Sources of pain

Superficial = skin

 - localized

Somatic = skeletal (muscles/joint pain)

 - More likely to be able to pinpoint pain

Visceral = deep pain (smooth muscles/organs)

 - frequently referred to other dermatomes

 - harder to define as limited to one area

Magnitude of acute pain

  How bad the pain can be...

Most common complaint presented to healthcare providers

National Center for Health Studies Data               >65 million injuries per year      >80% cause acute pain

>24 million surgical procedures per year          Millions of lost work days per year

Pain Management Principles

• Pain is a universal experience
• Each person’s pain experience is unique
  
• Pain is subjective
• Included as the 5th vidtal sign
• Pain impairs healing and decreases immune function
  

Nurses' roles in Pain Management

• Nurses must appropriately assess pain
• Nurses need to be knowledgeable about pain and how to relieve it
• Potent analgesics are available, safe, and effective when properly used
• If the med being used is not effective and nonpharmacologic  interventions do not work, you must consult with MD

Managing Acute Pain

• Treat pain aggressively - as early as possible

• Risk of pain > risk of drugs
• High doses often needed to establish comfort
• Assess and reassess pain regularly
• Empower and encourage patients to report pain
• Establish pain management plans
• Clearly defined lines of responsibility

Nursing management of Pain

• Accurate and frequent assessments
• Adequate intervention
• Pharmacologic
• Nonpharmacologic
• Monitor effect of intervention
• Onset and peak depends on drug and route
• Side effects

Nursing Process in Pain Management

 Assess your patient before giving any analgesic

• Take vital signs  
• Check pupils (PERLA)  
• Check allergies  
• Know other medications the patient is on
• Document medication after it is given:
• Educate patient
• administer pain medication before pain reaches its peak to maximize effectiveness
• Evaluate and monitor response
• Refusal

Most important vital sign to monitor while a patient is on pain medications

RESPIRATIONS!

Analgesic Classifications

 
Narcotic (addictive)

• Narcotic: can cause narcosis (stupor)
• Can lead to drug dependence      
• Abuse potential is high
• Examples: Morphine, Hydrocodone,
• Can be called the Opiates: opium poppy

• Non-narcotic (not addictive)
• Less potent than the narcotic analgesics
• Generally do not lead to drug dependence
• Examples: ASA, Tylenol, Ibuprofen

ANALGESIC ACTION

Narcotics

• Act on the central nervous system=CNS     (brain and spinal cord)
• Produce greater analgesia than even high doses of non-narcotics

Non-narcotics

• Act primarily on the peripheral nervous system  (voluntary and autonomic)

Opioid Analgesics

Mechanism of action is r/t binding with receptors

• Mu (μ), kappa (ĸ), delta (δ), sigma (σ)
• Produce analgesia, altered perception of pain   
• Also the unwanted effects (constipation, respiratory depression, etc)

NARCOTICS

Also called narcotic analgesics or narcotic agonists

• An agonist = a drug that produces a response     
• binds with receptor
• Partial agonist—produces a partial response
• Agonist-antagonist—mixed effects on receptors

Action

Suppress pain impulses

• Morphine – moderate to severe pain
• Codeine – mild to moderate pain

Suppress respiratory and cough centers in the medulla

• A drug that suppresses a cough is called an antitussive

NARCOTICS: SIDE EFECTS

• Respiratory depression
• Normal respiratory rate = 12-20 breaths per minute in an adult 
• Respiratory depression = < 10
• Decrease in Blood Pressure (B/P):   
• Normal 120/80 mmHg    
• Low B/P = 90/60 mmHg
• Respiratory Depression   
• Onset within minutes IV    
• Persists for 4-5 hours
• If given via spinal routes, can last longer  
• Must be prepared to intervene
• BVM (bag valve mask) & supplemental 0₂
• Reversal drugs
• Protect airway (suction and positioning)

 NARCOTIC OVERDOSE 

Example: morphine overdose

• Pinpoint pupils     
• Bradypnea < 8    down to  respiratory arrest

Opiates increase the effect of:

• Alcohol
• Sedatives (to sedate)  
• Hypnotics (for sleep)
• Antipsychotic meds       
• Muscle relaxants

ANTIDOTES: Narcotic Antagonists

Drugs used for overdose of narcotic analgesic       

• A narcotic antagonist
• Blocks receptor site and displaces the narcotic
• Action: these drugs have a higher affinity to the opiate receptor site than the narcotic taken

• Narcan (Naloxone)
• reverses the effects of respiratory and CNS depression!
• Half life is shorter than the narcotic. Usually must repeat
• If unknown OD substance, give anyway

Other common SE of opioids

• Constipation & biliary colic      
• Orthostatic hypotension       
• Urinary retention
• Nausea especially in ambulatory patients      
• Sedation    
• High falls risk; cannot operate machinery
• DWI         
• Cannot make legal decisions (Consent forms)

NARCOTIC: MORPHINE

Used for moderate to severe pain    

e.g., chest pain, acute myocardial infarction (MI) 

ADME

• Administration    
• PO, IM, IV, SC, PR, epidural, intrathecal
• Distribution     
• Wide, passes blood-brain barrier

MORPHINE: Effects

 CNS:  drowsiness, lethargy, apathy, alters mood; decreases anxiety

 Resp:  depression (effect on resp center)

 Assess rate and depth

 GI:  stimulates vomiting center, decreases peristalsis and increases sphincter tone

 Eye:  miosis

 GU:  diminished sensation to void

 CV:  hypotension, flushing of upper body (not allergy)

Morphine Dose     

Dependent on Route

• IV:  1-10 mg per dose    
• PCA:  (Patient Controlled Analgesia)
• IM:  5-20mg      
• PO:  10-30mg

• SQ (same as IM)
• Epidural, intrathecal  (must be preservative free- don't want preservative-induced meningitis)
• Rectal

Morphine: Indications

Indications:  Moderate to severe pain

• Higher doses initially, or if patient is developing tolerance
• More effective before pain reaches intolerable levels
• Schedule pain-causing activities for when drug will be most effective (e.g., bandage changes)

Fixed schedules more effective than “as needed”

More common for MD or RN to give too little than too much narcotic

PCA now commonly used to deliver

PCA   

Patient Controlled Analgesia

• Pump with controller to push for a dose     
• Set dose with each request
• mg per dose and # times per hour
• Can also have a basal rate      
• Some drug is constantly provided
• Lock out prevents too many doses given in too short a time

Benefits of PCA

• No waiting in agony for nurse to come
• Smaller doses = less sedation and respiratory depression
• Patient is empowered
• Studies show less over use of opioids post op than if given on schedule or prn.

Tolerance (Morphine, opioids)

• Larger and larger doses needed for same effect
• analgesic, euphoric, sedative and respiratory depression effects
• Tolerance to respiratory depression is good because when need higher doses of drug, the risk remains relative
• There can be cross tolerance between drugs

Physical Dependence on Opioids

The body reacts when dose drops or not given

Occurs about 6-10 hours after last dose

Reactions include: severe body aches, cramps, racing heart, shivering, shaking, fever,  runny nose and keen irritability

Dose helps, but stimulation of Dopaminergic Reward system never reaches original high.  Need more and more to sorta achieve it.

Who should not get a basal rate on their PCA pump?

Narcotic-naive

A person who does not typically take pain meds

Other Pure Narcotic Agonists: Meperidine (Demerol)

Action: same potency but shorter action than Morphine

• Does NOT have an antitussive (cough suppressant) effect
• Given to patients after surgery
• For pain control if allergic to morphine
• To stop the massive shivers that can get when awakening

Other Pure Narcoic Agonists: Fentanyl (Sublimaze, Innovar, Duragesic

Is 100 X stronger than morphine!!

