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A. Medications.
1. Nonsteroidal anti-inflammatory drugs (NSAIDS). These agents are believed to
lead to analgesia via central and pe'fipheral mechanisms. They function through
the inhibition of the arachidonic acid cascade, leading to a decreased production
of prostaglandins. Patients may have varying reSponses to differ- ent agents in
this class. These agents can be classified based on activity of agent against
cyclooxygenase [/11 activity (COX). COX 1/ nonselective agents in- clude
ibuprofen, naproxen, and piroxicam. Celecoxib is currently the only COX 1]
selective agent available in the United States. Paracnxib, an intravenous COX [1
selective agent, is not currently available in the United States. Common side
effects of NSAIDs include renal dysfunction, gastrointestinal bleeding, and ulcer
formation. The antiplatelet effects are not seen in celecoxib and other COX ll
selective agents.
2. Opioids. These drugs are naturally occurring alkaloids or may be synthetically
produced. These agents Function to varying degrees at the opioid receptors. in the
central nervous system (CNS) and the periphery. These agents are classified based
on chemical structure. Opium plant derivatives (plienthrenel include morphine
and codeine. Agents that are synthetically derived from the phennnthrenes (semisynthetic) are hydrocodone, oxymorphone, and oxycodone. Synthetic agents not
derived from the phenanthrene; include the anilindopiperidincs, fentanyl
(transdermal. buccal, sublingual), 'sutentanil, reinitentnnil. 'l'he phenylpiperidines
are meperidine and tmtnadol; phenylpropylamines include propoxyphene,
methadone, and loperarnide. Pentazocine is a benzomorphane, oripavane
(buprenorphinel), and morphinan drugs include butorponal and nai- buphine.
Buprenorpiine is an opioid receptor agnnist.fanlngonist that has also been used in
pain management [Table 50.1].
Clinicians should utilize preparations w ith the least abuse potential and side
effects. Agents that contain an anti-inflammantory / acetaminopen to decrease the
dose of opioid required fox analgesia should be considered first-line drugs
Prescribing physicians should notifyp atients about the clinics prescription policy via the use of a "narcotics contract or narcotics agreement." Common side
effects include respiratmy depression, sedation, cognitive impairment livel dvsfunction, and testosterone deficiency in men both with long-term use Tolerence
addiction potential, and withdrawal from sudden cessation are also common.
1 mg IV q 4-6 hr
Goal dose
Side effect
use
preparation
with least abuse respirotary distress
potential
sedative,
cognitive
impairment
use
combination
agent that contain
an
anti liver dysfunction with
inflammatory
to long-term use
decrease
opioid
dose
testosterone
deficiency
Hydrocodone
(available 1 tablet q 4-6, not
with
acetaminophen to exceed 3-4 g of
norco, vicodin, lorbab), acetaninophen qd
addiction potential
Available with inbuprofenvicoprofen)
patch: start @ 25 may
utilize
withdrawal
with
Fentanyl
meg/q72 hr
narcotic contract to
cessation
control abuse
15-35 mg/hr IV
Meperidine
50-100 mg po qid,
max 400 g/qd; if
Tramadol (also available in
>75 yrs, hepatic or
combination
with
renal dysfunction,
acetaminophen)
max daily dose 200
mg/qd
65 mg q 4 hr
Propoxyphene
2,5 mg to 10 mg q
Methadone & loparemide
8-12 hr
Pentazocin in formullation 1 tablet q 4hr PRN
with aspirin and/or naloxone
Buprenorphine
(also variable
with
available in formulation formulation
with naloxone)
1 mg to 4 mg q 3-4
Butorphanole
hr by MDI
Nalbuphinc
10 mg/70 kg body
wt 3-4 hrs PRN.
