PAIN MANAGEMENT
DR MOTHATA-MOTSWALEDI
Pain
Pain is defined as “an unpleasant sensation caused by noxious
stimulation of the sensory nerve endings.
Pain is a cardinal symptom of inflammation and is valuable in the
diagnosis of many disorders and conditions.
It may be mild or severe, chronic or acute, lancinating, burning, dull or
sharp, precisely or poorly localized, or referred.
Experiencing pain is influenced by physical, mental, biochemical,
psychological, physiologic, social, cultural, and emotional factors”
(Mosby’s Medical Dictionary, 2012).
Types of pain Location Quality of Localization sources Examples
pain
Nociceptive- Skin, Burning, Well localized to Traumatic Surgery,
somatic muscles, sharp, diffuse and events,strain,injury ,isch burns,
tissue, dull, radiate aemia, inflammation cuts ,
tendons, aching, &dermatological confusion,
joints & cramping arthritis,
bones tendonitis
Nociceptive- Visceral organs Sharp, Well or poorly Ischaemia ,inflammation Appendicitis ,
visceral stabbing or localized , organ distension, Pancreatitis,
deep aching muscle spasm gastric ulcer,
bladder distension
Neuropatic peripheral Sensitivity, Diffuse can be Peripheral nerve damage Diabetic neuropathy,
burning, difficult to lesions, neuralgia,
aching, determine compressive metabolic carpal tunnel
shoootin, disorders, syndrome,
cramping , ishaemia, phantom limb pain ,
throbbing , circulatory impairment & post stroke
numbness & CNS disease
tingling
Acute pain Chronic Pain
• unpleasant experience with an • Pain that persists at least three months
identifiable precipitating cause. beyond the expected course of an acute
injury or illness.
• Acute pain can also be seen as a • Chronic pain has no protective purpose
reflexive and protective response
• Pain can be continuous or intermittent , with
• Pain associated with degree of tissue or without acute exacerbations .
damage which decreases with healing
of injury. • Depressed mood ,irritability, social
withdrawal , fatigue, changes in daily
activities of living, disrupted social
relationships.
Pain assessment
The three most common scales recommended for use with pain
assessment are:
The numeric scale
The Wong-Baker scale (also known as the FACES scale)
The FLACC scale
(Health Care Association of New Jersey, 2011)
PAIN ASSESSMENT
Numeric scale
Wong-Baker Scale
FLACC Scale:
FLACC Scale:
0 1 2 3
FACE No particular Occassionaly grimace /frown, Frequent to constant frown ,
expression of smile withdrawn , clenched jaw ,
disinterested quivering chin
LEGS Normal position / Uneasy, restless or tense Kicking or legs drawn up
relaxed
ACTIVITY Lying quietly, Shifting back and forth or tense/ Arched , rigid or jerking
normal position, squirming
moves easily
CRY No crying Moans or occasional complaint Crying steadily,
(awake or asleep) screams or sobs,
frequent complaints
CONSOLABILITY Content, Reassured by occasional touching, Difficult to console or comfort
relaxed or hugging or talking to.
Distractable
(American Pain Society, 2007; Health Care Association of New Jersey, 2011)
y
TPain management strategies include pharmacological and non-pharmacological
approaches (Amer
PHARMACOLOGICAL APPROACH
Analgesic Paracetamol (Acetaminophen)
Non-steroidal anti-inflammatories Ibuprofen , naproxen and ketorolac
(NSAIDs)
Steroidal anti-inflammatory drugs: Hydrocortisone, methylprednisolone and dexamethasone,
Anxiolytics Benzodiazepines, ie midazolam, diazepam and lorazepam
Anticonvulsants carbamazepine , gabapentin and pregabilin.
Tricyclic antidepressants (TCAs) Amitriptyline, nortriptyline and desipramine
Selective serotonin reuptake Fluoxetine , paroxetine , serotonin, and sertraline
inhibitors (SSRIs)
alpha2 agonists, Clonidine and dexmedetomidine.
Local anesthetics Epidurals or Nerve blocks
Inhalational agents Entonox® is inhaled nitrous oxide.
