Fundamentals of Nursing test 3

Unpleasant sensory and emotional experience associated with actual or potential tissue damage

Pain exists whenever the person says it does!

Protective mechanism

Tissue damage may not be proportional to extent of pain experienced

Pain thresholds are similar for all people BUT pain tolerance & perception greatly differ

level of intensity that triggers neuropathways resulting in pain sensation

level of intensity needed to cause an action potential and neuron firing

amount of pain a person perceives as tolerable

Acute
Sudden onset
Short duration: <3 months
Cause: usually can identify
Course: pain decreases over time

Chronic
Gradual or sudden onset
Duration: >3 months
Cause: may not know
Course: does not go away; pariods of waxing/waning

Chronic pain

50% or 1/2 of the people

Cutaneous (superficial)- caused by stimulation of nerve fibers in skin (burning/sharp)

Somatic (deep)- non-localized, originates in support structures strong pressure on tendons, bones, ligaments (aching/throbbing)

Visceral- arises from internal organs, difficult to localize (stomach, intestines)

damage to nerves

shooting, burning, pins & needles, intense

Phantom- sensation perceived when body limb or part is missing

Diabetic neuropathy- damage to nerves in the body that occurs due to high blood sugar levels from diabetes

perceived at the source and extends to nearby tissue

chronic pain in the absence of any identifiable cause

pain felt in different body area of body than actual tissue damage

pain from a mental event, no physical cause identified

pain highly resistant to relief (ie: bone ca)

when there is enough tissue injury to reach a pain threshold

Neurotransmitters (excitatory) are released which spread pain message and also stimulate the inflammatory response
(examples of these neurotransmitters are histamine, lactic acid, prostaglandins, bradykinin, Substance-P

Impulses travel along primary afferent neurons to the dorsal horn of spinal comuln-Substance-P released- pain sensation transmitted via spinothalamic tract

Acute pain runs up large A fibers (myelinated)
Fast transmission-Sharp pain

Diffuse pain runs up smaller C fibers (unmyelinated)
Slower transmission- throbbing pain

Stimulus received by thalamus; transmitted to cortex where pain is consciously perceived

Activation of endogenous opoids/neuromodulation system. Body releases pain blocking substances: endorphins, enkephalins, serotonin.
Efferent message sent to muscles to withdraw from pain stimulus.

Thalamus

Cortex

Hypothalamus/Limbic system

Theory that describes how external stimulation and cognitive techniques can affect pain transmission

Impulses traveling on small diameter C fibers act to "open the gate" to pain

Impulses traveling on large diameter A fibers act to "close the gate" to pain

External stimulation such as massage/heat/cold/TENS/acupuncture on large A fibers "close the gate" to small C fibers and pain

Also, cognitive techniques such as biofeedback, distraction, guided imagery can "close the gate"

Gate located @ dorsal root or spinal cord

Previous experience with pain
Fatigue
Anxiety/stress
Support systems
Attention
Coping style: locus of control
Neurological function
Age
Cultural factors

Meaning of pain may be exacerbated
Interference with functional status has greater impact on body systems
Not a normal sign of aging or inevitable

Additional RISKS:
-under-reporting of pain
-analgesic toxicity

Meaning of pain
Spiritual factors
Cultural beliefs and values
-acceptable expression of pain
-need for nurse self-assessment
Communication obstacles
Variation in acetylator rates of meds

Beging with acceptance of client report

Includes:
Subjective description-
Client statement
Use of a pain-rating scale

Objective assessment-
physical examination

A- ask about pain regularly
assess pain symmetrically

B- believe the client and family

C- choose appropriate pain control options

D- deliver interventions in timely fashion

E- empower the client and family

Where is your pain?
When did your pain start?
What does your pain feel like?
How much pain do you have now?
What makes the pain better or worse?
How does pain limit your function/activities?
Why do you think you are having pain?
What are your expectations regarding pain and pain relief?

Descriptive:
No pain-mild-severe

Numerical:
0-10

Visual analog:
Wong Baker

Behavioral:
Peyen PBS

Inspect the site of pain

Take vital signs

Note behavioral and affective signs

Involuntary
Sympathetic response (fight or flight):
Increased BP, HR, R, Pallor, Diaphoresis

If prolonged, deep, severe leads to parasympathetic response:
Decreased BP, HR, N & V, fainting

Guarding, Rubbing, Grimacing, Moaning, Immobilization, restlessness

Anxiety, fear, fatigue, anger, depression, withdrawal-isolation, decreased attention

Acute pain r/t tissue damage (mechanical, thermal, chemical) AEN.......

Chronic pain r/t tumor progression AEB.......

Related:
Self care deficit r/t pain
Ineffective airway clearance r/t pain

Client will...

Utilize a pain rating scale to identify pain and determine comfort level

Report that pain management regimen relieves pain to satisfactory level

Describe how unrelieved pain will be managed

Establish trusting nurse-client relationship

Comfort measures:
-administering analgesics
-modifying environment
-non-pharmacologic relief measures

Client teaching is an important part of a pain management plan

Explore strategies that have been effective for the client in the past

Physician
Pharmacist
Physical therapist
Occupational therapist
Pain specialist

Used with pharmacologic
-Distraction
-Guided imagery
-Relaxation
-Music
-Cutaneous stimulation: TENS, massage, heat, cold, acupressure

Removing or altering cause of pain:
-Loosening of a tight binder
-Emptying a distended bladder

Altering factors affecting pain tolerance:
-Environmental control
-Quiet, dim lighting
-Allow client to rest
-Position for comfort

Non-opoid
acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs) such as ASA, ibuprofen

Opoids (narcotics)
Ex:morphine,codeine

Adjuvants/co-analgesics
drug developed for use other than analgesic but enhances effect of opoids by providing added relief

Decreases inflammatory response

Works on peripheral nervous system

Blocks release of excitatory neurotransmitters (ie:histamine)

Slower onset-longer peak action

Side effects: stomach irritation, liver and renal damage, bleeding, ASA toxicity-tinnitus, hearing loss

Acetaminophen- N & V, low BS and pH. Max dose= no more than 4g daily. Watch for combo medications.

Provide synergistic additive effect

Antidepressants- Elavil
Muscle Relaxants- Flexeril
Corticosteroids- Decadron
Anti anxiety- Valium
Anticonvulsants- Neurontin
Antihistamines- Vistaril

Decreases cognitive perception of pain

Works on Central Nervous System

Blocks (locks into) pain receptors

Faster onset- shorter duration

Side effects- orthostatic hypotension, dizziness, sedation, nausea, constipation, urinary retention, respiratory depression

Emergency Rx for overdose= Narcan
narcan= narcotic antagonist

Give regularly instead of PRN, ATC, or PCA

Recognize side effects and treat appropriately

Use combinations that enhance analgesics

Individualize dosing specific to patient

Monitor for tolerance and treat appropriately

Monitor for physical dependence- body physically adapts to opoids and withdrawal symptoms can occur upon sudden stoppage. THIS IS NOT AN ADDICTION

Addiction (psychological dependence)- compulsive drug use; craving for opoid for effects other than pain relief

Function/cause of pain
When pain can be anticipated
How to use pain scale
What pain control measures will be used
Other measures to control pain
Methods for pain relief after discharge

Goals met?
Pain controlled?
Comfort level acceptable to patient?
Quality improvement considerations