PAIN

Mary J. Aigner RN, FNPC

 How big of a problem is
PAIN?
 Per Lewis (in U.S.):
 15-20% acute pain from surgery/injury
 Chronic persistent pain (eg. arthritis)
• 25-30% of population
 Back pain in 25-30% of 20-64 year olds
 Leading cause of disability <45 years
 Migraine HAs affect 25 million
 9 of 10 have a nonmigraine HA yearly
 Jaw/facial pain 20 million
 Fibromyalgia (mostly) 4 million
Other pain problems
 Poor pain relief
 Estimated
30% Ca pts have adequate
 Consequences include
• Unnecessary suffering
• Physical/psychosocial dysfunction
• Immunosuppression
• Sleep problems
• Can result in increased morbidity
 Financial costs
 Unrelieved/inadequate mgmt = $100 billion/yr
 Lost workdays estimated $50 million/yr
 So … what is pain?
 “whatever the person experiencing
the pain says it is, existing wherever
the person says it does”. Bo th em
Sub phasize
jecti
v
data e
 “…an unpleasant sensory and
emotional experience associated
with actual or potential tissue
damage, or described in terms of
such damage” (Int’l Assn Study Pain).
Nociception & Suffering

 Nociception: activation of free nerve

endings (primary afferent nerves)
 Respond differently to noxious stimuli
 May not be perceived as pain

 Suffering: a “state of severe distress

associated with events that threaten the
intactness of the person”.
 Can occur even if there is no pain
 Acute vs Chronic

1. Is one worse than the

other?

2. Is one easier to control?

3. Is pain always bad?

4. Can you have both?

 Physical vs Emotional

1. Is physical pain more

real?

3. How do emotions
affect physical pain?

5. How does physical

pain affect emotions?
How does fear affect pain?
 Pathophysiology of Pain:
the simple explanation
 Noxious stimuli
 Tissue damage occurs
 Stimuli is sensed
 Sensation is transmitted
 First
to spinal cord
 Then to brain or thalamus

 Brain sends back signal

 Painis perceived
 We react to the pain
 Want an example?
 Consider dysmenorrhea (menstrual cramps)
Two types: 1) no pathology or primary, and 2) pelvic
disease is underlying cause…we’ll look at primary.
Basically, it is caused by excess of prostaglandin F and/or
2

> sensitivity to prostaglandin.

•Estrogen in endometrium is stimulated, then progesterone
•This results in large increase of prostaglandin produced
by the endometrium
•When menses start, the endometrium releases the
prostaglandin…this actually begins 12-24 hrs before
menses
  Released prostaglandins cause
 local myometrial contractions
 constriction of small endometrial blood
vessels
• Tissue ischemia results
• Pain receptors have > sensitization
 Result is menstrual pain
• Most severe lst day, may last 2 days
 Prostaglandins absorbed in bloodstream
 May cause HA, diarrhea, vomiting

Primary dysmenorrhea usually starts a few yrs after menses with

Onset of regular cycles
 4 steps to physiologic pain:

1. Transduction
1. Conversation of stimuli to action potential
2. Occurs at level of peripheral nerve (free
endings or nocioceptors)
3. Causes release of chemicals into area
around peripheral afferent nociceptor or
PAN
 Some will excite/sensitize PAN
 If PAN activited – action potential produced
Substances that stimulate
the norciceptors:
• Bradykinin: a powerful vasodilator that increases
capillary permeability and constricts smooth
muscle. Plays a role in chemistry of pain at site of
injury.

• Postaglandins: hormone-like substances that

send additional pain stimuli to CNS

• Substance P: believed to act as a stimulant at

pain receptor sites and may influence
inflammatory response
 Step 2: Transmission
 Generated action potential travels
 Along entire nerve route to spinal cord
 very long cell (eg toe to s.c.)
 This is called the afferent fiber
 Can be blocked by Na channel inhibitor or
a lesion in the fiber
 Two fiber types
A (alpha, beta, delta)
C
 Do fiber types matter?
A vs C
 A fibers
 A-alpha and A-beta
are larger  C fibers
 A-delta medium  Smallest of all

 A’s are myelinated  No myelin sheaths

 M. sheaths allow
faster transmission  Transmit slowest
 Larger = faster
Fibers have different
sensations per type
 A-alpha (sensory muscle) and A-beta
(sensory skin)
 Transmit nonpainful sensations (usually)
• Eg. light touch, vibrations
 A-delta (visceral)
 Pricking,sharp, well localized pain
 Short duration

 C (visceral)
 Dull,aching, burning
 Diffuse nature, slow onset, longer duration
 All fiber types …

 Extend from
periphery

 Enter through dorsal

root ganglia

 To dorsal horn of
spinal column
 How do they get there?

