Pain and Suffering

4 Pain Mechanisms

• Transduction

• Transmission

• Perception

• Modulation

Transduction

Noxious stimuli causes cell damage with the release of sensitizing chemicals (prostaglandins, bradykinin, serotonin, substance P, histamine).

• These substances activate nociceptors and lead to generation of an action potential.

• Ex) NSAIDS inhibit prostaglandins which is one of the sensitizing chemicals

Transmission 

Action potential continues from the site of injury to the spinal cord, then to the brainstem and thalamus, then to the cortex for processing.

• ex) Opioids bind to presynaptic receptors and decrease Ca conduction 

Perception

Conscious experience of pain 

• ex) Cognitive strategies such as distraction, relaxation, hypnosis, etc 

Modulation

Neurons originating in the brainstem descend to the spinal cord and release substances that inhibit nociceptive impulses 

• ex) Antidepressants 

What causes nociceptive pain?

Damage to somatic or visceral tissue

Superficial Somatic Pain

Arises from skin, mucous membranes, and subQ tissues

• It is sometimes described as sharp, burning, or prickly

Deep Somatic Pain

Arises from bone, joint, muscle, skin, or connective tissue

• It is sometimes described as dull aching or throbbing, squeezing

Visceral Pain

Results from activation of nociceptors in the internal organs and lining of the body cavities

• It is sometimes described as deep aching, cramping, pressure

What causes neuropathic pain?

Damage to peripheral nerve structures in the CNS

• It is sometimes described as numbness, tingling, “shock-like”, “burning”

Acute Pain

• Caused by a precipitating event (illness, surgery, injury)

• Time limited; less than 3 months

• May have observable signs like increased HR, RR, and BP. May also have confusion, anxiety, agitation, diaphoresis, pallor, and urine retention

• Treatment involves pain control with ability to take part in recovery activities and minimize side effects of treatment

Chronic Pain

• Cause may not be known, original cause of pain may differ from mechanisms that maintain the pain

• Persists > 3-6 months

• Vegetative, depressive signs, autonomic adaptation

• May experience fatigue, flat affect, decreased physical activity, withdrawal from social interaction

• Treatment involves pain control to the extent possible. Focus on enhancing function and quality of life. Minimize side effects of treatment

Consequences of Unrelieved Pain on Endocrine System / Metabolism

• Increased RR, HR, BP

• Fluid overload

• Glucose intolerance

• Hyperglycemia

• Loss of lean body mass

Consequences of Unrelieved Pain on the Cardiovascular System

• Hypertension 

• Unstable angina 

• MI 

• Deep vein thrombosis 

Consequences of Unrelieved Pain on the Respiratory System

• Atelectasis (collapse of lung)

• Pneumonia 

Consequences of Unrelieved Pain on the Urinary System

• Fluid overload 

• Electrolyte imbalance 

Consequences of Unrelieved Pain on the GI System

• Constipation 

• Anorexia 

• Ileus 

Consequences of Unrelieved Pain on the Musculoskeletal System

• Immobility 

• Weakness and fatigue 

Consequences of Unrelieved Pain on Neurological System

• Confusion

• Impaired ability to reason and make decisions

• Increased risk of chronic pain, allodynia, hyperalgesia

Consequences of Unrelieved Pain on the Immune System

• Infection

• Sepsis

Consequences of Unrelieved Pain on the Psychological System

• Anxiety 

• Demoralization 

• Depression

Consequences of Unrelieved Pain on Social System

Withdrawing from hobbies, loneliness

Consequences of Unrelieved Pain on Spiritual System

• May challenge sense of meaning in life

• Destructive beliefs

Elements of Pain Assessment

• Pattern

• Location

• Intensity

• Quality

• Associated symptoms and aggravating factors

• Management strategies and alleviating factors

• Impact of the pain

• Patient beliefs, expectations, and goals

Non-Opioids

• Nonsalicylates: acetaminophen

• Salicylates: aspirin

• NSAIDs

Acetaminophen

• MoA: inhibiting COX pathways in the central nervous system to reduce pain and fever

• Few side effects

• Hepatotoxicity at high dose – recommended to limit total daily intake to 3,000mg or less

• Use for pain and fever, not for inflammation

• Given IV form over 15 min

Aspirin

• MoA: irreversibly inhibits COX enzymes, which stops the body from making prostaglandin. Also has anti-platelet effect

• Side effects: increased risk of bleeding (especially GI bleeding)

• Used more in low doses as a cardioprotective measure than for its analgesic properties

NSAIDs

• Ibuprofen, naproxen, and ketorolac

• MoA: Inhibit COX to reduce prostaglandin production

• Many side effects

• GI bleed risk (less than aspirin though)

• Renal effects (fluid retention, electrolyte imbalances, high BP, renal failure)

• Hypersensitivity reaction risk

• Used for pain, fever, and inflammation

• Don't use during 3rd trimester of pregnancy

• Don't take on empty stomach

• May increase cardiovascular events

Opioids

• Ex) morphine, oxycodone, hydrocodone, hydromorphone, and fentanyl

• MoA: Bind to opioid receptors to block pain signals - relieves pain, relief of anxiety, improved mood, decreased dyspnea

• Not recommended for chronic pain

• Adverse Effects:

  • Probable:

  • Constipation

  • nausea

  • Sedation

  • delirium

  • Sweating

  • Dry mouth

  • Pruritus

  • Physical dependence

• Possible effects:

  • Urinary retention

  • Myoclonus (spasms)

  • Hyperalgesia (heightened sensitivity to pain)

  • Seizure

  • Hypogonadism

  • Sleep disordered breathing

  • Respiratory depression

• Monitor pain

• Use sedation scale (RASS scale) to assess alertness

• Assess RR and O2sat before and after administering

Adjuvant Medications for Pain

• Antidepressants

• Antiseizure drugs (Gabapentin)

• GABA receptor agonists (Baclofen)

Antidepressants

ex) Amitriptyline and nortriptyline (TCAs)

• MoA: Antidepressants work by increasing the levels of specific brain chemicals (like serotonin, norepinephrine, and dopamine) in the spaces between nerve cells

• For neuropathic pain

• Side effects vary with each agent

• Decreased arousal and desire to have sex

Gabapentin

Antiseizure

• MoA: regulates electrical channels ( the boosting of calming chemicals, or the reduction of exciting ones)

• For neuropathic pain

• Side effects vary - dizziness, drowsiness, fatigue, edema, ataxia

• Start with low doses, increase slowly

Baclofen

• Binding to GABA receptors in the central nervous system to increase inhibitory signaling and reduce neuronal excitability

• side effects: drowsiness, dizziness, weakness, headache, and nausea

• For neuropathic pain and muscle spasms 

• Monitor for weakness and urinary problems 

• Avoid abrupt discontinuation bc of CNS irritability 

Non-Pharmacologic Therapies

Basic comfort measures

• Positioning

• Environmental conditions (lighting, noise, temp)

• Pacing activities / rest

• Supportive devices

Cutaneous stimulation/physical strategies

• Heat

• Cold

• Vibration

• Massage

• Exercise

• TENS

Cognitive and behavioral

• Distraction

• Relaxation

• Music

• Humor

• Imagery

• Education

• Supportive therapy