Foundations of Pain

Foundations of Pain

Understanding pain requires recognizing that it is not merely a sensation, but a complex biopsychosocial stressor that triggers widespread physiologic responses. This is why pain assessment and management are core nursing responsibilities. Pain follows the Biopsychosocial Model, meaning it is influenced by biological (pathology), psychological (mood, coping), and social (cultural, environmental) factors.

I. Definition of Pain

  • ‑An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.‑ Pain is characterized by:

    1. Sensory and Emotional Components:

      • Sensory: Nerve activation, tissue injury, signal from the body (Nociception).

      • Emotional: Fear, anxiety, distress, memory, and suffering.

    2. No Requirement for Visible Tissue Damage:

      • Pain can exist in the absence of an identifiable physical cause.

      • Examples:

      • Neuropathic pain: Damage to the nervous system itself.

      • Phantom pain: Pain in a limb that has been amputated.

      • Chronic centralized pain: Like fibromyalgia, where the CN amplifies signals.

    3. Subjective Nature of Pain:

      • McCaffery’s Principle: ‑Pain is whatever the experiencing person says it is, existing whenever he says it does.‑

      • Nursing Implication:

      • Self-report is the gold standard.

      • Vital signs (HR, BP, RR) are unreliable for chronic pain and only supportive for acute pain.

      • Failure to treat pain leads to a persistent catabolic state.

II. Unrelieved Pain Responses (The Stress Response)

  • Unrelieved pain is interpreted by the brain as a threat to survival, activating a global systemic response:

    1. Sympathetic Nervous System (SNS) Activation: The "Fight or Flight" response.

    2. Hypothalamic–Pituitary–Adrenal (HPA) Axis: The endocrine cascade.

III. Harmful Effects of Unrelieved Pain

A. Endocrine & Metabolic (The Catabolic State)

  • Pain triggers the hypothalamus to release hormones that mobilize energy at the expense of tissue building:

    • ↑ ACTH → ↑ Cortisol: Promotes gluconeogenesis and protein breakdown.

    • ↑ Catecholamines (Epinephrine/Norepinephrine): Mobilize glucose and cause vasoconstriction.

    • ↑ ADH & ↑ Renin → Angiotensin II → Aldosterone: Leads to water and sodium retention.

    • ↑ Glucagon / ↓ Insulin: Causes hyperglycemia and insulin resistance.

    • ↓ Testosterone: Conserves energy for survival but impairs long-term repair.

  • Clinical Consequences: Hyperglycemia (even in non-diabetics), poor wound healing, muscle wasting (negative nitrogen balance), and increased risk of infection (IL-1, IL-6 proinflammatory cytokine surge).

B. Cardiovascular Effects

  • The Catecholamine Surge:

    • ↑ HR (via \beta_1 stimulation), ↑ Contractility, ↑ Myocardial oxygen demand.

    • ↑ Peripheral Resistance (\alpha_1 vasoconstriction) → ↑ Blood Pressure.

    • Hypercoagulability: ↑ Platelet aggregation and ↓ Fibrinolysis.

  • Clinical Consequences: Myocardial ischemia (angina/MI), Stroke (CVA), and Deep Vein Thrombosis (DVT).

C. Respiratory Effects

  • Patients with pain, especially abdominal or thoracic, engage in "Splinting" (shallow breathing to avoid pain).

  • Results: ↓ Tidal volume, ↓ Lung expansion, and ↓ Cough reflex.

  • Clinical Consequences: Atelectasis (alveolar collapse), pneumonia due to retained secretions, and hypoxemia.

D. Genitourinary & Gastrointestinal

  • GU: Fluid overload and ↓ urine output due to Aldosterone/ADH.

  • GI: Suppression of the Parasympathetic system (Vagus nerve).

  • Result: ↓ Gastric emptying and ↓ bowel motility leading to Paralytic Ileus, constipation, and anorexia.

IV. Types and Categories of Pain

  • Acute Pain: Protective, identifiable cause, short duration, SNS activation (tachycardia, hypertension).

  • Chronic (Persistent) Pain: Lasts >3-6 months, not protective, degrades quality of life, often lacks SNS signs as the body adapts.

  • Breakthrough Pain (BTP): A transient flare of moderate-to-severe pain that "breaks through" otherwise controlled baseline pain.