TPain management strategies include pharmacological and non-pharmacological
NMDAapproaches (American
ANTAGONISTS Pain Society,
(EXCITATORY Ketamine2007; Health Care Association of New Jersey, 2011)
AMINO ACID ANTAGONISTS)
Classification for opioids:
Opioid agonists
Dipipanone HCl (Wellconal®)
Papaveratum (Omnopon®)
Dihydrocodeine tartrate (DF- 118®)
Codeine
Propoxyphene
Oxycodone
Pethidine
Opioid dualists:
Buprenorphine,
Pentazozine &
Tilidine
Opioid antagonist: Naloxone
Atypical opioids: Tramadol
Ultra-short acting:
Remifentanil
Medium acting:
Classification of opioids according
Short acting: Fentanyl
to
Alfentanil Sufentanyl
their duration of action
Long acting:
Morphine
Pethidine
Pentazocine
Buprenorphine
Tramadol
Paracetamol
ANILIDE
INDICATION:
Pyrexia
mild-moderate pain
ROUTE OF ADMINISTRATION: Oral, intravenous, rectal
ADVERSE EFFECTS:
Rare –hypersensitivity skin reaction,thrombocytopenia
Toxicity-→occur if glutathione stores are depleted eg overdose
Management:
• Activated charcoal, unless antidotes are given orally
ANTIDOTES:
• Acetylcysteine,
• Methionine,
• Carbocisteine
Non-steroidal anti-
inflammatory drugs(NSAIDs)
NSAIDs are chemically dissimilar agents that differ in the antipyretic,
analgesic and anti-inflammatory activities.
The class includes:
Salicylic acid- Aspirin
Proprionic acid – Ibuprofen
Acetic acid – Diclofenac
Indomethacin
Ibuprofen-Proprionic acid
Diclofenac-Acetic acid
Aspirin
Aspirin is a salicylic acid
Aspirin is differentiated from other NSAIDs because it is an irreversible inhibitor of
cyclooxygenase(COX-1).
MOA:
Irreversibly acetylates cyclooxygenase→deacetylated by esterases to form
Salicylate→decreasing prostaglandin E2 synthesis→ preventing sensitization of
pain receptors→ depressing pain stimuli at subcortical sites (thalamus&hypothalamus)
THERAPEUTIC USES:
Relief of mild to moderate pain
Pyrexia
Prophylaxis of platelet aggregation
Rheumatic fever
Acute and chronic inflammatory disorders
primary and secondary prevention of ischaemic heart disease, ischaemic stroke and
transient ischaemic attacks(TIA)
Aspirin
ADVERSE EFFECTS:
Gastrointestinal effects:
Bleeding:
Pseudo-allergic reactions →bronchospasm, rhinitis, urticaria, anaphylactic shock
Hepatotoxicity
CNS effects: Tinnitus, decreased hearing,
Renal effects: NSAIDs prevent the synthesis of PGE2 and PGI2 (prostaglandins are
responsible for renal blood flow) → decreased synthesis of prostaglandins→ retention of
sodium and water →oedema
Selective COX-2 inhibitor
Other cox-2 inhibitors(Meloxicam, Parecoxib, Etoricoxib)
Celecoxib
Selective COX-2 inhibitor (reversible)
INDICATIONS:
Rheumatoid arthritis
Osteoarthritis
Pain following dental procedures
ADVERSE EFFECTS:
GIT : abdominal pain, dyspepsia, nausea& vomiting, diarrhoea, flatulence.
Skin reaction (rare)
Morphine
INDICATIONS
Analgesic
Antitussive
Antidiarrhoeal
Anaesthesia adjunct
PHARMACOKINETICS:
Analgesic effect occur within 10-30min depending on the route of administration.
