 Topical local anesthetics such as the lidocaine 5% patch may
be helpful for incisional pain, but its efficacy is limited due to lack of penetration
D.K. should have acetaminophen started at 1,000 mg orally scheduled every 8
hours as soon as he is alert enough to swallow medication without risk of aspiration.
NSAIDs should be avoided in the immediate postoperative period until his renal
function can be evaluated. If D.K.’s creatinine clearance is >50 mL/minute, ibuprofen
600 mg orally every 6 hours as needed can be used for pain because this was the
patient’s NSAID choice. Prior to admission, D.K. was reporting pain shooting down
the right leg but was not taking medication for neuropathic pain. If the shooting pain
persists postoperatively, gabapentin started at a low dose of 100 mg orally scheduled
3 times a day may be helpful. Caution should be used with gabapentin in patients with
renal insufficiency which may require a dose adjustment. Intravenous lidocaine is
generally not a first-line option for postoperative pain management and should be
used only if pain control is suboptimal after maximizing other multimodal
medications. Before D.K. is discharged, plans should be made for prescribing the
oral multimodal medications for a short duration of time because acute postoperative
pain generally abates after one to 2 weeks.
Low back pain occurs at a rate of 1.39/1,000 person-years in the United States,
including 3.15% of all emergency visits. These are typically injuries occurring in the
It has been reported that low back pain affects 70% to 85% of adults at some
point in their lives, and 12 months after the onset of low back pain, 45% to 75% of
56,57 There is a bimodal distribution with peaks between 25 and
29 years of age (2.58/1,000 person-years) and 95 to 99 years of age (1.47/1,000)
without differentiation by underlying etiology.
56 There is an association between
psychological factors and the occurrence of low back pain, including anxiety,
depression, somatization symptoms, stress, and negative body image. Chronic low
back pain patients have higher rates of emotional distress and depression (25%)
relative to acute low back pain subjects (2.9%).
include job dissatisfaction, physical work, psychologically stressful work, low
educational achievement, and workers’ compensation insurance.
and physical work factors such as heavy lifting, repetitive motion, non-neutral body
postures, and vibration are established risks for back disorders.
pain also creates a large financial burden on the workplace. Low back pain accounts
for almost $20 million in lost productivity annually, and patients who have been on
disability for more than 1 year rarely return to work.
Low back pain, by definition, affects the lumbosacral spine and associated
muscles and nerves. It is multifactorial in nature, either nociceptive (musculoskeletal,
myofascial), neuropathic (radicular pain), or has a central sensitization component.
In about 85% of cases, no pathophysiologic cause can be found.
spinal unit is made up of two vertebral bodies, two zygapophyseal (facet) joints, the
intervertebral disc, and the supporting ligamentous structures (Fig. 55-5). The facet
joints of the spine form the junction where vertebral bodies meet. The joint space is
maintained by cartilage and fluid in the joint. Like all weight-bearing joints of the
body, the spine also develops joint space narrowing, bony hypertrophy, and
deterioration of cartilage with normal use, resulting in the musculoskeletal pain of
OA. If the spine is used more, as with jobs involving heavy lifting and manual labor,
the joints deteriorate faster. In addition to deterioration of the facet joint spaces, the
intervertebral discs lose water content with time and may become desiccated,
reducing the cushion between the vertebral bodies. These discs are fragile and can be
torn or damaged and may herniate into the spinal canal foramen (Fig. 55-5). If
vertebral bodies shift because of deterioration, spondylolisthesis may occur. This
shift, or a herniated disc, may impinge on the spinal nerve root, or cause nerve root
irritation, which can produce radicular neuropathic pain. This is sometimes referred
to as sciatica. Shifting of the vertebral bodies may also reduce the size of the foramen
where the nerves exit the spinal cord (spinal stenosis). If the vertebral bodies shift
too far into the central spinal canal, pressure can be exerted on the spinal cord, which
may lead to spinal cord injury and subsequent loss of sensory and motor nerve
function (paralysis). If the motor nerves are affected (as with lower extremity muscle
weakness, bowel or bladder incontinence), a “red flag” is present and surgery may
be necessary to preserve function. Table 55-9 lists other serious conditions that call
for immediate medical or surgical attention.
64 Sometimes low back pain is more
intense than would be expected, or is much more widespread than imaging would
predict. These are hallmarks of central sensitization.
Figure 55-5 Spine anatomy and disc herniation.
Myofascial pain is very common in patients with chronic low back pain.
