Pain Assessment
Development of Pathologic Pain
Pain develops through two main pathways: nociceptive and/or neuropathic processing.
Patients present with diverse symptom types, leading to varied clinical responses to therapy.
Accurate pain assessment is crucial for developing effective non-pharmacologic and/or pharmacologic strategies to achieve improved clinical outcomes.
Neuroanatomic Pathways
Pain receptors (nociceptors) detect painful sensations.
Transmit signals via primary sensory (afferent) fibers (Aδ and C fibers).
Enter the spinal cord through posterior nerve roots into the dorsal horn via the tract of Lissauer.
Fibers synapse with interneurons in the substantia gelatinosa (Lamina II) of the spinal cord.
Pain signals then cross the spinal cord and ascend to the brain via the anterolateral spinothalamic tract.
The pathway continues through the medulla and thalamus, ultimately reaching the cerebral cortex, where pain is perceived.
Physiology of Pain: Nociceptors and Nerve Fibers
Nociceptors:
Specialized nerve endings designed to detect painful sensations.
Transmit sensations to the central nervous system (CNS) using two primary sensory (afferent) fibers: Aδ and C fibers.
Aδ Fibers:
Myelinated and larger in diameter.
Transmit pain signals rapidly to the CNS.
Result in localized, short-term, and sharp sensations.
C Fibers:
Unmyelinated and smaller.
Transmit signals more slowly.
Sensations are diffuse and aching, persisting after the initial injury.
Peripheral sensory Aδ and C fibers:
Enter the spinal cord via posterior nerve roots within the dorsal horn, traveling through the tract of Lissauer.
Substantia Gelatinosa:
A specific area of the spinal cord (considered Lamina II) where Aδ and C fibers synapse with interneurons.
This area receives sensory input from various body regions.
After synapsing, pain signals cross to the contralateral side of the spinal cord and ascend to the brain via the anterolateral spinothalamic tract.
Nociception Process and Phases
Nociceptive Pain:
Develops when functioning and intact nerve fibers in the periphery and CNS are stimulated.
Triggered by external events causing actual or potential tissue damage.
Nociception is divided into four phases:
Transduction
Transmission
Perception
Modulation
Phase 1: Transduction
Occurs in response to noxious (harmful) stimuli.
Injured tissue releases a variety of chemical mediators, including:
Substance P
Histamine
Prostaglandins
Serotonin
Bradykinin
These neurotransmitters propagate the pain message.
An action potential moves along afferent nerve fibers to the spinal cord, terminating in the dorsal horn.
Phase 2: Transmission
The pain impulse moves from the spinal cord to the brain.
In the dorsal horn, a second set of neurotransmitters (Substance P, glutamate, and adenosine triphosphate (ATP)) carries the pain signal.
If the pain signal is not stopped, it ascends via various fibers within the spinothalamic tract to the thalamus.
Phase 3: Perception
This is the conscious awareness of the pain signal.
Cortical structures, such as the limbic system, contribute to the emotional response to pain.
Pain is only perceived as a painful experience when it reaches the cerebral cortex. The perception of pain is highly individualized and influenced by psychological and cultural factors.
Phase 4: Modulation
This phase involves the body's natural pain-inhibiting processes.
Descending pathways from the brainstem release neurotransmitters such as serotonin, norepinephrine, GABA, and endogenous opioids (e.g., endorphins, enkephalins) into the spinal cord.
These neurotransmitters inhibit pain transmission by blocking the release of pain-producing substances from the afferent nerve fibers or by decreasing the excitability of postsynaptic neurons in the dorsal horn.
This process can reduce or alter the perceived pain.
Types of Pain
Acute Pain:
Short-term, self-limiting, dissipates after injury heals.
Serves as a warning sign; identifiable cause.
Example: surgery, trauma, kidney stones.
Chronic Pain (Persistent Pain):
Pain continues for 6 months or longer, typically after the injury has healed.
Can be malignant (cancer-related) or non-malignant (arthritic, back pain).
Does not stop when injury heals; can be difficult to treat.
Often accompanied by symptoms such as fatigue, insomnia, weight changes, depression, and irritability.
Nociceptive Pain:
Arises from actual or threatened damage to non-neural tissue.
Usually responsive to opioids and non-opioid medications.
Divided into:
Somatic Pain:
Originates from musculoskeletal tissues or body surface.
Usually well-localized and described as throbbing, aching, or gnawing.
Examples: tissue injury, bone metastasis, surgical incision.
Visceral Pain:
Originates from internal organs (e.g., stomach, intestine, gallbladder).
Often poorly localized, dull, aching, squeezing, or cramping.
Can be referred to other body sites.
Examples: tumor pressing on an organ, bowel obstruction, appendicitis.
Neuropathic Pain:
Caused by a lesion or disease of the somatosensory nervous system.
Implies an abnormal processing of pain messages from damage to nerve fibers.
Often perceived as burning, shooting, tingling, or electrical-like sensations.
