Pain management

Zeina al-saddar
Rama mawajdeh
Teeba al- shammari
Manar qarqash

Pain never
killed any one.
True or False?

Postop pain can delay healing and

contribute to complications that may be
lifethreatening.

Pain
An unpleasant
sensory and
emotional experience
associated with actual
or potential tissue
damage.
Whatever the
patient says it is!

Nociception
Stimulation
In acute pain, free nerve endings (nocicep-tors) are
stimulated in response to noxious stimuli
Transmission
And then the sensation is transmitted through the
nerve fibers of the primary afferent system.
When the transmission is through A-delta (A)
nerve fibers, the pain is generally sharp and localized, whereas when it is transmitted through Cafferent fibers, the pain can be described as dull
and aching.

 Perception
The pain is then perceived by the brain
Modulation
finally the sensation is modulated through
various processes that affect how the body
responds to the pain and medications used to
treat the pain.

 that pain is modulated is via the endorphinergic

system. In this process, endogenous opioid
compounds bind to the , , and receptors in
the central nervous system (CNS) and mediate
the effect of analgesia. Neurotransmitters, such
as norepinephrine and serotonin, are also
involved in this complex endogenous modulation
system. Inflammation may be part of the
nociceptive pain process causing endogenous
chemicals, substance P, serotonin, histamine,
acetylcholine, and bradykinin to be released and
activate other nocioceptors.

 Acute pain
Useful physiologic process warning individuals of
disease states and potentially harmful situations.
Acute pain usually nociceptive, but it can be
neuropathic in nature.
Common causes : post surgery , acute illness,
trauma, labor, medical procedures.
Chronic pain
Continuous , episodic pain that persists more than 6
months to years it serves no biologic protective
purpose and can cause stress and suffering/
Can be nociceptive, neuropathic or both.

Chronic pain
Subtypes include :
Pain related to chronic disease ( pain
secondary to osteoarthritis ).
pain that persists beyond normal healing time
for acute injury (e.g., complex regional pain
syndrome).
pain without identifiable organic cause (e.g.,
fibromyalgia).
pain associated with cancer.

Pain
Level

Typical
Corresponding
Numerical
Rating (0 to 10
Scale)

WHO Therapeutic
Recommendations

Example Medicines for

Initial Therapy

Comments

Mild
pain

1-3

Nonopioid analgesic:
taken on a regular
schedule, not as
needed (prn)

Acetaminophen 650 mg
every 4 hr
Acetaminophen 1,000 mg
every 6 hr
Ibuprofen 600 mg every 6
hr

Consider adding adjunct analgesic

or using an alternate regimen if pain
not reduced in 12 days
Consider step up if pain not
relieved by two different regimens

Modera
te pain

4-6

Add opioid for

moderate pain (e.g.,
moderate potency
analgesic). Use on a
schedule, not prn

Acetaminophen 325
mg/codeine 60 mg every 4
hr
Acetaminophen 325
mg/Oxycodone 5 mg every
4 hr
Tramadol 50 mg every 6 hr

Consider adding adjunct analgesic

or using an alternate regimen if pain
not reduced in 12 days
Consider step up if pain not
relieved by two different regimen

Severe
pain

7-10

Switch to a high
potency (strong)
opioid; administer on
a regular schedule

Morphine 15 mg every 4
hr
Hydromorphone 4 mg
every 4 hr
Morphine controlled
release 60 mg every 8 hr

Consider alternate regimen (e.g.,

different strong opioid) if pain not
reduced in 12 days
Consider increased dose of strong
opioid, or addition of nonopioid
agents, if pain not adequately
relieved by two regimens

Pain Treatment Options

Non pharmacologic :
Heat/cold therapy
Massage
Physical/Occupational
therapy
Aromatherapy
Music therapy
Spiritual/Religious

Pharmacologic :
Non opioids
Opioids

Nonopioids
Acetaminophen
NSAIDS (Nonsteroidal antiinflammatory
drugs)
Corticosteroids

Chief Complaint
My belly hurts, and I cant stand the sight of
food.

HPI
Charles Porter is a 68-year-old man who presents to the
Family Practice Center with a 2-day history of nausea,
vomiting, and epigastric and RUQ abdominal pain. The
patient states that the pain began several hours after eating
a double sized cheeseburger, french fries, and a chocolate of
milkshake at a local fast food restaurant. The pain intensified
and was associated with escalating nausea followed by
several episodes of vomiting. The vomiting finally ceased
but the abdominal pain has persisted and is made worse
after meals. The pain is now dull, and achy in nature. Lying
up in bed or sitting in a chair seems to relieve some of the
pain. Since the initial episode, his appetite has decreased
and he has been avoiding fried or fatty foods. He denies any
change in stool color or consistency.