Myofascial pain is localized to specific regions or muscle groups. It affects all age
groups and is associated with numerous other pain conditions. It is classically
associated with muscle knots called “trigger points.” A trigger point is described as
a hyperirritable spot in skeletal muscle that is associated with a palpable “taut band”
of muscle. Trigger points are hypothesized to evolve from excessive acetylcholine
release from the motor endplate, leading to sustained muscle fiber contracture.
Development of trigger points is usually associated with mechanical overuse or
overload of a muscle group (as with repetitive work). It is also associated with
postural problems, prolonged static positions, emotional stress (causing muscles to
tense), and nutritional deficiencies (such as vitamins B1
magnesium, and zinc) or metabolic problems such as thyroid disease. It is thought that
low-intensity exertions related to static posture cause small muscle fibers to be
continuously activated, leading to the development of trigger points.
are abundant in muscle nerves, and there are a variety of nociceptors that can be
stimulated by substances such as prostaglandins, bradykinin, protons, ATP, 5-HT,
and glutamate, which are released from damaged tissue. The neuropeptides,
substance P and CGRP, are also found in the nociceptor terminals, which stimulate
the inflammatory cascade, leading to peripheral sensitization and the clinical
manifestation of muscle pain. Continuous activation of muscle nociceptors leads to
release of substance P and glutamate from the presynaptic terminal at the dorsal root
ganglion. These substances activate postsynaptic AMPA and NMDA receptors,
respectively, and subsequently may lead to neuroplasticity (Fig. 55-3).
Red Flags for Potentially Serious Conditions that Cause Back Pain
Possible Fracture Possible Tumor or Infection
Age <20 or >50 years Saddle anesthesia
Minor trauma or strenuous lifting in
older or potentially osteoporotic
History of cancer Recent onset of bladder dysfunction
(e.g., urinary retention, increased
frequency, overflow incontinence)
Constitutionalsymptoms (recent
fever, chills, unexplained weight
Severe or progressive neurologic
deficit in the lower extremities
Risk factors for spinal infections:
Pain that worsens when supine Perianal/perinealsensory loss
Severe nighttime pain Major motor weakness:
Ankle plantar flexors, evertors, and
Acetaminophen is considered the safest choice for the management of
musculoskeletal pain. Its mechanism of action is not well defined, but it has analgesic
activity in the CNS. It has no peripheral clinical effect on prostaglandins, so it lacks
typical anti-inflammatory activity. Use of acetaminophen therefore avoids the GI,
renal, and cardiovascular toxicities associated with NSAIDs. NSAIDs reduce pain
and inflammation by inhibiting cyclooxygenases (COX-1 and COX-2) at the site of
injury and along the ascending pain pathway. The NSAIDs are equally effective
across the drug class, although some patients may respond to one agent better than
another. They are more effective as monotherapy for acute low back pain than in
combination with a muscle relaxant or an opioid. A meta-analysis showed that
NSAIDs are better than placebo for back pain without neuropathic symptoms, but not
for back pain with neuropathic symptoms.
66,67 COX-2 selective inhibitors are as
effective as traditional NSAIDs for analgesia but are better tolerated.
the only COX-2 selective inhibitor available in the United States. Acetaminophen
may be used in combination with NSAIDs for additive analgesia.
There are several guidelines published for the management of low back pain. Koes
et al. reviewed evidence-based management guidelines from 13 different countries
and 2 international committees that were published between 2000 and 2008.
55-10 presents a summary of common recommendations. All guidelines were in
agreement with the use of simple analgesics such as over-the-counter acetaminophen
and NSAIDs for first-line therapy for both acute and chronic low back pain. Both of
these medication classes are considered effective for short-term use, although their
effects are modest. Because the guidelines have been published, a meta-analysis of
acetaminophen versus placebo for spinal pain and osteoarthritis found acetaminophen
to be ineffective for long-term use in chronic pain.
ideal first-line analgesic, if there are no contraindications.
Most guidelines recommend either muscle relaxants or weak opioids as third-line
choices for short-term use in either acute or chronic low back pain. Despite the fact
that muscle relaxants are used commonly, there is no evidence that they are effective
for chronic low back pain. Agents such as cyclobenzaprine and tizanidine, as well as
benzodiazepines such as diazepam, show moderate efficacy in the short-term (<2
weeks) but are associated with a higher incidence of adverse effects than placebo.