Difficult to treat; often requires adjuvant analgesics.
Examples: diabetic neuropathy, shingles (postherpetic neuralgia), sciatica, phantom limb pain.
Referred Pain:
Pain felt at a particular site but originates from another location.
Both sites are innervated by the same spinal nerve, making it difficult for the brain to differentiate the origin.
Example: myocardial infarction pain refers to the left arm or jaw.
Breakthrough Pain (BTP):
A transient flare of moderate to severe pain superimposed on a persistent pain syndrome.
Can be predictable (e.g., with movement or dressing changes) or unpredictable.
Requires rapid-onset, short-acting medication.
Clinical Manifestations of Pain
Physiologic Responses (Acute Pain):
Sympathetic nervous system activation:
Tachycardia
Increased blood pressure
Tachypnea
Pupil dilation
Diaphoresis
Muscle tension
Anxiety, fear
These responses may lessen over time, even with persistent pain, as the body adapts.
Behavioral Responses (Acute Pain):
Crying, groaning, moaning
Guarding, grimacing
Restlessness, agitation
Inability to concentrate
Changes in appetite
Behavioral Responses (Chronic Pain):
Often subtle and less obvious than acute pain.
Bracing, rubbing
Diminished activity, reduced range of motion
Sighing
Changes in sleep patterns
Isolation, withdrawal
Flat affect, decreased spontaneity
Depression, anxiety, fear of re-injury.
Pain Assessment Approaches
Pain is always subjective; it is whatever the experiencing person says it is.
Believe the patient's self-report of pain.
Subjective Data - Pain History
Location:
Where is your pain? Ask the patient to point.
Intensity/Severity:
How bad is your pain? Use a pain rating scale.
Quality:
What does your pain feel like? (e.g., sharp, dull, throbbing, burning)
Onset:
When did the pain start?
Duration:
How long does it last? Is it constant or intermittent?
Timing (Pattern):
What makes the pain better or worse? Does it follow a pattern?
Alleviating and Aggravating Factors:
What relieves the pain? What causes it to worsen?
Associated Symptoms:
Any other symptoms accompanying the pain (e.g., nausea, fatigue, numbness)?
Impact of Pain on Activities of Daily Living (ADLs):
How does the pain affect sleep, appetite, mood, personal hygiene, walking, social interactions?
Patient's Goals:
What is a realistic pain goal for the patient? (e.g., function improvement, pain reduction to a tolerable level)
Objective Data - Physical Examination
Observe the patient for nonverbal behaviors of pain. (Note: The absence of these behaviors does not mean the absence of pain).
Vital Signs:
While vital signs can indicate acute pain (e.g., increased heart rate, blood pressure, respirations), they are not reliable indicators for chronic pain due to adaptation.
Musculoskeletal Examination:
Inspect and palpate joints and muscles for swelling, tenderness, guarding, or limited range of motion.
Neurological Examination:
Assess sensation, motor strength, and reflexes if neuropathic pain is suspected.
Abdominal Examination:
Palpate for tenderness, guarding, distention, or masses in cases of visceral pain.
Facial Expression:
Grimacing, clenched teeth, furrowed brow.
Body Movement:
Restlessness, pacing, guarding a painful area, stooped posture, reduced mobility.
Pain Rating Scales
Unidimensional Scales:
Measure only pain intensity.
Numeric Rating Scale (NRS):
A scale from 0 to 10 (or 0 to 5).
0 = no pain, 10 = worst possible pain.
Commonly used for adults and children \ge 10 years.
Verbal Descriptor Scale (VDS):
Uses words to describe pain intensity (e.g., no pain, mild, moderate, severe, worst pain possible).
Visual Analog Scale (VAS):
A 10-cm line on which the patient marks pain intensity.
0 = no pain, 10 = worst possible pain.
Multidimensional Scales:
Measure pain intensity, quality, impact on function, and emotional response.
McGill Pain Questionnaire (MPQ):
Comprehensive tool; describes sensory, affective, and evaluative aspects of pain.
Brief Pain Inventory (BPI):
Assesses pain severity and interference with daily activities.
Pain Assessment in Specific Populations:
Infants and Children:
FLACC Scale (Face, Legs, Activity, Cry, Consolability):
Used for nonverbal children aged 2 months to 7 years.
Scores range from 0 to 10 (no specific LaTeX instruction was provided for
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Uses 6 faces ranging from happy (no pain) to crying (worst pain).
Suitable for children \ge 3 years.
Older Adults:
Many older adults may underreport pain due to fear of addiction, belief that pain is a normal part of aging, or cognitive impairment.
PAINAD (Pain Assessment IN Advanced Dementia) Scale:
Observational tool for assessing pain in nonverbal patients with advanced dementia.
Assesses breathing, negative vocalization, facial expression, body language, and consolability.
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Patients with Communication Barriers:
Consider behavioral cues, vital signs, and involve family members for insights.