PMH

HTN since 1992; poorly controlled

Type 2 DM since 1987; under fair control
History of gout; last attack in 1995
hyperlipidemia

FH
Father deceased (CVA), age 76; mother
deceased (MI), age 83; brother alive and well,
age 65; sister with breast cancer and gallbladder
disease, age 58

SH
Is a retired bar owner. He lives with his wife
(married for45years) on a 10-acre farm. He
has two dogs and a cat. He has a 50 pack-year
history of smoking and a history of binge
drinking.
ROS
As per HPI; otherwise negative

Meds
Atorvastatin 20 mg po once daily
Hydrochlorothiazide 25 mg po once daily
Lisinopril 20mg po once daily
Glibizide 10 mcg po BID
Metformin 500 mg po BID
Aspirin 81 mg po once daily
Insulin glargine 10 units subQ at bedtime
Maalox TC 30 ml po. PRN heartburn
MVI 1 po once daily

All
Erythromycinabdominal pain(1997)
Morphinehives and mild wheezing(1987)
Physical Examination
Gen
A pleasant, ealderly white man in mild-to-moderate acute
distress; appears his stated age
VS
BP 145/95 mm Hg (sitting), P 84 bpm, RR 20, T 37.8C; pain
4/10, dull, somewthat achy; Wt 78 kg, Ht 510
HEENT
PERRLA, fundi with mild AV nicking; TMs WNL; mucous
membranes moist
Chest
Clear to A & P

 Heart
Normal S1 and S2; without murmur, rub, or gallop
Abd
Normal bowel sounds, without organomegaly,
moderate RUQ pain with deep palpation with mild
guarding
Genit/Rect
normal prostates; guaiac () stool
Ext
Good strength throughout, reflexes intact, mild
decreased pinprick sensation to both lower
extremities; no CCE

Lab results :
Na 138 mEq/L (135-152)

Hgb 12.6 g/dL

(12-16)

AST 78 units/L

(13-35)

K 3.3 mEq/L

(3.5-5.3)

Hct 36%

(37-47%)

ALT 67 units/L

(10-35)

Cl 97 mEq/L

(97-110)

Platelets 340 103/mm3

(140-440)

Alk phos 180 units/L (30-122)

CO2 23 mEq/L

WBC 12.0 103/mm3 (4-10)

T. bili 3.4 mg/dL

(up to 1.1)

BUN 15 mg/dL (1.8-7.1)

Neutros 76%

D. bili 2.6 mg/dL

(up to 0.3)

SCr 1.3 mg/dL (0.7-1.35)

Bands 4%

Glu 160 mg/dL (70-110)

Eos 2%

(1-6%)

Lymphs 18%

(26-45%)

Crcl 60

(40-75%)

Amylase 130 units/L (

Lipase 50 units/L

 Assessment
Acute RUQ abdominal pain; R/O cholelithiasis,
acute cholecystitis, ascending cholangitis, acute
pancreatitis.

Problem Identification
1.a. Create a list of the patients drug therapy problems.
Hepatic disease (elevated liver function tests) >>alcohol abuse.
Hypertension inadequately controlled diuretic and
angiotensin II receptor blocker (acute pain may elevate blood pressure); further
evaluation
Type 2 diabetes inadequately controlled >>(glipizide and metformin)
and basal insulin
Dyslipidemia managed with atorvastatin that requires further
evaluation to assess adequacy of treatment regimen.
Hypertriglyceridemia may precipitate acute pancreatitis

 Potential problem:
Metformin >>lactic acidosis>abdominal discomfort
hydrochlorothiazide>> Hypokalemia secondary
>>acute abdominal discomfort.

 1.b. What clinical information indicates the

presence of an acute pain syndrome?

Pain reported as 6/10 on physical exam.

Hypertension (BP 160/95)
acute abdominal pain after a high-fat meal.
Dull, constant, moderate RUQ epigastric pain boring to his
back for 2 days.
Moderate epigastric pain and mild guarding with abdominal
palpation.