Primarily used as an adjunct to anesthesia   

Can be used in PCA pump

Patch for severe chronic pain;

Actiq:  lollipop (will kill a child)

• Effects like oral or IV opioids
• Heat lamps and hot packs will increase absorption rate     

Other Pure Narcotic Agonists: Codeine

• 1/10th the analgesic potency of MS, 5 times the potency of ASA or acetaminophen
• Is metabolized to morphine!
• Some folks have genetic block to metabolizing it
• Mild to moderate pain      Not as sedating; no increase in ICP like MS
• Common to mix with ASA or acetaminophen to achieve two different types of analgesia

More pure narcotic agents: Diacetyl morphine (Heroin)

• More lipid soluble than MS, enters brain faster; but not stronger on pain
• Converted to MS in the body
• Schedule I drug—no legal use in US
• Frequently “cut’ with other substances    
• Those substances may be lethal or cause the OD

More pure narcotic agonists: Methadone

Analgesic = MS

Longest duration of action of any narcotic

Used for detox or maintenance (withdrawal is milder, more gradual)

Patient is still using a narcotic

May be delivered daily at a clinic     

Has less of a “buzz” than MS  

Tolerance develops and seek other drugs

Hydrocodone (Vicodin)

• Used as an analgesic and antitussive
• Commonly prescribed for outpatients

Oxycodone (Percodan, Percocet)

• 10 x more potent than codeine, available in combo with ASA or Tylenol and ibuprofen,
• extended release form (OxyContin)
• Commonly Rxd for outpatients

Narcotics For Non-Narcotic Uses:

Lomotil

diphenoxylate/atropine

For managing diarrhea

(Davis p. 453 if more info needed)

Narcotics for Non-Narcotic Uses: Antitussives

• Codeine and hydromorphone—effective but have abuse potential
• Dextromethorphan—chemically related to opiates but few effects other than antitussive so is in many OTCs

-dan

(drug name suffix)

-cet

(suffix in drug name)

Opioid-Like Analgesic

Prototpye:  tramadol (Ultram)

• Synthetic, not related to opioids but binds to mu receptors
• For moderate to moderately severe pain
• Not for use in patients who have a narcotic dependence or are addicted
• Has high street value

Non-narcotic Analgesics: NSAIDS

• Nonsteroidal anti-inflammatory drugs (NSAIDS) – reduce pain by inhibiting chemical mediators
• Inhibit prostaglandins by interacting and interfering with cyclooxygenase  (COX1)
• Analgesics         
• Antipyretics

Blocking COX1: pros/cons

BAD

• Gastric ulcers that can bleed to death
• Definite gastritis issues

Possible Good

• Inhibition of platelet aggregation
• Antipyretics
• Don’t need to use opioids

Asprin (acetlysalicylic acid)

ADME

• Well absorbed in GI tract, acidic environment improves absorption, buffering slows it but protects gastric mucosa to some extent
• Half life of 15 min in single usual dose but can be extended to 20 hrs in overdose situations (can’t be excreted fast enough)

Highly protein-bound

Asprin: Effects

• Inhibits enzyme cyclooxygenase which is needed in the synthesis of prostaglandins
• works in peripheral sensory nerves, no physical dependence;
• doesn’t work for visceral pain but is good for HA, muscle and joint pain and especially when inflammation present

Asprin: actions

• Anti-inflammatory
• Suppresses inflammation (antiprostaglandin)
• Antipyretic
• Inhibits formation of fever-causing substances that raise body’s thermostatic controls
• Antiplatelet
• Decreases the stickiness of platelets ~ 7 days
• Prevents colon cancer
• Prophylaxis of recurrent MI or stroke

Asprin: Indications

• Indications
• Pain, inflammation, or fever
• Associated with Reye’s syndrome in children when given for viral illnesses

Asprin: Drug-drug interactions

• Heavily protein bound
• Anticoagulants
• Alters pH (metabolic acidosis)
• Gastric irritation is additive with NSAIDs
• ETOH—both are ulcerogenic

Asprin: Toxicity

Mild (salicylism)

• Tinnitus, HA, dizziness, drowsiness, confusion, paresthesias, ventilatory stimulation, GI distress

Salicylate poisoning

• Altered resp (increased rate, then depression)
• Altered fluid/lytes and acid-base balance (alkalosis to acidosis)

