EMERGENCY SEDATION AND PAIN MANAGEMENT - PART 5 pps

The majority of randomized, controlledNSAID trials for acute low back pain have demonstratedthe superior efficacy of NSAIDs over placebo, but nonehas demonstrated that one NSAID is super

CyclobenzaprineDiazepamMetaxoloneOrphenadrineOpiatesSteroidsAntidepressantsHeat/IcePhysical therapy/Exercise therapy/Spinal Manipulation/AcupunctureFacet Injections/Epidural Injections

FOLLOW-UP CONSIDERATIONS

SUMMARY

BIBLIOGRAPHY

SCOPE OF THE PROBLEM

Acute low back pain is a very common problem that

affects 60–80% of adults during their lifetimes Fifty

percent of working-age adults will have at least one

episode of low back pain during any given year At any

one point in time, 15–20% of the population will report

having low back pain, 1% of the population will be

temporarily disabled, and 1% of the U.S population will

be chronically disabled from back pain This equates to

24.5 million adults in the United States reporting back

pain during the year 2000 Low back pain usually starts

between age 30 and 50, with the median age of onset at 48

years Men and women are equally affected by this

problem and it crosses all social and racial boundaries

Epidemiologic studies have shown similar prevalence

worldwide Low back pain is second only to upper

re-spiratory problems as the most common symptom-related

reason for a physician visit In 2000, 44 million scriptions were written for low back pain, includingprescriptions for nonsteroidal anti-inflammatory drugs(NSAIDs) (16.5%), COX-2 inhibitors (10%), and musclerelaxants (18.5%)

pre-Low back pain accounts for a huge financial diture Although patients who become disabled owing tolow back pain represent less than 5% of those with lowback pain problems, they account for up to 60% of thesocietal costs for this disorder In 1990, the directmedical costs for treating low back pain exceeded $24billion, and total expenditures of $35–56 billion havebeen estimated when disability costs are included

expen-CLINICAL ASSESSMENT

The majority of low back pain is due to mechanicalmusculo-ligamentous injury Low back pain may arise

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from spinal structures including ligaments, facet joints,

vertebral body periosteum, perivertebral musculature

and fascia, blood vessels, the annulus fibrosis, and nerve

roots However, up to 85% of patients with isolated low

back pain cannot be given a precise neuroanatomical

diagnosis The remainder of the cases can be roughly

divided between mechanical, nonmechanical, and

vis-ceral causes (Table17-1)

The emergency provider’s approach to low back pain

is not that different from the general practitioner’s

Because the majority of low back pain is self-limiting

and lacks a neuroanatomical diagnosis, imaging studies

are usually of little utility When assessing the patient,

the emergency provider should be vigilant for the ‘‘Red

Flags’’ that are indicators of a more serious cause of low

back pain (Table17-2) Although up to a third of patients

may report a red flag symptom, only 1–10% of those will

have potentially serious pathology (Table 17-3) The

sensitivities and specificities of various historical and

physical exam elements are included in Table17-4

Neurologic involvement as a cause of pain is gested by the presence of sciatica, neurogenic claudica-tion, or symptoms of cauda equina syndrome Sciatica is

sug-a unilsug-atersug-al leg psug-ain thsug-at ususug-ally extends psug-ast the kneeand arises from a lumbar radiculopathy The absence ofsciatica makes the presence of a clinically important discherniation unlikely The presence of sciatica can beconfirmed by the reproduction of pain on straight legraise of less than 60

Neurogenic claudication is the presence of leg pain onstanding or after walking that mimics claudication, butunlike claudication, which improves when a patient rests(even in an upright posture), neurogenic claudicationoften requires sitting with the back in flexion to relievesymptoms Although the sensitivity of neurogenicclaudication for the detection of spinal stenosis is only60%, the specificity is thought to be quite high Caudaequina syndrome is suggested by the presence of urinaryretention (sensitivity 90%) with overflow incontinence,saddle anesthesia (sensitivity 75%), and bilateral lower

Table 17-1 Differential diagnosis of low back pain

Mechanical low back or leg pain Nonmechanical spinal conditions Visceral disease

Degenerative disk disease Multiple myeloma Gastrointestinal disease

Degenerative facet disease Metastatic carcinoma Pancreatitis

Ligamentous instability Shingles

Inflammatory arthritis Ankylosing spondylitis Psoriatic spondylitis Reiter’s syndrome Inflammatory bowel disease Osteochondrosis

Paget’s disease Source: Adapted from Deyo RA, Rainville J, Kent DL What can the history and physical examination tell us about low

back pain? JAMA 1992;268:760–765.

extremity weakness, pain, or sensory abnormalities(sensitivity 80%).