 1.c. What is the pathophysiologic basis for the

development of acute pain?
We talked about it

 1.d. Could the patients problem have been caused by

drug therapy?
Yes, various medications have been associated with the
development of acute pancreatitis.
metformin>>GI side effects(nausea, vomiting, abdominal pain,
and dyspepsia). initiallyy
Metformin >>lactic acidosis >>abdominal pain.
(nausea/vomiting/Abdominal or stomach discomfort/diarrhea/sleepiness )

Atorvastatin, an HMG CoA reductase inhibitor>> elevated

hepatic enzymes, cholestasis, jaundice, and rarely
pancreatitis.

 Desired Outcome

What are the goals of pharmacotherapy in this

case?
Acute pain: 1. Relieve the patients abdominal pain 2. increase his
functional status 3.minimize ADE 4.treat the underlying
condition causing the pain.
Hypertension: 1. determine the need to adjust the medication
regimen 2.adherence. 3.The BP goal <140/90 mm Hg.

(Presumed) acute alcoholic pancreatitis: 1.Relieve the patients

abdominal pain 2. risk of complications 3. prevent further
pancreatic damage.

 Hyperglycemia: 1.adjust the medication regimen based on

(concomitant illnesses /blood glucose records /prospective blood

glucose monitoring. 2.Rule out other causes) 3.Obtain A1C level
Treat to A1C goal of <7%

Dyslipidemia: 1.adjust current medication regimen (lipid profile)

2. Consider adding a fibric acid derivative. Dec. TG/removal of TG from blood
/Fibrates lower blood triglyceride levels by reducing the liver's production of VLDL

Heartburn: Determine frequency and severity of heartburn

symptoms, 2.assess adequacy of current medication regimen with

an H2-receptor antagonist 3.determine need for diagnostic testing.

Hypokalemia: 1.we Initiate potassium supplementation PO

(moderete-severe) but he is mild ??

2.Goal serum potassium should be 4.0 mEq/L (diabetes history of
cardiovascular disease.)

Therapeutic Alternative

 3.a. What feasible pharmacotherapeutic alternatives

are available for the treatment of acute pain?
Options for visceral pain include :
Corticosteroids
intraspinal local anesthetic agents
NSAIDs
opioids

1. Nonopioid agents
Acetaminophen (APAP)
analgesic and antipyretic prop.
minor pain.
comparable effectiveness to aspirin
no peripheral anti-inflammatory activity or effects on platelet
function.
fewer GI and renal adverse effects than NSAIDs.
The max.daily dose (adult) is 4 g.
Hepatic toxicity >> 1.acute acetaminophen overdose
2. usual doses in certain high-risk conditions (e.g., alcohol ingestion, cachexia or
malnutrition, and concomitant drugs that induce hepatic enzymes)

 NSAIDs

(aspirin, choline salicylate, diflunisal, meclofenamate,

mefenamic acid, etodolac, diclofenac, ibuprofen, fenopro- fen, ketoprofen,
magnesium salicylate, naproxen, ketorolac) and cyclooxygenase-II enzyme
selective inhibitors (celecoxib)

mild to moderate acute pain.

MOA inhibit prostaglandin synthesis.
caution GI bleeding (>60 years old, history of a GI event, Med.
Corticosteroids>internal bleeding/peptic ulcer
Possibility of Inc. cardiovascular events
cyclooxygenase-II enzyme inhibitors : dose and duration of
therapy should be limited.

2.Opioids

Analgesia results because the perception of

pain within the CNS as well as the patients
emotional response to pain is altered,
therefore modifying the sensory and
affective response.

 Opioid adverse effects

nausea /vomiting /constipation urinary retention/ sedation
/altered mental status/ respiratory depression/ vertigo/
hypotension.
Tolerance to opioid-induced side effects (after a few days of adm).
tolerance to constipation does not occur >>routine stimulant
laxatives for persons requiring chronic opioid therapy.

If the side effects do not lessen over time>> adjunctive drug

therapy( antiemetic or stimulant)

 Opioid classes include the phenanthrenes (morphinelike),

phenylpiperidine (meperidinelike), and diphenylheptane
(methadonelike).
True type 1 hypersensitivity (anaphylactic) > uncommon after
administration of opioid agonists.

If this does occur, an opioid from a different chemical class may be

prescribed under close medical supervision.

Opioids /release of histamine >> itching (local or diffuse), flushing,

or urticaria.
oxymorphone or fentanyl >>less histamine release>>less itching and
urticaria. Premedication with antihistamines may also be helpful.

 Tolerance to the analgesic effects of opioids (common

phenomenon)
(larger does V.S lower doses. )
Physical dependence is commonly observed in patients
requiring chronic opioid analgesics and is manifested by s&s of
withdrawal after abrupt discontinuation or rapid dose reduction
of the medication.