Asprin Toxicity Treatment

Treatment—the sooner the better, no antidote

• Induce emesis,
• Ventilatory support,
• Correct acid-base balance
• Hasten excretion
• Watch for possible GI bleeding
• Expect effects of severe anticoagulation
• Renal failure if already renal insufficiency

Other NSAIDS (basics)

• Not salicylates but share many of the common SE and contraindications
• All have the same general pharmacokinetics
• Indications are similar, cost is greater
• May give less frequently
• All are ulcerogenic but not as great as ASA
• Many different drugs on the market, many are OTC

Ibuprofen

• Very common use, Rx and OTC strengths
• Causes sodium and water retention
• Caustic to stomach and intestinal lining
• Massive GI bleeds
• Can occur without warning
• Can cause renal damage
• Good Pain control
• Anti-inflammatory

NSAIDS & Muscle Injury

Strain (stretch-induced injury)

Animal studies:  Delayed healing

Human study:  No different than placebo

NSAIDS & Contusions

• No studies in humans
• Equivocal at best or slow adaptation to training
• At best NSAIDs are disappointing

NSAID & Ligament Injury

• Injuries heal best with controlled mobilization
• If NSAIDS promote mobilization, then perhaps beneficial.
• Most heal in spite of us
• Not sure if effect is from pain relief or anti-inflammatory effect

NSAIDS & Bone

• Animal studies show inhibit fracture healing.
• Indomethacin and naproxen inhibit ossification after hip fracture and total hip replacement
• Marked association between non-union and delayed healing in those who take NSAIDS

How to decrease risk of RENAL issues when taking ibuprofen

COX-2 Inhibitors

• Prototype: celecoxib (Celebrex)
• Pain relief similar to ibuprofen or naproxen—inhibits cyclooxygenase (COX)
• Less ulcerogenic (?), fewer SE      
• More expensive
• Now used for acute post-op or trauma pain
• Probable increase CV risk
• Even Celebrex
• Even Naproxen and Ibuprofen, but to a lesser degree

NSAIDs: Things to ponder

• If taken ASA and Cox-1 ASA effect stopped
• Less likely with COX-2
• NSAIDS should not be popped like candy
• Patients should not remain in pain for slight risk of CV event for short term use
• Other therapeutic interventions are very important---not just drugs

Acetaminophen: Effect & ADME

Analgesic (but not anti-inflammatory)

Effects

• Antiprostaglandin but apparently effects only certain types of cells – inhibits the synthesis of prostaglandins thereby reducing pain – more central mechanism than peripheral

ADME

• Well-absorbed, metabolized in liver

How acetaminophen differs from ASA

• No anti-inflammatory action
• Does not inhibit platelet aggregation
• Rare gastric irritation
• Not likely to cause bronchoconstriction in patients allergic to ASA
• Fewer drug-drug interactions
• No risk of Reye’s

Tylenol Indications & Side Effects

• Relief of mild pain and fever

Side effects:

• Few with normal dosage
• Danger is with long-term use or OD
• Liver damage if also ETOH 2-4X a day
• Can’t be used by liver cancer or cirrhosis patients

MAKE NOTE:  Max dose just changed to 3 GM a day

Tylenol Toxicity

 Fairly common (OD 25 gm for an adult)

• At its worst, fatal liver damage
• 12-24 hr:  GI cramping, N/V
• 2nd day:  no obvious signs, relief; urine output drops, hematuria, pain in URQ
• 3-5 days:  hepatic necrosis, irreversible

• Treatment:  N-acetylcysteine (Mucomyst)
• Interacts with toxic metabolite, protects liver cells
• Best if given within 10-12 hrs after ingestion

Anesthetics

• CNS depressants
• Loss of sensation, esp. to pain
• Types
• General—state of unconsciousness, surgery
• Regional—larger body region, target nerves
• Local—small body region, procedural area

Pre-anesthetics

Action: reduce undesirable effects of anesthesia, reduce apprehension

Common agents

• Narcotics—
• Barbiturates or Benzodiazepines
• Phenothiazines—like promethazine for nausea control
• Anticholinergics— like atropine (for airway secretion control)
• Skeletal muscle relaxants