Because 95% of disk herniations involve the L5 or S1nerve roots, the physical exam should focus on the distalsensory and motor exam (Table17-5) The most com-mon impairments are weakness of ankle and great toedorisflexion (L5), loss of sensation on the foot (L5, S1),and loss of ankle reflex (S1) Although ankle plantarflexion is a function of the S1 nerve root, only severeimpairments can be detected Pin prick should be testedbilaterally for symmetry along the medial (L4), dorsal(L5), and lateral (S1) aspects of the feet, as this is moreaccurate than light touch or temperature

In the absence of findings suggestive of systemic disease

or cauda equina syndrome, imaging is rarely neededunless patients have failed 6 weeks of conservative ther-apy Plain radiographs can be used to identify fractures,but are not able to adequately date compression fractures

Table 17-2 Red flag indicators to prompt consideration of radiographic imagingfor patients with acute back pain

Indicators of cancer

 History of cancer

 Unexplained weight loss

 Unrelenting night pain or pain at rest

 Recent significant trauma or milder trauma, age >50

 Prolonged use of oral corticosteroids

 Osteoporosis Indicators of cauda equina syndrome

 Loss of bowel or bladder control

 Saddle anesthesia

 Symmetric distal numbness or leg weakness Other

 Clinical suspicion of ankylosing spondylitis

 Progressive neurological dysfunction

Table 17-3 Prevalence of potentially severe causes

of acute low back pain in

Source: Adapted from Deyo RA, Rainville J, Kent DL What can

the history and physical examination tell us about low back pain?

JAMA 1992;268:760–765.

Patients with a high pretest probability for other serious

diseases will require additional imaging, as plain

radio-graphs are not sufficiently sensitive to detect other serious

pathology Computed tomography (CT) has the same

sensitivity as magnetic resonance imaging (MRI) indetecting herniated disks and central stenosis CT candetect pathology at the foraminal and extraforaminal nerveroot, but is not effective for evaluating the intrathecal

Table 17-4 Sensitivity and specificity of history and physical exam for disease processes

Disease to detect Historical or physical exam finding Sensitivity (%) Specificity (%)

Age  50 or hx of CA or unexplained Weight loss or failure to improve w/Rx

Note: ca, cancer; IVDA, intravenous drug abuse; UTI, urinary tract infection.

Source: Adapted from Deyo RA, Rainville J, Kent DL What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765.

Table 17-5 Physical examination findings for specific nerve roots

dorsiflexion

Medial ankle/foot Patella

S1 Ankle plantar flexion Lateral plantar foot Achilles

nerve root MRI appears to be the superior modality for

imaging the spine

PAIN CONSIDERATIONS

The vast majority of patients will not have a readily

identified neuroanatomical diagnosis for their low back

pain Expectations of an exact diagnosis, disease-specific

treatment, and complete relief of pain lead patients to

believe that their pathology has been missed or that their

symptoms are doubted by the medical practitioner

Unsuccessful treatments reinforce a patient’s belief that

the cause of their pain is not known, further adding to

the psychological distress of chronic pain

Given that 90% of individuals will have resolution of

pain by 6 weeks, initial therapy should be tailored to

support patients through this initial period of pain The

patient should be encouraged to remain active during

this period of time, being reassured that the pain

asso-ciated with physical activity is not causing further

damage to the spine This avoids the impairment that

frequently accompanies chronic low back pain Patients

should be informed that up to 50% of those presenting

with acute low back pain will have at least one

recur-rence in the first 12 months

Further complicating the expression as well as the

perception of pain are a number of psychosocial factors

including depression, anxiety, job satisfaction, and the

monetary reimbursement that may accompany disability

from low back pain Waddell has described a number of

criteria on examination that might lead one to believe that

a patient’s back pain is of nonorganic etiology (Table17-6)

Understanding the pain pathway helps one

under-stand the treatment of low back pain In the periphery,

injury directly stimulates peripheral nerves or causes

release of inflammatory mediators that stimulate

noci-ceptors The pain stimulus is transmitted to the spinal

cord by fast-conducting, myelinated delta fibers and

slow-conducting, unmyelinated C fibers In the dorsal

horn of the spinal cord, pain transmission is modulated

by opioid receptors

Once a pain stimulus has become severe enough to

result in central transmission, the signal is carried by the

spinothalamic tracts to the medulla and thalamus and

eventually to the cerebral cortex The signal is once again

modified by serotonin, norepinephrine, GABA,

dopa-mine, and opioid receptors prior to effecting a response.NSAIDs and muscle relaxants, epidural and facet blocks,and exercise, physical therapy, and osteopathic manip-ulation modify the pain response at the level of theperipheral nerve Opiates and transcutaneous electricalnerve stimulators have analgesic efficacy at the spinallevel, and opiates, antidepressants, neuroleptics, andneurostimulants have efficacy at the cortical level Painshould be initially managed with NSAIDs, musclerelaxants, and/or analgesics, with additional optionsconsidered if pain continues

PAIN MANAGEMENT

NSAIDsU.S guidelines on the treatment of low back pain statethat there is good evidence for the use of NSAID med-ications for short-term symptom control (Figure 17-1,Table 17-7) The majority of randomized, controlledNSAID trials for acute low back pain have demonstratedthe superior efficacy of NSAIDs over placebo, but nonehas demonstrated that one NSAID is superior to another.NSAIDs do not appear to be as effective in acute low backpain accompanied by the neurologic symptoms of sciatica

or radiculopathy There is conflicting evidence regardingthe effectiveness of NSAIDs over acetaminophen, whereneither has proven to be superior in the treatment ofacute low back pain Similarly, there is no evidence thatNSAIDs are superior to muscle relaxants or opiates forthe treatment of acute low back pain