Total daily dose <
160 mg/qd
Nortiptyline
Duloxetine
diabetic
neuropatic pain
Starting dose
Goal dose
50 mg qhs
150 mg qhs
25 mg pq qhs
150 mg qhs
60 mg qd
120 mg qd
300 mg/day
Phenytoin
Carbamazepine
Lamotrigine
Topiramate
Levetiracetam
diabetic
neuropatic
trigelminal
100 mg BID
neuralgia,
post
stroke pain, post
herpetic
neuralgia,
neuropathy
20-50 mg po qHS
cold-induced
pain, trigeminal
neuralgia,
neuropathy
diabetic
50 mg qHS
neurophaty, post
herpetic
neuralgia,
intercostal
neuralgia, CRPS
500 mg po bid
300-400
mg/day
300-1,000
mg/day
in
divided bid
doses over 2
wks
Side effect
Sedation,
dry
mounth,
impotenci,
hyponia thermia,
withdrawal
Dry
mputh
constipation,
orthostatic
hypotension,weig
ht gain, dizziness,
unmasking
of
mania in bipolar
patients
on
tramadol
gingival
hyperplasia,
hirsutism,
coarsening
of
features.
gait disturbances,
hyponatremia,
neucopenia,
aplastic anemia,
agranulocytosis.
rash,
stevens300-500
jhonson syndrom,
mg/day
in decreased efficacy
divided bid with
codoses over 2 administration or
wks
carbamazepine,
phenytoin
sedation, kidney
200 mg po
stone,
ocular
bid
granuloma
1,500 mg bid
rash,
hives,
neuropatic pain
pregabalin
diabetic
neurophaty, post
herpetic
neuralgia, CRPS
150 mg/day
100 mg/day
Zonisamide
neuropatic pain
0-3-1 nanograms/hr
Conopeptide
Baelofen
5 mg dd
4 mg qd
Tiagabine
neuropatic
spaticty
pain,
Diazepam
Tizanidine
Cyclobenzaorin
e
Chlorzoxasone
muscle spasms,
spaticty
2 mg bid
muscle spasms,
spaticty,
spinal
cord
injurypost
troke pain
4 mg/qd
muscle spasms
muscle spasms
30-40 mg/qd
250 mg tid/qid
4,800 mg po
divided
in
TID dosing
600 mg/day
for
neurophatic
pain;
450
mg/day for
fibromyalgia
itching, dizziness
fatigue,
somnolence,
dizziness
dizziness, blurred
vison,
weight
gain, diminished
cognition
ataxia,
rash,
kidney
stones,
600 mg/day
oligohydramnios,
pediatric
hyperthermia
sedation, tremor,
hypotension,
histaminergic
reaction
confusion, ataxia,
80-100
hallucination,
mg/day
in
lifetheatring
devided doses
withdrawal
12-22 mg/qd
for pts not on
epilepsi drugs seizures, aphasia,
32-53 mg/qp sedation
for pts on
AEDs
sedation,
dependence, risk
of seizures and
deadth
with
20-30 mg/qd withdrawal
increase by 4- headache,
6 mg/wk to digestive change,
36 mg/mq
dry mouth
sedation,
dry
30-40 mg/qd mouth
1,000-2,000
GI disturbances,
mg/qd
liver dysfuntion,
Carisoprodol
methucarbomol
muscle
spasms,spaticty
350 mg tid/qid
muscle spasms
1000 mg/tid
muscle spasms
800 mg tid/qid
Metaxolone
Orphenadrine
neuropathic,muscl
e spasms
60-80 mg q 8 hrs
Dystonia,
spaticity,
migraine,
botulinum toxin
torticallis,
myofascial pain, varies base on site of
GI, GU spam
injection
sedation
sedation, tremor,
350 mg po altred cognition,
tid/qid
addiction potential
3000-4000
sedation, altered
mg/qid
cognition
hemolytic anemia,
800
mg elevated
liver
tid/qid
function test
ortbostic
hypotension,
urinary retention,
60-80 mg q 8 dizziness,
hrs
euphoria
myalgia,
dysphagia,
discomfort
Treatment is initiated at 150 mg/d up to a goal of 300 to 450 mg/d. The side effect
profile is similar to lidocaine.
6. Calcium channel blockers. Gabapentin is a membrane stabilizer binding at the
alpha-2 delta subunit of the L-calcium channel (Table 50.2). The name of the drug is
a misnomer as gabapentin has no activity at the GABA receptor but is struc- turally
similar. Gabapentin is used for many neuropathic pain states including diabetic
neuropathy, postherpetic neuralgia, and CRPS. Treatment is started at 100 to 300
mg at bedtime, increasing to 4,800 mg per day divided in three times a day dosing.