Weak opioids such as tramadol have also shown modest relief with short-term use
70,71 There are several studies showing some efficacy for most long- and
short-acting opioids, but they do not show any long-term functional improvement or
A few guidelines, including those from the American Pain Society (APS),
recommend use of antidepressants or anticonvulsants for neuropathic pain
70 Antidepressants, specifically the TCAs, have shown modest analgesia
compared with placebo, but they have not been shown to be effective for acute low
back pain, nor have they shown demonstrable improvement in function.
Duloxetine, an SNRI, has shown efficacy and safety for the treatment of low back
77 There have been a very small number of trials using the anticonvulsants
topiramate and gabapentin for back pain. Anticonvulsants traditionally have been
helpful for treating neuropathic pain (e.g., peripheral neuropathies) but produce only
small improvements for back pain with radiculopathy.
Summary of Common Recommendations for Treatment of Low Back Pain
Reassure patients that diagnosis is not serious
Prescribe medication if necessary
Third line: muscle relaxants, opioids, antidepressants, or anticonvulsants as coanalgesics
Do not recommend supervised exercise program
Discourage use of alternative therapies (ultrasound, electrotherapy)
Short-term use of medication/manipulation
NSAIDs, nonsteroidal anti-inflammatory drugs.
Myofascial pain treatment is aimed at correcting precipitating behaviors including
ergonomic factors. Physical rehabilitation is essential for teaching patients
appropriate stretching and strengthening exercises, as well as postural support and
stabilization. Some clinicians inject the trigger point(s). There are several techniques
that are all equally effective, including dry needling, saline injection, local anesthetic
injection or botulinum toxin. Several other pharmacologic therapies may be used, but
none have more than anecdotal support. General approaches to pain management,
including NSAIDs, muscle relaxants, antidepressants, anticonvulsants, and opioids,
may be helpful for individual patients. Vitamin D deficiency has been linked to
chronic musculoskeletal pain, although this is somewhat controversial.
available. He reports that his blood pressure is usually around 150/80 mm Hg with a pulse around 75
The presentation and assessment of back pain can be very complex given its
multifactorial nature. Acute low back problems are defined by the Agency for Health
would fit this definition. When J.P. has acute exacerbations of his back pain, the
numeric pain scale is an accurate assessment tool (Table 55-2, Fig. 55-4). His rating
of 10 out of 10 indicates severe acute pain. Clinicians should also consider a
patient’s vital signs, which may be elevated with acute pain. If a patient is unable to
communicate (e.g., on a respirator), changes in vital signs may be the only indicator
J.P.’s chronic back pain assessment must rely heavily on the history he provides,
because there is minimal objective evidence to base the assessment on, other than his
findings on physical examination or imaging studies. He indicated that his chronic
pain is about 7 out of 10 on the numeric pain scale. Even though the numeric pain
scale has been validated for chronic pain, it is less useful in this setting because it
only gives a snapshot of the whole pain picture. A multidimensional tool, such as the
Brief Pain Inventory or the McGill Pain Questionnaire, is more useful to assess
18,19 Physical activities, sleep, diet, and social interactions
may be affected by chronic pain. J.P. notes that his pain is worse with physical
activity. He reports sleeping poorly and has limited physical activity and minimal
social interaction. All of these factors contribute to a patient’s pain experience and
must be considered (Fig. 55-1). Assessment of chronic pain is not only more
complex, but is more extensive, because the perception and response to chronic pain
is widely variable. Each patient experiences pain in his/her own way. A
psychological assessment is essential to identify comorbidities such as depression or
anxiety and any history of abuse (e.g., physical, verbal, sexual) or previous trauma,
as well as to assess a patient’s coping ability. It may be helpful to ask J.P. about his
spirituality and cultural values, because these may offer unique opportunities (or
barriers) to any proposed treatment plan.
If opioids are being considered, many clinicians endorse the use of a substance
abuse screening tool such as the Screener and Opioid Assessment of Patients with
Pain-Revised (SOAPP-R), Opioid Risk Tool (ORT), or Diagnosis, Intractability,
83 J.P. drinks alcohol, smokes tobacco, and has used his
sister’s acetaminophen/codeine. These factors may warrant use of a screening tool to
assess his risk for opioid abuse.
J.P.’s chronic pain has been present for several years and has gradually worsened.