NSAIDs tend to be well tolerated in the short-termtreatment of back pain patients, with withdrawal rates of2–13% secondary to side effects Side effects are typicallygastrointestinal, including abdominal pain and diarrhea,but can also include edema, dry mouth, rash, dizziness,headache, and fatigue Adverse effects of NSAIDs includegastrointestinal bleeding, nephropathy, and worsening ofheart failure and hypertension There is no reported dif-ference in the number or severity of adverse eventsamong trials of different NSAIDs

Skeletal Muscle RelaxantsOne commonly proposed mechanism of low back pain

is the spasm-pain-spasm cycle According to this theory,muscle spasm activates afferent pain fibers, whichstimulate the anterior horn cells, causing increased

Table 17-6 Waddell’s test

Having three or more of the following five criteria is a strong indicator of a nonorganic cause of low back pain Refer to the appropriate mental health individual if appropriate.

1 Superficial or nonanatomic tenderness

a Cutaneous hyperesthesia

b Pain on gently rolling the skin

2 Pain on simulated maneuvers

a Axial loading on the top of the head in upright individuals

b Pain on passive range of motion of the shoulder and hip in the same direction

in the standing individual

3 Straight leg raising discrepancy

a Lying and sitting straight leg disparity

b Normal sitting straight leg raise with distraction

4 Nonphysiologic distal examination

a Stocking glove sensory distribution

b Pseudocogwheeling – voluntary muscle contraction with recurrent giving way

5 Overreaction

Low back pain

History and physical exam

Uncomplicated low

back pain

Uncomplicated sciatica

Suspect major mechanical injury Suspect infection

Suspect major neurological injury

NSAID

± muscle relaxant + early return to activity/work

Immobilize

Negative

Labs and imaging

Consult

MRI

Positive X-ray

Consult

Add opiate Consider antidepressant

Consider physical modalities

No improvement

Positive

Figure 17-1.Algorithm for evaluation of acute low back pain.

muscle contraction For this reason, muscle relaxants

would be expected to have a significant affect, breaking

the spasm-pain-spasm cycle However, clinical and

physiologic studies, including electromyogram (EMG)

studies, have failed to support this hypothesis The term

‘‘skeletal muscle relaxant’’ is a misnomer because at the

usual prescribed doses, skeletal muscle relaxants do not

depress neuronal conduction, neuromuscular

transmis-sion, or muscle excitability and do not appear to relax

skeletal muscle to a significant degree

Oral muscle relaxants have been shown to improve

pain to a greater degree than placebo A systematic

re-view of the literature looking at 40 trials demonstrated

that skeletal muscle relaxants are as effective as NSAIDs

for the treatment of acute low back pain, but found little

benefit in the treatment of chronic low back pain

Comparisons of combination therapy of a NSAID plus a

muscle relaxant compared to NSAID therapy alone have

yielded conflicting results in comparative trials

The major side effects of skeletal muscle relaxants are

similar for all the medications in this class, although there

are some less common side effects that are unique to each

agent The primary side effects include central nervous

system (CNS) effects, including headache, drowsiness,and dizziness, and GI effects, including nausea, vomiting,and anorexia After prolonged administration of musclerelaxants, withdrawal symptoms may occur on abruptcessation Few studies have compared the various skeletalmuscle relaxants for the management of acute back pain

Carisprodol

Carisprodol is prescribed as 350 mg QID Head-to-headstudies of cyclobenzaprine and carisprodol demon-strated equal effectiveness and similar side-effect profilesexcept for autonomic side effects, which were moreprevalent in cyclobenzeprine Comparative studies ofcarisprodol to diazepam have demonstrated improvedefficacy of carisprodol in relieving muscle stiffness,muscle tension, and activity impairment with less sideeffects than diazepam therapy

The major concern for carisprodol use is its potentialfor abuse Meprobamate, a metabolite of carisprodol, isclassified by the Food and Drug Administration (FDA) as

a schedule IV controlled substance Although carisprodoldoes not carry this classification by the FDA, many stateshave assigned it their own schedule IV classification

