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Chapter 10 - pain assessment

Jarvis Chapter 10
STUDY
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we understand pain to develop by two main processes
nociceptive and neuropathic processing
a highly complex and subjective experience from the CNS, PNS, or both
pain
specialized nerve endings designed to detect painful sensations from the periphery and transmit them to the CNS
nociceptors
nociceptor locations
within the skin, connective tissue, muscle, and thoracic, abdominal, and pelvic viscera
nociceptors can be stimulated
directly by trauma or injury, or secondarily by chemical mediators that are released from the site of tissue damage
nociceptors carry the pain signal to the CNS by two primary sensory (afferent) fibers
Aδ and C fibers
myelinated and larger in diameter, transmit the pain signal rapidly to the CNS. The sensation is very localized, short term, and sharp in nature
unmyelinated and smaller, transmit the signal more slowly. the seconday sensations are diffuse and aching and they last longer after the initial injury
C fibers
Aδ and C fibers fibers synapse with interneurons located within a special area of the spinal cord called the
substantia gelatinosa
pain signals cross over to the other side of the spinal cord after synapsing with the interneurons and ascend to the brain by the
anterolateral spinaothalamic tract
develops when nerve fibers in the periphery and in the CNS are functioning and intact
nociceptive pain
occurs when a noxious stimulus in the form of traumatic or chemical injury, burn, incision, or tumor takes place in the periphery. Chemicals such as substance P, histamine, prostaglandins, serotonin, and bradykinin are released
transduction
substance p, histamine, prostaglandins, serotonin, and bradykin
neurotransmitters that propagate a pain message, or action potential, along sensory afferent nerve fibers to the spinal cord
second set of neurotransmitters carry the pain impulse across the synaptic cleft to the dorsal horn neurons
substance p, glutamate, and ATP
the pain impulse moves form the level of the spinal cord to the brain. within the spinal cord, at the site of the synaptic cleft, are opioid receptors that can block this pain signaling with our own endogenous opioids or with exogenous opioids if they are administered. If not stopped, the pain impulse moves to the brain via various ascending fibers within the spinothalamic tract to the thalamus
transmission
indicates the conscious awareness of a painful sensation. Cortical structures such as the limbic system account for the emotional response to pain, and somatosensory areas can characterize the sensation. Only when the noxious stimuli are interpreted in these higher cortical structures can this sensation be identified as "pain"
perception
the pain message is inhibited. fortunately our bodies have a built in system that will eventually slow down and stop the processing of painful stimulus. If not, we would continue to experience pain from childhood injuries and beyond. Descending pathways from the brain stem to the spinal cord produce a third set of neurotransmitters that slow down or impeded the pain impulse, producing an analgesic effect
modulation
neurotransmitters that slow down or impede the pain impulse producing a analgesic effect
serotonin, norepinephrine, neurotensin, GABA, and our own endogenous opioids, beta endorphins, enkephalins, and dynorphins
nociceptive processing is
protective. nociceptive pain is typically predictable and time limited based on the extent of the injury
examples of nociceptive pain
skinned knee, kidney stones, menstrual cramps, muscle strain, venipuncture, or arthritic joint pain
pain that does not adhere to the typical and rather predictable phases in nociceptive pain
neuropathic pain
neuropathic pain implies
an abnormal processing of the pain message from an injury to the nerve fibers. it is the most difficult pain to assess and treat
nociceptive pain can change into neuropathic pain
over time when pain has been poorly controlled
conditions that may cause neuropathy include
diabetes mellitus, herpes zoster, HIV/AIDS, sciatica, trigeminal neuralgia, phantom limb pain, and chemo. further examples include CNS lesions such as stroke, MS, and tumors
visceral pain
originates in the larger interior organs: kidney, stomach, intestine, gallbladder, pancreas
the pain impulse is transmitted by ascending nerve fibers along with nerve fibers of the autonomic nervous system in visceral pain
this is why it often presents along with vomiting, nausea, pallor, and diaphoresis
comes from sources such as blood vessels, joints, tendons, muscles, and bone
deep somatic pain
derived from the skin surface and subcutaneous tissues, the injury is superficial with a sharp, burning sensation
cutaneous pain
term attributed to pain with no known cause and assumed to have a psychiatric or emotional cause
psychogenic pain
pain that is felt at a particular site but originates from another location. may originate from visceral or somatic structures
referred pain
pain that is short term and self limiting, often follows a predictable trajectory, and dissipates after the injury heals
acute pain
an acute type of pain that happens predictably when certain movements take place
incident pain
persistant/chronic pain
diagnosed when the pain continues for 6 months or longer.