Areas on skin innervated by one spinal cord segment

 More: dorsal horn processing
 Once there, nociceptive signal is processed in the
dorsal horn of sc
 Neurotransmitters are released
• From afferent fiber into synaptic cleft
• They bind to receptors on close cell bodies and dendrites (in
dorsal horn)
 These activate or deactivate other cells
• Which then release neurotransmitters

 Special wide dynamic range (WDR) cells

 Mainly receive stimuli from A-delta/C fibers
 Also indirect dendritic projections * this may be the
why of referred pain
 Got that?
What about sensitization?
NMDA=
 Sensitization or enhanced excitability N-methyl-
 Think D-aspartate
of “Bob” commercials
 As input (variety) received, neurotransmitters
released at level of sc…especially substance P and
glutamate
 Sc neurons may respond in an exaggerated or
prolonged manner
 Glutamate acts through NMDA receptors
• If chronically activated will lead to neural remodeling which
increases the # areas activated responsive to input
So what if area is sensitized?
 Increased responses
to input leads to
increased pain
perception

 Therefore … therapy
goals are to prevent
pain and prevent
sensitization.
Where does the impulse go?
 From the dorsal horn (sc) to
brain
 Nociceptive stimuli go to a 3rd
order neuron mainly in
thalamus, or other parts of
brain
 There are several pathways
into the brain
 The cerebral cortex is believed
to be where pain perception
occurs
 Perception ……...Modulation
 Descending pathways
 Several structures in activated to transmit pain
brain involved signal
 Somatosensory  M. can occur in
system = • Cerebral cortex
localization/char- • Brainstem
acterization of pain • Sc
• Periphery
 Limbic system =
emotional/behavioral  Chemicals released
No Brain = response to pain  Serotonin
No Pain  Cortical structures =  Epinephrine
behavioral response  Gamma-aminobutyric
acid (GABA)
 Endogenous opiods
Five Pain Dimensions …

1. Sensory = recognition of pain

 Pattern, area, intensity, nature (PAIN)

2. Affective = emotional response

 Anger, fear, depression, anxiety
 - emotions impair QOL

3. Behavioral = observable actions to express

or control pain
 facial expression, posturing, ADLs
More dimensions …(3+2=5)

1. Cognitive = beliefs, attitudes, memories,

and meaning of pain
 Also includes pain-related beliefs
 Cognitive coping strategies
 Determines pt’s goals/expectations

2. Sociocultural = demographics, support,

social roles, culture
 Age, gender, education all influence pain
 Family may act as gatekeepers
 Pain Types
 Nociceptive = damage
to
 Neuropathic = damage
 Somatic tissue (bone,
to
 Nerve cells
joint, muscle, skin,
connective tissue  Changes in sc
• Aching, Throbbing processing
• Well localized • Burning
 Visceral tissue • Stabbing
• Arises from internal • Electrical
organs • Brief or lingering
• Poorly localized • Sudden, intense
• N/V,<BP,restless
 Assessment of Pain
 Our goal as nurses =
 describe the 5 dimensions of a pain experience
• What are they?

 Our purpose as nurses =

 implement pain management techniques
• What are some?
 Identify
pt goal and self-mgmt resources
 Make collaborative decisions (pt, MD, etc.) re mgmt
Sensory component of pain
 Pattern  Area
 Onset?  Location?
 Duration?  Radiates?
 Frequency? • Where?
 What worsens?
 What helps?  Ask patient to
 Describe site
 Breakthrough is one  Point to area
pattern type  Or mark on a pain
map
• (drawing of body)
  Intensity
 Severity 6 on 0-10
 Pain scales
helpful  A comprehensive
• What are some assessment
types of scales?
includes
evaluation of all
 Nature 5 dimensions
 quality or charac-
teristics?
• Eg. throbbing,
 Should be
stabbing, sharp, completed on
itchy admission to a
facility or service
3 on 0-10
 The other dimensions
 Need to be assessed also
 Effect on sleep
 Effect on ADLs
 Relationships with others
 Physical activity
 Emotional well-being
 How expressed
 Coping strategies or how controlled

 Chronic pain may need more detailed

assessment
 Pain Assessment Methods

 ABCDE:
A = ask regularly, assess pain systematically
 B = believe reports of pain & what relieves
 C = choose appropriate options for control
• Approp. For pt/client, family, setting
D = interventions timely, logical, coordinated
 E = empower pt/family
• Enables them to control course as much as possible
 Another method:
 PQRST:
P = what “precipitated – palliated – is pattern
of” - pain?
 Q = what is “quality, quantity” of pain?
• Sharp? Stabbing? Aching? Burning? Stinging?
Deep? Crushing? Viselike? Gnawing?
R = what is “region of, radiation of” pain?
 S = what is severity of pain?
 T = Timing: when begins/began, lasts how
long, how related to other events in client’s
life?
Another: assessment form in
textbook (Lewis)