Table 17-7 Medications for analgesia in acute back pain patients

Muscle relaxantss

Opiates

Cyclobenzaprine is prescribed in 5 or 10 mg tablets TID

A large, randomized controlled trial comparing

cyclo-benzaprine at multiple doses to placebo demonstrated

that cyclobenzaprine recipients had significant

im-provement in all primary efficacy variables, including a

30% reduction in time to complete resolution of

symptoms A meta-analysis of 14 randomized controlled

trials demonstrated that patients treated with

cyclo-benzaprine were five times more likely to have symptom

improvement at day 14 Adverse events in these trials

were more common with the 10 mg dose than the 5 mg

dose Somnolence is reported in 18–38% of patients and

dry mouth in 21–32%

Diazepam

Diazepam in 5–10 mg doses is often prescribed as a muscle

relaxant A single study of 50 patients comparing diazepam

to placebo failed to identify any benefit of diazepam for the

treatment of acute low back pain, but demonstrated

increased CNS side effects Two studies of tetrazepam use

in chronic low back pain have demonstrated superiority

over placebo in treating chronic low back pain Although

there may be some benefit of benzodiazepines for the

treatment of acute low back pain, appropriate evidence is

currently lacking in the medical literature

Metaxolone

The recommended dose of metaxolone is 800 mg TID

Although no quality trials of metaxolone have been

published, the low incidence of sedation and short

elimination half-life suggest that metaxolone may be a

muscle relaxant with less likelihood of the typical side

effects of this group of medications The only

random-ized controlled trials in the literature evaluating

metaxolone include studies used for FDA approval from

the 1960s and 1970s, where metaxolone demonstrated

superiority to placebo in the treatment of acute low back

pain or acute exacerbations of chronic low back pain

The majority of adverse events reported with its use

include gastrointestinal effects

Orphenadrine

Few studies have addressed the use of orphenadrine The

benefit of this medication includes its ability to be used

as an intravenous or intramuscular injection A high

quality study demonstrated that a single intravenousdose produced significant relief in 45 min when com-pared to placebo

OpiatesNarcotic analgesics are commonly prescribed for backpain There are few studies in the literature evaluatingthe effectiveness of opiates in the treatment of acuteback pain, but a wealth of clinical experience suggeststhat they are efficacious for pain syndromes

A few principles should be considered in prescribingnarcotics In treating an acute episode in the emergencydepartment, opiate options include oral therapy or in-travenous therapy Intramuscular (IM) and subcutane-ous (SC) injections have unreliable and erratic drugabsorption, and it is difficult to give repeated dosessecondary to patient discomfort Because IM and SCdelivery routes have an onset of action that approx-imates that of oral agents, there is no benefit to thesemethods The maximum dose of oral analgesics com-bined with acetaminophen or ibuprofen is limited by thepresence of the nonnarcotic portion of the medication.Codeine, propoxyphene, hydrocodone, and oxycodoneare common narcotic preparations in this class.Studies have demonstrated that physicians routinelyineffectively treat pain with intravenous opiates Thetypical dose of morphine is 0.1–0.15 mg/kg, with similarequipotent dosing of hydromorphone as 0.015 mg/kg,and fentanyl as 1–2 mcg/kg

Side effects of narcotics include CNS depression,nausea mediated by histamine release, gastroparesis,constipation, and hypotension

SteroidsSteroids are occasionally used by practitioners for thetreatment of acute low back pain, particularly in thosepatients with a radicular component Data regarding theutility of treating acute low back pain with steroids arelacking

A single study comparing systemic steroids to placebofor the treatment of acute low back pain did not dem-onstrate any benefit of a dexamethasone taper whencompared to placebo with pain assessments at 7 days,less than 1 year, and greater than 1 year A more recentarticle evaluating large dose IV corticosteroids forsciatica demonstrated a statistically significant, but

clinically irrelevant decrease in pain at 3 days, but no

lasting effect (see reference 10)

Antidepressants

There is no available evidence to support the use of

antidepressants for acute low back pain management

However, there is evidence that antidepressants effective

in blocking norepinephrine reuptake (tricyclics and

tetracyclics) are mildly to moderately effective in

de-creasing chronic low back pain

Heat/Ice

A Cochrane review evaluating data through 2005 found

that heated wraps applied to the low back provided

short-term pain relief and improvement in disability when

compared to placebo tablets or nonheated wraps One

study comparing heat to ibuprofen or acetaminophen

found that a heated back wrap provided significantly

better relief than ibuprofen or acetaminophen at 1 and 4

days of therapy Likewise, heat has compared favorably to

both exercise and educational booklets Studies of heat vs

cold, cold vs placebo, or cold vs other interventions have

been few and of poor methodological quality

Physical therapy/Exercise therapy/Spinal

Manipulation/Acupuncture

A recent meta-analysis reviewed 11 of the highest quality

studies of the MacKenzie technique of physical therapy

for low back pain Although there was a statistical

benefit to physical therapy for low back pain, the

dif-ference between physical therapy and other techniques is

probably not clinically meaningful

A meta-analysis identifying 11 trials of exercise

ther-apy for acute low back pain found no benefit over no

treatment or other conservative therapies There was

moderate evidence to suggest that exercise is effective in

the care of subacute and chronic low back pain For

years, bed rest had been advocated based on the

obser-vation that certain types of back pain get better with rest

Studies have demonstrated that prolonged

immobiliza-tion with back rest can actually be harmful in the

treatment of acute low back pain

A Cochrane review of studies comparing spinal

ma-nipulation versus sham treatments for acute low back

pain demonstrated that although patients receiving

spinal manipulation had a clinically significant response

compared to sham treatment, the analgesic differencebetween groups did not reach statistical significance.There is no evidence in the medical literature to supportthe use of spinal manipulation for chronic low backpain When compared to other accepted therapies forlow back pain, of both acute and chronic duration,spinal manipulation does not appear to provide signif-icant pain relief or functional improvement