General Anesthesia

2 classes of anesthetics

• Inhalation (gases or liquids)
• IV agents

Balanced anesthesia involves a combo of drugs, each with a specific effect

Pre-op agents

Intra-op agents

Stages of General Anesthesia

• Stage 1 – analgesia     
• Administration to loss of consciousness
• Stage 2 – excitement    
• Reflexes still present, may be exaggerated
• Stage 3 – surgical anesthesia     
• Increasing depth of anesthesia, affects respiration, loss of reflexes, flaccidity, lower body temperature
• Stage 4 –
• medullary paralysis (toxic)     
• Respiratory arrest and vasomotor collapse

Inhalation Anesthetics

• Nitrous oxide     (Not nitric oxide)
• Most often used in dental surgery
• 100% excretion through lungs
• High analgesia unlike other gases, but with low anesthesia

Volatile Liquids (mixed with oxygen)

• Halothane, Isoflurane, Ethrane
• Can be mixed with nitrous

IV Anesthetics

• Used for induction and/or maintenance, seldom used alone

Recovery Considerations

 Most anesthetic agents are lipid-soluble...

• Take VS every 15 minutes or sooner
• RR and airway: critical to monitor
• Some folks shiver as SE of med     
• Can also be from cold room
• Warm them up!
• Groggy and uncoordinated
• High falls risk
• Can’t drive home

Regional & Local Anesthesia

• Action
• Stabilizes or elevates threshold of excitation of nerve cells, prevents depolarization and transmission of nerve impulses
• Effect    
  
• loss of sensation without skeletal muscle involvement
• Types
• Topical
• Infiltrates—tissue, nerve, spinal

Topical Anesthetics

• Solution, ointment, cream, placed directly on skin or mucous membranes
• Effect
• Affects distal nerve endings, relieves pain or itching (loss of pain first, then warmth, pressure)
• “BenGay” is real medicine
• Choice depends on duration of action
• Short—1/2-1 hr     (lidocaine)     
• Intermediate—1-3 hr
• Long—3-10 hr   (Marcaine)
• Some contain epinephrine—local vasoconstriction

“Fingers, Ears, Nose, Toes and OHs”

What adverse reaction can occur r/t genearl anesthesia drugs?

Local Anesthetics: ADME

• Alert: When used in mouth can interfere with swallowing/gag reflex
• We don't want to cause an aspiration because we didn't check the gag reflex! 
• Viscous Xylocaine for sore throat
• Sprays given prior to endoscopy

Malignant Hyperthermia

Happens to certain groups of individuals (genetically predisposed)

Hypothalamus goes "offline" and temperature rises uncontrollably

Certain drugs more likely to have this effect than others

Local anesthetics: Nursing Management

• Monitor VS, watch for SE
• Watch for systemic effects
• If mixed with epinephrine can cause ischemia in the area.
• Why it's especially important to avoid epi on distal extremities
• Can be mixed with anti-inflammatory for dual action

Spinal Anesthesia

 Putting numbing agents into CSF to cause numbness from waist down.

• Can awaken with HA (headache)
• ??if occurs due to suggestion
• Nursing research showed that when people weren't warned of possible headache, they didn't occur.
• Usually only with larger loss of fluid
• Typically on flat position bedrest X 12 hours
• Cannot be released if cannot void
• Shaking and moving extremities does not hasten recovery
• Don't try and "shake it off"
• High falls risk 

Propofol

• IV anesthetic
• Rapid onset and short duration
• Can be used outside OR in continuous infusion

• SE:  PROFOUND respirations and hypotension
• Caution in hypovolemia and CVD

• Increase risk of bacterial infection WHY????
• You can't flush it with a lot of stuff (it's thick, stickier... bacteria like to stick to it)
• Can’t be used with Egg allergies
• egg protein

Non-pharmacologic Interventions in Pain Management

Positioning

Ice/heat (though needs an order, officially)

Distraction (TV)

"Massage" (but don't call it that, also requires an order)