V. Classification by Pathology

A. Nociceptive Pain (Normal Processing)

  • Somatic: Arises from skin, bone, or muscle. Well-localized, "throbbing" or "aching."

  • Visceral: Arises from internal organs. Poorly localized, "cramping," or "gnawing." Often shows Referred Pain (e.g., gallbladder pain felt in the right shoulder).

B. Neuropathic Pain (Pathophysiology)

  • Damage to peripheral or central nerves. Described as "burning," "electric shocks," or "tingling."

  • Includes Diabetic Neuropathy, Postherpetic Neuralgia (Shingles), and Trigeminal Neuralgia.

VI. Nociception: The Four Processes

  1. Transduction: Tissue damage releases the "Sensitizing Soup" (Prostaglandins, Bradykinin, Serotonin, Substance P, Histamine). These open ion channels to create an electrical impulse.

    • NSAIDs work here by blocking Cyclo-oxygenase (COX 1 & 2) to prevent Prostaglandin synthesis.

  2. Transmission: The signal travels from the periphery to the spinal cord (Dorsal Horn) via:

    • A-delta fibers: Fast, myelinated; Sharp, localized pain.

    • C fibers: Slow, unmyelinated; Dull, diffuse, burning pain.

    • NMDA Receptors: Activated in the dorsal horn by Glutamate; blocking these (e.g., with Ketamine) reduces signal intensity.

  3. Perception: The Thalamus (relay station) sends signals to the Cortex. This is where the patient becomes "aware" of the pain.

  4. Modulation: The brain sends descending signals to inhibit pain.

    • Endogenous Opioids (Endorphins/Enkephalins) and Neurotransmitters (Serotonin/Norepinephrine) inhibit the "gate."

    • SNRIs/TCAs work here by increasing the availability of Serotonin/Norepinephrine.

VII. Neuropathic Pain Mechanisms

  • Allodynia: Pain from non-noxious stimuli (e.g., a cotton ball or bed sheet).

  • Hyperalgesia: Excessive response to a normally painful stimulus.

  • Wind-Up Phenomenon: Repeated stimulation of C-fibers causes the dorsal horn to become hyper-responsive (NMDA activation and calcium influx). The pain "snowballs."

  • Central Sensitization: A state of constant high reactivity in the CNS; the brain "learns" pain, leading to chronicity.

VIII. Pain Assessment & Nursing Management

  • Hierarchy for Nonverbal Patients:

    1. Attempt Self-Report.

    2. Search for potential causes (e.g., full bladder, surgery).

    3. Observe patient behaviors (PAINAD or CPOT scales).

    4. Surrogate reporting (family insight).

    5. Analgesic Trial: Administer a low dose and observe if behavior improves.

  • Pasero Opioid-Induced Sedation Scale (POSS):

    • S: Sleep, easy to arouse (Acceptable).

    • 1: Awake and alert (Acceptable).

    • 2: Slightly drowsy, easily aroused (Acceptable).

    • 3: Frequently drowsy, drifts to sleep during conversation (Unacceptable; monitor RR, decrease dose).

    • 4: Somnolent, minimal/no response to stimuli (Unacceptable; Stop opioid, consider Naloxone).

IX. Pharmacological Interventions

  • Acetaminophen (APAP): Max 4,000\text{ mg/day} (healthy) or 3,000\text{ mg/day} (frail/elderly). Watch for hepatotoxicity.

  • NSAIDs: Inhibit COX. Risks include GI bleed, Renal failure, and Cardiotoxicity. Ketorolac (Toradol) is limited to 5 days max due to high renal/GI risk.

  • Opioids:

    • Pure Mu Agonists: (Morphine, Fentanyl, Hydromorphone). No "ceiling effect"—dose can be titrated up until side effects occur.

    • Side Effects: Constipation (requires bowel program), Pruritus (common, not an allergy), Nausea, and Sedation (precursor to respiratory depression).

X. Patient-Controlled Analgesia (PCA)

  • Safety: ONLY the patient pushes the button (NO PCA by proxy).

  • Lockout Interval: Prevents overdose by limiting frequency.

  • Basal Rate: Continuous infusion; usually avoided in opioid-na've patients as it increases Opioid-Induced Respiratory Depression (OIRD) risk.