A Cochrane review of 35 randomized controlled trials

of acupuncture vs placebo or sham treatment for lowback pain was only able to identify three relevant trials.These studies were of small sample size and poormethodological quality, preventing decisive conclusions.Facet Injections/Epidural Injections

A Cochrane review to determine the effectiveness of jection therapy in the treatment of acute and chronic lowback pain found, on pooled analysis of the four ran-domized, placebo-controlled trials, no significant benefit

in-to epidural corticosteroid injections It is difficult in-to drawconclusions from these trials secondary to the degree ofheterogeneity in patients, medications, injection techni-ques, small sample sizes, and the significant effects ofplacebo (20–30% recovery in the placebo group)

FOLLOW-UP CONSIDERATIONS

Patients evaluated for acute low back pain should betreated with NSAIDs with or without a muscle relaxantand referred to a primary care physician for continuedtreatment Although 79% of back pain patients see only theinitial physician who began their care for low back pain,

a substantial minority (21%) will see multiple providers.The suggestion of disc herniation (symptoms of sciatica)should not rule out a course of conservative therapy.Ultimately, the decision to pursue a more aggressivesurgical approach is based on clinical factors, not radio-graphic studies This decision is also typically based onthe presence of severe, uncontrolled pain, profound orprogressive neurologic symptoms, or failure to respond toconservative therapy (Table17-8)

SUMMARY

Most acute low back pain is self-limited, does notrequire radiographic evaluation, and will resolve in 6weeks After the initial health-care provider has ruled

out potentially serious causes of low back pain,

treat-ment should emphasize NSAID therapy

Opiates and skeletal muscle relaxants can be added to

the pain medication regimen for more severe pain at the

cost of added CNS side effects Patients should be

encouraged not to use bed rest for prolonged periods of

time and should be referred to a primary care physician for

reevaluation and further treatment if the back pain persists

BIBLIOGRAPHY

1 Bigos S, Bowyer O, Braen G, et al Acute low back problems

in adults Clinical practice guideline no 14 AHCPR Publ

no 95-0642 Rockville, MD: Agency for Health Care Policy

and Research, December 1994

2 Liu X, Pietrobon R, Curtis LH, Hey LA Prescription of

nonsteroidal anti-inflammatory medications and muscle

relaxants for low back pain in the United States Spine

2004;29(23):E531–E537

3 Deyo RA, Weinstein JN Low back pain N Engl J Med

2001;344:363–370

4 Spengler DM, Bigos SJ, Martin NA, Zeh J, Fisher L,

Nachemson A Back injuries in industry: A retrospective

study I Overview and cost analysis Spine 1986;11

(3):241–256

5 O’Malley AS, DiGiuseppi C Counseling to prevent low back

pain U.S Preventive Services Task Force Guide to Clinical

Preventive Services, 2nd edn, chapter 60 Washington, DC:

U.S Department of Health and Human Services, Office of

Disease Prevention and Health Promotion, 1996

6 Deyo RA, Rainville J, Kent DL What can the history and

physical examination tell us about low back pain? JAMA

1992;268:760–765

7 Schnitzer TJ, Ferraro A, Hunsche E Kong SX Acomprehensive review of clinical trials on the efficacyand safety of drugs for the treatment of low back pain JPain Symptom Manage 2004;28:72–95

8 Koes BW, Sholten RJ, Mans JM, Boeter LM Efficacy ofnon-steroidal anti-inflammatory drugs for low back pain:

A systemic review of randomized clinical trials AnnRheum Dis 1997;56:214–223

9 van Tulder MW, Sholten RJ, Koes BW, Deyo RA steroidal anti-inflammatory drugs for low back pain Asystematic review within the framework of theCochrane Collaboration Back Review Group Spine2000;21:2501–2513

Non-10 Haimovic IC, Beresford HR Dexamethasone is notsuperior to placebo for treating lumbosacral radicularpain Neurology 1986;36(12):1593–1594

11 Beebe FA, Barkin RL, Barkin S A clinical and logic review of skeletal muscle relaxants for musculoskele-tal conditions Am J Ther 2005;12:151–171

pharmaco-12 van Tulder MW, Koes BW, Bouter LM Conservativetreatment of acute and chronic nonspecific low back pain:

A systematic review of randomized controlled trials of themost common interventions Spine 1997;22:2128–2156

13 van Tudler MW, Touray T, Furlan AD, Solway S, Bouter

LM Muscle relaxants for nonspecific low back pain:

A systematic review with the framework of theCochrane Collaboration Back Review Group Spine2003;28:1978–1992

14 Toth PP, Urtis J Commonly used muscle relaxant therapiesfor acute low back pain: A review of carisoprodol,cyclobenzoprine hydrochloride, and metaxalone Clin Ther2004;26:1355–1367