Metabolised in the liver→ morphine-6-glucuronide (higher analgesic potency)
→ morphine-3-glucuronide
Glucuronide metabolites & unchanged drug are excreted in urine
DRUG INTERACTIONS:
CNS depressants alcohol.anaesthetic,sedatives,antidepressants,antihistamines,etc
Antidiarrhoeals→severe constipation
Anticholinergics→atropine- increase risk of constipation &urinary retension
Cimetidine→increase risk of toxic effects e.g CNS & resp depression
Morphine
ADVERSE EFFECTS
Respiratory and circulatory depression with rapid IV administration
CNS- sedation,euphoria & miosis
RESP- truncal rigidity
RENAL-difficulty micturating
GIT-nausea , vomiting, constipation-slow gastric emptying
Tolerance and dependence may develop with prolonged use
ALLERGIC REACTIONS-pain at injection site, flushing, sweating & itching due to
histamine release
NALOXONE –is the antidote for opioid overdose
The classic triad of opioid toxicity is an altered mental status, respiratory
depression and miosis (constricted pupils)
Pethidine
Has no proven beneficial effects over morphine
It is neuro- & cardiotoxic and should be used with caution
Neurotoxicity is attributed to the accumulation of its long acting metabolite,norpethidine
Pethidine has the potential to release serotonin &must be used cautiously with other serotonergic
agents
INDICATIONS :
Analgesia for moderate to severe pain
CAUTION:
Elderly ,neonates & during labour (naloxone)
Renal impaired patients →at high dose there is risk of accumulation of norpethidine→which is
neurotoxic and may increase CNS excitation including seizures
75mg pethidine equivalent/= 10mg morphine imi
Pethidine
ADVERSE EFFECTS:
Dizziness,nausea and vomiting
Constipation&urinary retention less frequent than morphine
Vagolytic action on the heart may cause tachycardia
Vasodilation&hypotention following rapid iv administration
Respiratory depression causing accumulation CO2 & elevation of intracranial pressure
Tolerance,dependence and withdrawal problems
DRUG INTERACTIONS:
Monoamine oxidase inhibitors-fatal
Cimetidine-decrease elimination of pethidine →increasing risk of toxic effect such as CNS
& respiratory depression
Serotonergic agents-e.g fluoxetine increase risk of serotonin syndrome
Fentanyl
INDICATIONS:
Chronic pain
Intraoperative pain
Neuraxial anaesthesia-intrathecally
Anaesthesia adjunct
PHARMACOKINETICS:
Highly lipophilic with rapid onset and short duration of action
It is usually administered intravenous, intrathecally and transdermally
It is metabolized to inactive metabolites by CYP3A4, drugs inhibiting this
isoenzyme may potentiate the effect of fentanyl
Fentanyl
ROUTE OF ADMINISTRATION:
• Oral, IV, IM, Intranasal, Transdermal, Epidural& Spinal
MECHANISM OF ACTION: binds to mu receptors
Metabolized in the liver by cytochrome CYP3A4
Given in high doses it can cause muscle rigidity
ADVERSE EFFECTS:
Itchy nose intrathecally
Mood alteration- euphoria& dysphoria
Respiratory depression
Vomiting
Constipation
Physical dependance
Tramadol
INDICATION
Moderate to severe pain
PHARMACOKINETICS:
Oral bioavailability is 75% ;analgesic effects occur within one hour after oral
administration
T1/2 = 6-7 hours
Metabolised in the liver
Excretion is renal with 30% excreted unchanged
CONTRAINDICATION:
Raised intracranial pressure/head injury
Respiratory depression
Tramadol
ADVERSE EFFECTS: same as morphine
Respiratory and circulatory depression with rapid iv administration
Histamine release→pain& reaction at injection site(urticarial), itching,
flushing,sweating
CNS→sedation, euphoria, miosis
Truncal rigidity
GIT→nausea &vomiting ,slow gastric emptying, BUT LESS RESP
DRUG INTERACTIONS:
Carbamazepine→increase metabolism of tramadol
CNS depressants, anaesthetic & Alcohol →potentiate the CNS depressive effect
Serotonergic agents e.g fluoxetine →serotonin syndrome
CYP3A4 inhibitors e.g ketoconazole inhibit metabolism of tramadol
Tilidine
INDICATIONS:
Postoperative
Severe pain
DOSAGES:
PAEDIATRICS: Oral 1 mg/kg/dose 6 hourly = 1 drop per 2,5kg body weight
ADULT: 50mg 3→4 times daily; postoperative 100mg 2hours later, then 100mg 4→5 hours
later thereafter normal dosage regimen
DRUG INTERACTIONS:
CNS depressants→ depressants effects of tilidine are enhanced
ADVERSE EFFECTS:
Dry mouth, constipation ,sweating and facial flushing
CNS effects →Confusion, dizziness, drowsiness
CVS →bradycardia ,papitations
Hydromorphone
INDICATIONS:
Severe chronic intractable pain
ADVERSE EFFECTS:
GIT-gastrointestinal discomfort, nausea , vomiting,
CNS-headache, confusion, somnolence ,dizziness ,vertigo ,blurred vision & anxiety
RESP- dyspnoea
RENAL-difficulty micturating
Arthralgia
Rash
CONTRAINDICATIONS-acute/postoperative pain,severe hepatic impairment
TCA- Amitriptyline.