persistant pain can be further divided into
malignant and nonmalignant pain
malignant pain
often parallels the pathology caused by the tumor cells. Is induced by tissue necrosis or stretching of an organ by the growing tumor. Pain fluctuates within the course of the disease
chronic nonmalignant pain
often associated with musculoskeletal conditions such as arthritis, low back pain, and fibromyalgia
chronic pain originates
from abnormal processing of pain fibers from peripheral or central sites. because the pain is transmitted on a cellular level, our current technology cannot reliably detect this process
the most important and reliable indicator for pain
patient self-report
pain that starts again or escalates before the next scheduled analgesic dose
breakthrough pain
although pain is a common experience among individuals 65+
it is NOT a normal process of aging
the most common pain producing conditions for aging adults
arthritis, osteoarthritis, osteoporosis, PVD, cancer, peripheral neuropathies, angina, and chronic constipation
people with dementia
do feel pain, the somatosensory cortex is generally unaffected by dementia of the Alzheimer type
women are two to three times more likely to experience
migraines during childbearing years, are more sensitive to pain during the premenstrual period, and are six times more likely to have fibromyalgia
various studies describe how black and hispanic patients are often
prescribed and administered less analgesic therapy than whites
pain is defined as an
unpleasant sensory and emotional experience associated with actual or potential tissue damage
pain is always
subjective
pain is multidemensional in scope
encompassing physical, affective, and functional domains
select the pain assessment tool based on
its purpose, time involved in administration, and the patient's ability to comprehend and complete the tool
use the pain tool consistently before and after treatment
to see if the treatment has been effective
standardized overall pain assessment tools
are more useful for chronic pain conditions or particularly problematic acute pain problems. examples are the initial pain assessment, the brief pain inventory, and the mcgill pain questionnaire
the clinician asks the patient to answer 8 questions concerning location, duration, quality, intensity, and aggravating/relieving factors. further, the clinician adds questions about the manner or expressing pain and the effects of pain that impair one's quaility of life
initial pain assessment
asks the patient to rat the pain within the last 24 hours using graduated scales with respect to its impact on areas such as mood, walking, and sleep
the brief pain inventory
asks the patient to rank a list of descriptors in terms of their intensity and to give an overall intensity rating to his or her pain
the short form mcgill pain questionnaire
unidimensional and are intended to reflect pain intensity. They can indicate baseline intensity, track changes, and give some degree of evaluation to a treatment modality
pain rating scales
asks the patient to choose a number that rates the level of pain for each painful site. 0 being no pain and 10 indicating worst pain ever
numeric rating scales
lists words that describe different levels of pain intensity, such as no pain, mild pain, moderate pain, and severe pain
descriptor scales
in cases in which the cause of acute pain is uncertain
establishing a diagnosis is the priority but symptomatic treatment of pain should be given while the investigation is proceeding
with occasional exceptions (the initial exam of the patient with acute abdominal pain)
it is rarely justified to defer analgesia until a diagnosis is made
crepitation
an audible and palpable crunching that accompanies movement
note the size and contour, measure the circumference for comparison with baseline, check passive and active ROM
the joints
inspect color, swelling, and any masses or deformities
the muscles and skin
absent pain sensation
analgesia
increased pain sensation
hyperalgesia
severe pain sensation is evoked with a stimulus that does not normally induce pain
allodynia
observe contour and symmetry, palpate for muscle guarding and organ size
abdomen
behaviors are influenced by a wide variety of factors with pain
including the nature of the pain (acute v. chronic), age, and cultural or gender expectations
acute pain behaviors
guarding, grimacing, vocalizations such as moaning, agitation, restlessness, stillness, diaphoresis, or change in vitals
cardiac acute pain responses
tachycardia, elevated BP, increased myocardial o2 demand, increased CO
pulmonary acute pain responses
hyperventilation, hypoxia, decreased cough, atelectasis
GI acute pain responses
nausea, vomiting, ileus
renal acute pain responses
oliguria, urinary retention
Musculoskeletal acute pain responses
spasms, joint stiffness
endocrine acute pain responses
increased adrenergic activity
CNS acute pain responses
fear, anxiety, fatigue,
immune acute pain responses
impaired cellular immunity, impaired wound healing
poorly controlled chronic pain responses
depression, isolation, limited mobility and function, confusion, family distress, diminished quality of life
chronic pain behaviors
persons try to give little indication that they are in pain and therefore are at higher risk for underdetection. behaviors include bracing, rubbing, diminished activity, sighing, and change in appetite
older adults will often deny pain for fear of
dependency, further testing or invasive procedures, cost, and fear of taking pain killers/becoming a drug addict
when you look for behavioral cues look at changes in functional status in aging adults
observe for changes in dressing, walking, tolieting, or involvement in activities
look for a sudden onset of acute confusion in aging adults
may indicate poorly controlled pain
people with dementia communicate pain through their behavior
agitation, pacing, and repetitive yelling
when asked if they are having pain, people with dementia may say no
words have lost their meaning
evaluates five common behaviors of breathing, vocalization, facial expression, body language, and consolability
the PAINAD scale, used on people with dementia
a score of 4 or more on the PAINAD scale
indicates a need for pain management
treat underlying cause, NSAIDS, opioid, muscle relaxant, corticosteriod, biphosphonate
treatments for somatic or visceral pain
primary lesion in neuropathic pain
neuroma
somatic pain descriptors
dull,aching, well localized, nocturnal
somatic pain associated disorders
postop pain, bone metastases, arthritis, sports injury, mechanical back pain
visceral pain descriptors
deep squeezing pressure, local tenderness and referred, poorly localized
visceral pain associated factors
liver metastases, pancreatic cancer
neuropathic pain descriptors
constant dull ache, burning, stabbing, vice like, electric shock like, numbness, tingling, allydynia, hyperalgesia, hyperpathia
neuropathic pain treatment options
tricyclic antidepressants (TCA), anticonvulsant, antidepressant, antineuroleptic, local anesthetic, biphosphonate, corticosteroid, opioid, interventional techniques
a chronic progressive nerve condition, characterized by burning pain, swelling, stiffness, and discoloration of the affected extremity. If affects both men and women, usually around 40-60 and occurs weeks to months after a nerve inury. involves a complex interaction of sensory, motor, and autonomic nerves, as well as the immune system. Nerve injury may modify the usual pain pathway causing a neuropathic windup or short circuit mechanism. KEY FEATURE: typically innocuous stimulus can create a sever, intense painful response.
Reflexive sympathetic dystrophy or complex regional pain syndrome