15 Browning R, Jackson JL, O’Malley PG Cyclobenzoprineand low back pain A meta-analysis Arch Intern Med2001;161:1613–1620

16 Borenstein DG, Korn S Efficacy of a low-dose regimen ofcyclobenzoprine hydrochloride in acute muscle spasm:Results of two placebo controlled trials Clin Ther2003;25:1056–1073

17 O’Connor AB, Lang VJ, Quill TE Underdosing ofmorphine compared to other parenteral opiates in anacute hospital: A quality of care challenge Pain Med2006;7:299–307

18 Finckh A, Zufferey P, Schurch MA, Balague F, Waldburger

M So AK Short-term efficacy of intravenous pulseglucocorticoids in acute discogenic sciatica A randomizedcontrolled trial Spine 2006;31:377–381

19 Staiger TO, Gaster B, Sullivan MD, Deyo RA Systematicreview of anti-depressants in the treatment of chronic lowback pain Spine 2003;28:2540–2545

20 French SD, Cameron M, Walker BF, Reggars JW, man AJ Superficial heat or cold for low back pain ACochrane review Cochrane Libr 2006;4750:3

Ester-21 Machado LA de Souza MS, Ferreira PH, Ferreira ML TheMcKenzie method for low back pain: A systematic review

of the literature with a meta-analysis approach Spine2006;31:E254–E262

Table 17-8 Indications for surgical referral of the

back pain patient

 Symptoms of cauda equina syndrome (loss of

bowel/bladder function, saddle anesthesia,

bilateral lower extremity weakness, pain, and

numbness)

 Progressive or severe neurologic deficit

 Persistent neuromotor deficit after 6 weeks of

conservative therapy

 Persistent sciatica after 6 weeks of conservative

therapy

 Persistent and disabling low back and leg pain

from spinal stenosis

22 Hayden JA van Tulder MW, Malmivaara AV, Koes BW.

Meta-analysis: Exercise therapy for nonspecific low back

pain Ann Intern Med 2005;142:765–775

23 Hagen KB, Jamtvedt G, Hilde G, Winnem MF The

updated Cochrane review of bed rest for low back pain and

sciatica Spine 2005;30:542–546

24 Assendelft, WJJ, Morton, SC, Yu Emily, I, Suttorp, MJ,Shekelle, PG Spinal manipulative therapy for low-backpain A Cochrane review Cochrane Libr 2006;447:3

25 Nelemans PJ, diBie RA, deVet HC, Sturmans F Injectiontherapy for subacute and chronic benign low back pain.Spine 2001;26:501–515

18 Analgesia for the Acute Abdomen Patient

According to the 2004 National Hospital Ambulatory

Medical Care Survey, abdominal pain accounts for more

that 7.5 million annual patient visits to emergency

departments (ED) throughout the United States

Ab-dominal pain is the most frequently reported principal

reason given by patients for visiting the ED, accounting

for almost 7% of all ED visits It is also the leading

discharge diagnosis in patients aged 22–49 years

Abdominal pain constitutes a very diverse group of

diagnoses ranging from benign and self-limited

condi-tions, such as gastroenteritis, to acute and

life-threat-ening diseases, such as ischemic bowel or ruptured

aortic aneurysms The challenge for emergency

physi-cians is to correctly differentiate those patients whose

abdominal condition may be imminently life

threaten-ing or require surgery, from those who require a more

extended evaluation and treatment or may be

dis-charged The ultimate challenge is to safely accomplish

this and at the same time providing the patient

maxi-mum comfort

CLINICAL ASSESSMENT

Until recently, patients presenting to the ED with

ab-dominal pain underwent a clinical evaluation consisting

of a routine history and physical examination, a panel of

laboratory tests, and perhaps plain radiographs Duringtheir ED stay these patients were kept NPO in case theymight require emergent surgery, and were rarely givenanalgesic medications prior to evaluation by a surgeon.Those without worrisome findings were dischargedhome (usually without analgesics), and those withconcerning findings were kept in the ED or hospitalizedfor continued observation and reexamination

Pundits have traced the dictum for withholdinganalgesia in these patients to the surgical teachings ofZachary Cope who, in the classical medical text, Theearly diagnosis of the acute abdomen, warned that ad-ministration of analgesics might mask symptom pro-gression or alter physical findings and thereby lead tomisdiagnosis, delayed surgical intervention, and unfa-vorable outcomes Although this has been the standard

of care for the last 100 years, a very dramatic changeappears to be taking place in how we evaluate andtreat patients with acute abdominal pain in the ED(Figure18-1)

PAIN CONSIDERATIONS

In the past two decades, following the publication ofseveral small ED clinical studies, the traditionalapproach of withholding analgesics in patients withabdominal pain has become controversial amongemergency physicians and surgeons alike Though there

120

is still no consensus as to whether opioids are completely

safe in this setting, it appears that a paradigm shift

toward more aggressive use of analgesia is indeed

hap-pening

How did this evolution in practice come about? Is this

new practice based on good scientific evidence? Or, as some

experts purport, is it based on studies with such severe

methodological problems and limitations that we should

question the wisdom of changing traditional practice?