INDICATIONS:
Anxiety & Depressive disorder
Sedative effects –useful in inducing and maintaining sleep
Panic states &
Phobic disorders-→imipramine
Obsessive-compulsive disorders-→clomipramine
In low doses-esp imipramine effective in chronic pain situations →Rheumatoid Arthritis,
neuralgias, neuropathies, migraine prophylaxis &malignancies
PHARMACOKINETICS:
Anticholinergic activity may slow gastric emptying & delay absorption
Protein binding 96% ,T ½ = 10-50 hrs
Extensively metabolised in the liver-nortriptyline metabolite
Eliminated in urine
TCA- Amitriptyline.
ADVERSE EFFECTS:
Confusion , disorientation, blurred vision, dry mouth, nausea, tachycardia, fatigue,
excessive sweating, weight gain, impotence &constipation.
DRUG INTERACTION:
Alcohol & other CNS depressants
Tramadol →seizure risk may be enhanced
Serotonergic agents e.g antidepressants →→serotonin syndrome →pyrexia,agitation,
restlessness , rigidity ,myoclonus& gastrointestinal symptoms
Protease inhibitors e.g lopinavir ,atazanavir →plasma concentration of amitriptyline
may be increased
Monoamine oxidase inhibitors →contraindicated with concomitant use
hypertension, hyperpyrexia, convulsions and death
Benzodiazepine
Ultra-short acting Short acting Intermediate acting Long acting
(t1/2 <6hours) (t1/2 6-12 hours) (t1/2 12-24 hours) (t1/2 >24 hours)
• Midazolam • Lorazepam • Bromazepam • Diazepam
• Triazolam • Lormetazepam • Alprazolam • Prazepam
• Oxazepam • Lorazepam • Clobazam
• Temazepam • Clonazepam
• Clorazepate
• Chlordiazepoxide
Benzodiazepine
MOA:
Benzodiazepines enhance the effect of the neurotransmitter gamma-
aminobutyric acid (GABA) at the GABAA receptor, resulting in
Sedative,
Hypnotic (sleep-inducing),
Anxiolytic ,
Anterograde amnesia
Anticonvulsant, and
Muscle relaxant properties
Benzodiazepine
THERAPEUTIC USES:
Acute alcohol withdrawal
Anxiety disorders
Amnesia
Muscular disorders (skeletal muscle spasticity)
Painful musculoskeletal conditions
Pre & intraoperatively ( sedation; muscle relaxation; anterograde amnesia; adjunct
during endoscopy)
Anticonvulsant
Sleep disorders (Flurazepam; Triazolam; Temazepam; Lorazepam-short term use)
Status epilepticus ( Diazepam;lorazepam)
Benzodiazepine
ADVERSE EFFECTS:
Drowsiness
Oversedation
Confusion
Ataxia- at high dose
Cognitive impairment-decreased recall and retention of new
knowledge
physical and psychological dependence
Benzodiazepine antagonist
Flumazenil
It is a GABA receptor antagonist; rapidly reverses the effects of
benzodiazepine by binding to the benzodiazepine receptor
Indications:
Reversal of central sedative effects of benzodiazepine in anaesthesia/ICU
Inadvertent/ self-administered benzodiazepine overdose
Pharmacokinetic:
Onset is rapid, duration-short with a half-life of 1hour
The anti-convulsant effect of benzodiazepine is also antagonized
Risk of seizures in patients who have been on benzodizepine for a long time
Local anaesthetics
Block the initiation and propagation of action potentials by preventing the
voltage-dependent increase in Na+ conductance
Produce loss of sensation to pain(analgesia) without loss of sensory
perception e.g touch ,vibration, proprioception & motor nerve activity-
referred to as local analgesics
Local anaesthetics
ESTERS AMIDES
Class • Cocaine • Lignocaine-30 amine
• Procaine • Ropivacaine
• Chloroprocaine • Bupivacaine
• Benzocaine • Levobupivacaine
• Tetracaine (amethocaine) • Prilocaine- 2o amine
Metabolism • Ester anaesthetics are metabolised • Amides undergo enzymatic
in the plasma by the enzyme degradation in the liver and
pseudocholinesterase excretion in the urine.