Based on his history and current physical examination, he appears to have
mechanical musculoskeletal pain. He is a former plumber, which involves bending
and lifting, which puts him at risk for facet joint arthritis. He describes the aching,
localized pain that is typical of arthritis, either in his spine–hip junction (sacroiliac
joint) or his zygapophyseal (facet) joints, which are the most common locations for
lumbosacral pain. He demonstrated localized tenderness at the L4–L5 level. This is
most consistent with facet joint disease. He also has tenderness along muscles in his
low back, reaching into his buttocks, which is very common, because the body
attempts to accommodate structural spine abnormalities. Muscular pain may radiate
into the mid-back or into the buttocks, but does not travel below the knees. J.P. did
not have pain that radiated below the knees. J.P. does not have any motor weakness,
past experiences, or comorbidities that would indicate a red ag (Table 55-9). J.P.’s
physical examination reveals radicular pain in the L5 dermatome (i.e., an area of the
skin supplied by nerves from a single spinal root). Unlike muscular pain, radicular
pain travels from the spine past the knee into the distal extremities. J.P. describes
burning and shooting pain that radiates from his spine down his right leg to his toes.
These are hallmarks of neuropathic pain. J.P. appears to have both
musculoskeletal/myofascial and neuropathic pain. This mixed picture is very
common with back pain and adds complexity to both diagnosis and treatment plans.
CASE 55-3, QUESTION 2: What comorbidities will affect J.P.’s presentation and pain assessment?
J.P. has a concurrent diagnosis of depression, which is quite common in patients
with chronic pain. The incidence of depression in chronic pain patients is 2 or 3
times higher than the general population.
84 Depression is often under-recognized in
the face of pain as a presenting symptom. Many times healthcare providers
investigate for a functional cause of the pain, but overlook the psychosocial aspects
of pain. Variables associated with depression in chronic pain are female sex,
younger age, lower socioeconomic status, unmarried, Caucasian, and higher pain
In fact, because pain severity worsens, depressive symptoms worsen,
medical visits become more frequent, and healthcare costs increase.
deficiency of NE and 5-HT that occur with depression makes the pain-blocking
function of the descending pain pathway less effective. As a result, J.P. may feel
more pain physiologically and may also have a greater emotional response to his
pain and other stressors. His depression may be contributing to his sleep disturbance
and his diminished social interactions. Untreated depression may be detected with a
multidimensional pain assessment tool. If identified and treated, his pain may
improve concurrently with his depression. Other psychiatric comorbidities that
commonly occur with chronic pain include anxiety, personality disorders, and
J.P. also has a diagnosis of hypertension. Although this will not directly contribute
to his pain, any acute exacerbations may cause an increase in his pulse and blood
pressure. Increases in blood pressure are associated with an increased incidence of
stroke. The presence of hypertension is also a factor when developing a treatment
plan. He is currently taking ibuprofen for pain, and NSAIDs are known to cause fluid
retention, compromise renal function, and diminish the benefits of antihypertensives
(such as J.P.’s lisinopril). Corticosteroids, which may be used during an
interventional pain procedure, may also increase blood pressure.
CASE 55-3, QUESTION 3: How can current low back pain treatment guidelines be applied to J.P.’s
Acetaminophen is considered first-line therapy for low back pain. J.P. has been
using acetaminophen up to 6,000 mg daily, which exceeds the recommended
maximum daily dose. He has also been using some acetaminophen/codeine that he
obtained from his sister. J.P. is at risk for liver toxicity from high doses of
acetaminophen. Additionally, he has not found the acetaminophen to be helpful, so it
to improve with a dose increase, but he may benefit from rotation to another NSAID
with a different chemical structure. Naproxen is an inexpensive agent that is also
available over the counter. He does not demonstrate any muscle spasm, so a muscle
relaxant is not indicated, nor is it recommended for chronic back pain. He has
radicular pain, so a trial of gabapentin may be helpful. He has been using the
codeine-containing product and notes that this has been helpful; however, opioids are
not recommended for long-term management and have not shown substantial benefit
with long-term use. He should be encouraged to reduce or discontinue use of the
opioid. Chang et al. recommend a trial of TCAs if NSAIDs and acetaminophen have
87 This may also help his chronic insomnia, but the doses used for analgesia
(typically less than 100 mg/day) may not be high enough to have true antidepressant
effects. Selective serotonin reuptake inhibitors (SSRIs) may be used to treat
depression, but have very little independent analgesic effects. However, if his
depression improves, we would expect to see a proportional improvement in his
pain. Because SSRIs are better tolerated than TCAs, and TCAs have not
demonstrated improvement in function in the long term, J.P. should have a trial of a
generic SSRI such as citalopram. SNRI’s may also be an effective and well-tolerated
option that would treat both his depression and pain.
different muscle relaxant be appropriate?
Muscle relaxants are commonly used to treat chronic musculoskeletal pain. They
are recommended for short-term use for acute low back pain (all are fairly equal).
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