An early pivotal study challenging the use of analgesia

in patients with acute abdominal was published in 1986

by Zolti and Cust, who compared sublingual

bupre-norphine (equivalent to about 6.6 mg of IV morphine)

vs placebo in a prospective double-blind trial of 288

hospitalized patients with acute abdominal pain, and

reported no effect on clinical diagnosis Critics of the

study, however, note that the buprenorphine dose was

no more effective in reducing pain than the placebo and

argue that it should, therefore, not be surprising that it

was not found to interfere with clinical diagnosis

Another study by Attard et al in 1992 compared asingle IM injection of ‘‘up to’’ 20 mg papaveretum(equipotent to about 12.5 mg of morphine) to placebo

in 100 patients with abdominal pain hospitalized on asurgical service They reported that those who received

a single IM injection of ‘‘up to’’ 20 mg papaveretum had

a significant reduction in pain and tenderness comparedwith those who received placebo, but there were nosignificant differences in the accuracy of diagnoses ormanagement decisions between the two groups Un-fortunately, the dose of the opioid used was not con-trolled (the dose varied) and the surgeons making thetreatment decisions were not blinded to the patients thatreceived opioids Furthermore, as in Zolti’s study, thistrial was limited to patients sufficiently ill to be hospi-talized, thus limiting applicability to patients in the EDsetting

In 1996, Pace and Burke compared the effects ofmorphine vs saline administration in 71 patients withabdominal pain in the ED They reported significant

History and physical exam

Alternative approaches

Repeat exam after pain treatment Repeat exam after pain treatment

Repeat exam at 30–60 min

Follow exam for changes until diagnosis made

Repeat pain treatment with subsequent exam until diagnosis made

Specific therapy initiated after diagnosis made

Fentanyl 1.5 mg/kg 0.5 mg/kg q3 min until pain free Morphine 0.1 mg/kg

Figure 18-1 Pain treatment in undifferentiated abdominal pain.

pain relief in patients who received morphine, but found

no differences between the groups in provisional

diag-nostic accuracy or final disposition Criticism of this

study included the small sample size, the variable dose of

morphine allowed, the lack of specifically defined

cri-teria of whether peritoneal signs were resolved, and the

lack of effective double blinding of the ED physicians to

patients receiving morphine

In 1997 LoVecchio et al reported that 50% of adult

patients with acute abdominal pain, whose management

plan had already been determined, had changes in their

abdominal exam in terms of tenderness or location in

response to either 5 or 10 mg of morphine, but only 6%

of patients who received saline had such changes

Sig-nificantly, neither group differed in either adverse events

nor delayed diagnosis, and the authors proposed that

early analgesia actually allowed for a more detailed

ex-amination of localized tenderness Traditionalists

dis-puted their conclusion, however, and argued that the

study in fact supported the concern that crucial physical

findings may be changed by opioid analgesia

adminis-tration

Based on these four small studies, emergency

medi-cine experts began espousing the benefits and safety of

analgesia administration to patients with abdominal

pain in the ED Many emergency physicians and

surgeons, however, continued to be ambivalent about

the liberalization of analgesia use in acute abdominal

pain

Over the next several years, studies purporting the

efficacy and safety of analgesia in abdominal pain

became highly scrutinized and criticized by surgeons

Thomas and Silen (see reference 12) cited disparity in

trial design and ‘‘insufficient enrollment to address with

any finality the issue of outcomes.’’ Nissman, Kaplan,

and Mann further expounded upon these studies’

numerous significant limitations and design flaws and

concluded that the trials were so problematic that they

should not support the practice of administering

anal-gesia prior to surgical evaluation They argued that the

studies in fact show that analgesia may alter the

sub-jective and obsub-jective clinical examination, that this

blunting of signs and symptoms may be dangerous, and

that it is the surgeon’s interpretation of the degree of

tenderness and guarding that determines whether a

patient needs rapid operative intervention

These authors cited examples from their personalexperiences in which opioid analgesia administration led

to ‘‘misses’’ or ‘‘near misses’’ in the proper diagnosisand subsequent management of patients with acuteabdominal pain and argued that analgesia should beused ‘‘far more judiciously’’ and ‘‘cannot be undertakenwith any certainty of safety.’’ A flurry of letters followed

in which surgeons cited personal experiences ofanalgesics masking peritoneal signs, and emergencyphysicians argued that anecdotal cases were not per-suasive arguments against the conclusions of the studies,even if these studies were flawed

Increasingly, the dialogue focused on three issues.First, does analgesia improve a patient’s subjectivecomplaint of pain? The studies suggest that it does.Second, does analgesia alter physical examination find-ings? Here the studies are contradictory with someshowing no significant change and others showingalteration in the physical examination Third, does an-algesia alter diagnostic accuracy? On this last issue, theanswer may depend upon the source of the abdominalpain