• Para-aminobenzoic acid (PABA) is an • The amino-amides are not
amino-ester metabolite, which metabolized to PABA and they
causes allergic reactions in some rarely cause allergic reactions.
patients • Amides are extremely stable in
• Esters are unstable in solution. solution
Local anaesthetics classification
according to duration of action &
potency
Long duration of action & high anaesthetic potency
Bupivacaine
Intermediate duration of action &intermediate anaesthetic potency
Cocaine
Lignocaine
Short duration of action& low anaesthetic potency
Procaine
Chloroprocaine
Toxicity of Local anaesthetics
Toxicity results from accumulation with repeated doses or inadvertent
IV injection
Treatment of local anaesthetic toxicity:
Seizures suppression→ with intravenous benzodiazepine/short acting
barbiturate
Airway management
Cardiopulmonary support
20% lipid emulsion infusion (intralipid 20%)
Contraindications of local
anaesthetis
History of known hypersensitivity reaction to LA drugs/their
metabolites
Epilepsy
History of known neurological disease e.g Myasthenia gravis-
Underlying uncorrected hypotension &hypovolaemia
Underlying liver disease→ impaired liver metabolism→ accumulation
of drug level→toxic blood levels
Under-Treatment of pain
Under-Treatment of Pain There are still many myths and misbeliefs about
the use of opioids and addiction which can lead to under-treatment of
pain.
This is particularly true of elderly patients, and those suffering from
chronic pain.
Unrelieved pain can lead to physical and psychological disruptions,
including hormone fluctuation, electrolyte and glucose imbalance,
hypertension, tachycardia, increased oxygen consumption, impaired
intake and output, fatigue, depressed immune response, reduced
cognitive function, insomnia, anxiety, depression, hopelessness, and
thoughts of suicide (American Pain Society, 2007; CPM Resource
Center, 2010a, 2010b, 2010c, 2010d).
Conclusion
Pain management is a vital component of patient care, and can be complex.
It is important to individualize plan of care for each patient. (City of Hope
National Medical Center, 2011)
Useful principles of pain management can be remembered with the “ABCDE
method” as follows:
A: Ask about pain regularly
B: Believe the patient’s and/or family’s reports of pain
C: Choose appropriate pain approaches and treatment options
D: Deliver interventions in a coordinated and timely fashion
E: Empower patients and their families (American Pain Society, 2007;
Denny & Guido, 2012; Health Care Association of New Jersey, 2011)
References
Alexander, L. Assessment and management of pain at the end of life. CME Resource, March 20,
2013, 1-16.
American Pain Society. (2007). Pain: Current understanding of assessment, management, and
treatments. Glenview, IL: American Pain Society.
Centers for Disease Control and Prevention. (2012). Summary health statistics for U.S. adults:
National health interview survey, 2010. Vital and Health Statistics, 10(252), 1-217.
City of Hope Medical Center Pain and Palliative Care Center. (2012). Knowledge and attitudes
survey regarding pain. Retrieved February 4, 2013 from http://prc.coh.org/Knowldege%20&
%20Attitude%20Survey%2010-12.pdf City of Hope National Medical Center. (2011). Pain
management competency. Retrieved February 4, 2013 from
http://prc.coh.org/pdf/COH_Competency.pdf
Courtenay, M., & Carey, N. (2008). The impact and effectiveness of nurse-led care in the
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