P A I N 1my Power Point

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 “…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).

th em Sub phasize jecti v data e

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  Pain

is 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 > sensitivity to prostaglandin. 2

•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. 2. 3.

Conversation of stimuli to action potential Occurs at level of peripheral nerve (free endings or nocioceptors) 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 C

(alpha, beta, delta)

Do fiber types matter? A vs C 

A fibers  A-alpha

and A-beta are larger  A-delta medium 

A’s are myelinated sheaths allow faster transmission  Larger = faster



C fibers  Smallest

of all



No myelin sheaths



Transmit slowest

 M.

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? 

Sensitization or enhanced excitability  Think



of “Bob” commercials

NMDA= N-methylD-aspartate

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 



Several structures in brain involved



 Somatosensory

No Brain = No Pain

system = localization/characterization of pain  Limbic system = emotional/behavioral response to pain  Cortical structures = behavioral response

Descending pathways activated to transmit pain signal M. can occur in • • • •



Cerebral cortex Brainstem Sc Periphery

Chemicals released   



Serotonin Epinephrine Gamma-aminobutyric acid (GABA) Endogenous opiods

Five Pain Dimensions … 1.

Sensory = recognition of pain 

2.

Affective = emotional response  

3.

Pattern, area, intensity, nature (PAIN)

Anger, fear, depression, anxiety - emotions impair QOL

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   

2.

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

Sociocultural = demographics, support, social roles, culture  

Age, gender, education all influence pain Family may act as gatekeepers

Pain Types 

Nociceptive = damage to  Somatic

tissue (bone, joint, muscle, skin, connective tissue • Aching, Throbbing • Well localized

 Visceral

tissue

• Arises from internal organs • Poorly localized • N/V,


Neuropathic = damage to  Nerve

cells  Changes in sc processing • • • • •

Burning Stabbing Electrical Brief or lingering Sudden, intense

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     

Onset? Duration? Frequency? What worsens? What helps?



Area  

• Where? 

Ask patient to 



Breakthrough is one pattern type

Location? Radiates?

 

Describe site Point to area Or mark on a pain map • (drawing of body)



Intensity  Severity  Pain

scales helpful

6 on 0-10 

A comprehensive assessment includes evaluation of all 5 dimensions



Should be completed on admission to a facility or service

• What are some types of scales? 

Nature  quality

or characteristics? • Eg. throbbing, stabbing, sharp, itchy

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)