Geiderman and Silka in 2000 argued that patientsexperiencing diseases characterized by visceral and pa-rietal peritoneum inflammation (e.g., more advancedappendicitis, cholecystitis, salpingitis) will haveimprovement of their pain with opioid analgesia, but areunlikely to have complete elimination of localizingphysical findings In contrast, patients with diseaseprocesses not characterized by inflammation of thevisceral peritoneum (e.g., pancreatitis, ischemic bowel,bowel obstruction), may not have ‘‘clinically helpful’’well-localized physical examination findings of tender-ness, but rather more diffuse tenderness Elimination ofthese patients’ subjective pain with opioid analgesia mayresult in misdiagnosis, delayed diagnosis, or delayedtreatment

A universal criticism of the literature published todate is the small sample size This is a significantproblem because most undifferentiated abdominal painresolves spontaneously without complications The lowevent rate of complications thus necessitates large groupsizes to adequately address the influence of analgesia onoutcomes

Lukens et al reported that almost 88% of patientswith undifferentiated abdominal pain in the ED were

pain free or improved 3 weeks later, and only 3%

required hospitalization Lee et al., on the other hand,

found in a prospective observational study of 860 ED

abdominal pain patients that 8% had an adverse outcome

(defined as obstruction, perforation, ischemia,

hemor-rhage, peritonitis, sepsis, or death) after 3 weeks, but

12.7% of the patients who received opioids had an

adverse outcome Using this adverse outcome rate, Lee

calculated that a randomized clinical trial of sufficient size

to establish the equivalent adverse outcome rate of opioid

analgesia administration vs placebo would require the

enrollment of 1,500 patients This is clearly far more

patients than all the existing studies combined to date

Most recently, Gallagher et al reported on the largest

clinical trail to date of opioid use in adult ED patients

with undifferentiated abdominal pain In this

random-ized placebo-controlled study, 153 patients with

ab-dominal pain received 0.1 mg/kg IV morphine or

placebo The endpoint was not change in their physical

examination, but diagnostic accuracy based on physical

examination In this study, IV morphine significantly

reduced pain severity but did not impact clinical

diag-nostic accuracy

A potentially important variable when considering

analgesia administration in patients with abdominal

pain is the wide availability and increasing use of

com-puted tomography (CT) scanning and ultrasonography

Although it has been argued that the physical

exami-nation is paramount in determining the need for

sur-gery, CT scanning and ultrasound imaging are now used

frequently to help determine not only the underlying

cause of a patient’s abdominal pain, but also the urgency

and type of surgical intervention that may be needed

Neighbor et al in 2005 reported that in an urban

teaching ED, the percentage of patients with right lower

quadrant (RLQ) abdominal pain receiving a CT doubled

between 1998 and 2003 and the percentage of patients

receiving opioid analgesia for their RLQ abdominal pain

more than doubled Their data suggested that the

observed increased analgesia use was not directly the

result of the increased utilization of CT scanning, and

may rather reflect a paradigm shift toward increasing

use of opioid analgesia in the ED

Although analgesic use in adults with abdominal pain

is controversial and yet becoming more accepted,

anal-gesic administration in children with abdominal pain

remains unclear There are few studies examining thisissue in children, and those that have been reported havesignificant limitations Most studies have been restricted

to a small sample of school-aged children

As with adult patients, the necessary large, multicenterstudies are unlikely to be performed in children to de-finitively answer the many questions regarding analgesicuse in abdominal pain, thus leaving providers to makedifficult clinical decisions in the absence of adequatedata

PAIN MANAGEMENT

What conclusions can be drawn from the nearly twodecades of study and debate? First, it must beacknowledged that much of the literature supporting theuse of opioids in undifferentiated abdominal pain hassignificant flaws and limitations Second, it is unlikelythat a study of sufficient size to answer all the necessaryquestions will be conducted in the near future

Conclusions are difficult to draw, and a lack of sensus among emergency physicians and surgeons islikely to persist for some time It must also be recognizedthat there is much suggestive evidence, perhaps even apreponderance of evidence, supporting the practice of

con-‘‘judicious’’ use of opioid analgesia in ED patients withacute undifferentiated abdominal pain

Perhaps the more relevant discussion and debateshould now be directed toward determining what

‘‘judicious’’ means Certainly a careful and thoroughhistory and physical examination must be performed onall patients with acute abdominal pain The morphinedose of 0.1 mg/kg does not appear to mask physicalfindings, and although it has been shown to be some-times an ineffective dose for pain relief, it likely repre-sents a ‘‘judicious’’ dose Alternatively, short-actingagents, such as IV fentanyl, allow for serial examsbetween doses in the absence of opioid effect, over ashorter period than longer acting opioids (Table18-1).The relative safety and efficacy of a low-dose strategy vs

a short-acting medication and allowing the pain toreturn has not been determined

In patients whose pain is severe enough to warrant theadministration of high doses of opioid analgesia, it may

be prudent to utilize ancillary imaging such as CTscanning or ultrasonography to facilitate diagnosis or