Common side effects include fatigue, somnolence, and dizziness. Pregabalin also
binds to the alpha-2-delta subunit at voltage-dependent calcium channels. This agent
is used for neuropathic pain states and for fi- bromyalgia. The starting dose of
pregabalin is 150 mg/d titrated to 600 mg/ d for neuropathic pain states; for
fibromyalgia the maximum daily dose is 450 mg/d. Side effects include dizziness,
blurred vision, weight gain, and diminished cognition.
Zonisamide acts at T- calcium and sodium channels.This drug in GABA
release. Zonisamide is started at 100 mg every day and increase 2 weeks by 200 m
g/Wk for a goal of 600 mg/ d. Common side effects 1 ataxia, rash, kidnegy stones
(carbonic anhychase inhibitor), oligohydia and pediatric hyperthermia.
-Couopeptides (ziconotide) acts on N-type calcium channels. Use trathecally
at 0.3 to 1 nanograms/ kg/ hr. The drug has been studied in
and HIV populations. Side effects include sedation, tremor, hypotension, and
histaminergic reaction. Nimodipine, diltiazem, verapamil, and nifedipine are agents
typically used for blood pressure control but may also have a role with other agents in
pain management. .
7. Gabaergic agents. Baclofeii is a derivative of GABA With activity at GABA-b
channels. It has both spinal and supraspinal activity (Table 50.2). This drug is used
For spinal cord injury and spasticity. Initial therapy begins at 5 mg three times a day
with titration to a daily dose of 80 to 100 mg/d. Baclofen may also be given
intrathecally. Common side effects include confusion, ataxia, and hal- lucinations.
Sudden cessation of therapy may lead to a withdrawal, which may be life-threatening.
Tiagabine acts as a GABA reuptake inhibitor. The drug is started at 4 mg daily
and increased by 4 to 8 mg/d to a final goal of 12 to 22 mg/d for patients not on
antiepileptic drugs (AED), or 32 to 52 mg/d for patients on AEDs. Common side
(ALS). Side effects include myalgia, dysphagia, and local discomfort. The amount of
agent on injection is tailored to the site of injection with attention to the degree of
spasm and the musculature being injected.
9. Other agents. Clonidine is an alpha 2 agonist that potentiates the analgesic action of
Opioids. It is useful in neuropathic pain states. A transdermal patch is started at a dose
of 0.1 mg/d changed every 7 days. Side effects include sedation, dry mouth, and
orthostatic hypotension. Capsaicin is an extract of chili pepper, which is thought to
cause analgesia by depletion of substance P. Clinicians should note that application
may lead to discomfort and irritation prior to analgesia.
B. Nonpharmacologic treatments.
1. physical therapy and occupational therapy. The use at heal, ultrasound, electrical
stimulation, and deep tissue massage may reduce discount. chronic pain states.
Additionally, in neurepathic pain states, targeting different fibers can lead to
decreasing the hypersensitivity (allodynia) that may be present as part of a painful
condition. The mainstay of treatment of certain conditions, including CRPS, is range
of motion and physical therapy. Prevention of contracture is important in maintaining
function and decreasing discomfort.
2. Electrical stimulation involves the use or eitner transcutaneous electrical nerve,
stimulation (TENS), spinal cord (dorsal column), or thalamic stimulators, which
can modulate pain. Patients with neuropathic pain states, muscular pain, central pain,
and axial low back pain may benefit from these therapies. The classical "gate control
theory in that stimulation of large fiber (a beta) closes the gate that has been opened
or initiated by the smaller diameter nociceptors. Contraindications for these therapies
include pregnancy and the presence of a pacemaker. I II . .- -L:.-.li.~ .xunxr
3. Psychological treatment is an important component or me pauem s mum. chronic p.
in treatment plan by addressing the psychological manifestations of the pain. A
support network for the patient involving family and friends may be conducive to the
healing process. Additionally, the use of biofeed- back along with adjunctive physical
therapy may help a patient cope with their discomfort.
Finally, the ultimate goal in the management or a patient with cronic pain is a
precise diagnosis with appropriate treatment for the painful condition. Referral to an
interventional pain physician may benefit the patient after conservative therapy has
failed. With the advent of technological advances, disease processes difficult to treat,