 Opioid analgesics available in a parenteral form for

severe pain are listed as follows
Morphine (prototypic opioid analgesic).
The most common adverse effects include (respiratory depression,
nausea, vomiting, constipation, and CNS effects (somnolence,
dizziness, euphoria).
Hydromorphone is more potent and has a shorter duration of
action than morphine, but it has a similar safety and efficacy
profile.

 Meperidine

has similar efficacy to morphine.. < duration of

action >risk for adverse effects.
Its use should be limited to a few days because of the risk for
accumulation of a renally excreted toxic metabolite (normeperidine) >>>agitation, tremors, seizures, and myoclonus.
AVOID 1. in patients with impaired renal function because
normeperidine can accumulate.
2.in patients taking MAOI because it can cause an accumulation of
serotonin >>>cardiovascular or neurologic adverse effects.
Meperidine (advantage over other opioids) less smooth muscle spasm
of the sphincter of Oddi, resulting in less pain in patients suffering
from biliary colic or pancreatitis. However, evidence of its
superiority in this regard over other opioids is lacking.

 Fentanyl

is structurally related to meperidine with a higher

potency and shorter duration of action. It can be administered
via a PCA pump (patch)

. Oxymorphone

has a higher potency than morphine but

has a similar safety and efficacy profile.

Methadone

has a long plasma half-life and accumulates

with continuous dosing, and therefore it should be used with
caution in the elderly. It is more often used for the treatment of
chronic pain.

Levorphanol

has a long plasma half-life that increases

with continuous administration of the drug.

3.Central analgesics
Tramadol relieves pain by two mechanisms of action.
1. It is a weak -opioid receptor agonist
2. inhibits the reuptake of the neurotransmitters serotonin and
norepinephrine.
The most common side effects are nausea, dizziness, drowsiness,
and constipation.

 3.b. What economic, psychosocial, and ethical

considerations are applicable to this patient?

The patient is a retired bar owner living on a farm; ( income,

insurance status, and accessibility to health care services need to
be evaluated.)>>>> discharge. medications

Optimal Plan

4.a. What drug, dosage form, dose,

schedule, and duration of therapy are
best for this patient?
Morphine P.O 5-15 mg then wait one hour.
Or morphine IV 1-3mg max(5mg) then wait 15 min

4.b. What alternatives would be appropriate if the initial

therapy fails or cannot be used?
NO adequate pain relief (initial dosing)>>the dose should be slowly
titrated upward. >>>regular patient monitoring for efficacy and
toxicity.>> intolerable side effects, it may be reasonable to
administer a lower dose of the drug with a revised lockout period
or consider changing to another appropriate opioid.

A new medication ???

Side effects that should be monitored include altered mental status,
constipation, urinary retention, respiratory depression,
somnolence, and mood changes. Due to intrapatient variability in
opioid response, switching from within an opioid class or to a
different class all together is a legitimate therapeutic strategy.
Meperidine???

Outcome Evaluation
What clinical and laboratory parameters are necessary
to evaluate the therapy for achievement of the
desired therapeutic outcome and to detect or
prevent adverse effects?

beginning of therapy to assess analgesic efficacy and to detect any

untoward effects from the drug. This will allow for therapeutic
changes if needed.
Observe the patients behavioral response to pain. Specifically
observe the patient for unusual facial expressions, guarding, or
rubbing of the abdomen.
.
A single-dimensional pain instrument (e.g., visual analog scale,
verbal numeric scale.

 Complete a focused physical exam of the abdomen. Light and deep

palpation ..
Measure vital signs, including pulse, respiratory rate, and blood
pressure, to assess the degree of pain relief and to monitor for
drug-related adverse effects.
Acute pain and opioid analgesics can both be associated with
changes in vital signs such as blood pressure, heart rate, and
respiratory rate. Importantly, the likelihood of opioid-induced
respiratory depression can be minimized with careful ongoing
assessment of respiratory status including pulse oximetry.

Monitor for adverse effects from the pain medications, such as

constipation (number of stools per day), drowsiness,
mood changes, and difficulty urinating.

Monitor amylase and lipase periodically since opioids can elevate

serum concentrations due to their effects on the hepatobiliary
system.
Monitoring would be especially important to distinguish disease
progression (e.g., hepatobiliary disease and biliary colic or
pancreatitis pain) from drug-induced changes.
Monitor electrolyte levels, specifically potassium, as hypokalemia
can contribute to abdominal pain.