Negative Effects Of Pain

1
Postoperative Pain Management

• Negative Effects Of Pain
• Short term effects
• Emotional and physical suffering
• Sleep disturbance
• Cardiovascular effects
• Impaired bowel movement
• Effects on respiratory function
• Delayed mobilization, promotes thrombosis.
• Long term effects
• Acute pain can lead to chronic pain
• Behavioral changes in children for a prolonged
  period after surgical pain.
• Goals Of Pain TreatmentImprove quality of life
  for the patientReduce morbidity Facilitate
  rapid recovery and return to full functionAllow
  early discharge from hospital.
• Categories Of PainPostoperative pain can be
  divided into acute pain and chronic painAcute
  pain is experienced immediately after surgery (up
  to 7 days)Pain which lasts more than 3 months
  after the injury is considered to be chronic.
• Types Of Pain
• Somatic (from skin, muscle, bone)
• Visceral (from organs within the chest and
  abdomen)
• Neuropathic (caused by damage or dysfunction in
  the nervous system).
• Patients can experience more than one type of
  pain.
• Pain Pathway

2

• Principles Of Pain Assessment
• Assess pain both at rest and on movement.
• Evaluate before treatment, than reevaluate after.
• If pain is intense, evaluate, treat, and
  re-evaluate frequently.
• On the ward, evaluate, treat, and re-evaluate
  regularly.
• Document pain and response to treatment,
  including adverse effects.
• Particular attention to patients who have
  difficulty communicating pain.
• Evaluate unexpected intense pain, particularly if
  associated with hypotension, tachycardia or
  fever.
• Family members are involved when appropriate.
• Tools For Pain Assessment
• Facial expressions
• Verbal rating scale (VRS)
• Numerical rating scale (NRS)
• Visual analogue scale (VAS).
• Currently the most frequently used approach to
  pain management is PRN based monotherapy.
• Whats wrong with this standard?
• Analgesic Gaps are specific periods of time when
  pain management is inadequate.
• By definition, PRN medications cause analgesic
  gaps (breakthrough pain).

3
Pharmacological Methods Of Pain Treatment
Non-opioid analgesics Paracetamol (Acamol), Dipyrone (Optalgin)
Non-opioid analgesics NSAIDs (including COX-2 inhibitors)
Weak opioids Codeine
Weak opioids Tramadol
Strong opioids Morphine
Strong opioids Pethidine
Strong opioids Oxycodone
Adjuvant Ketamine
Adjuvant Gabapentine (Neurontin), Pregabalin (Lyrica)
Adjuvant Clonidine, Dexmedetomidine (Precedex)

• Non-opioids Paracetamol (Acamol)
• Inhibits COX-3 in the hypothalamus, very low
  activity on COX-1, possible 5-HT activity.
• No anti-inflammatory properties.
• Rapidly absorbed from GI tract, reaches a peak
  plasma level in 30 to 60 min, rectally 2-2.5 h.
• Metabolized in liver half life is 2 hours.
• Associated with hepatotoxicity when taken in
  large doses (10 to 15 g).

Administration RectalOral (as soon as possible).
Dosage 1 g x 4 /day PO, rectal dose 50 higher.
Comments Should be combined with NSAID and/or opioids or loco-regional analgesia for moderate to severe pain.

• Non-opioids Dipyrone (Optalgin)
• Popular in some regions (Middle East, Asia,
  S.Africa, S.America, part of Europe), but
  prohibited in others (USA, EU, Australia).
• Presumably inhibits COX-3 in spinal cord.
• No anti-inflammatory properties.
• IV administration can result in hypotension.
• Questionable risk of agranulocytosis.

Administration IV, IM, Rectal Oral (as soon as possible).
Dosage The single dose in all age groups is 8 to 16 mg/kg BW up to 1g x 4/day, 3 days max.
Comments Should be combined with NSAID and/or opioids or loco-regional analgesia for moderate to severe pain.
4
Non-opioids NSAIDs
Administration Intravenous (30-60 min before end of surgery)
Administration Intramuscular (painful)
Administration Oral (as soon as possible).
Monitoring Renal function in patients with renal or cardiac disease, elderly patients, or patients with episodes of severe hypotension. Gastrointestinal side effects.
Comments Can be added to the premedication. Would be combined with proton inhibitors (i.e. Omeprasol) in patients at risk of gastrointestinal side effects.

• Analgesia
• Ceiling effect
• Effects are evident in 1-2 hr
• Administration limited to 1-2 wks If inadequate
  results, change to another NSAID.

• Opioids
• Opiate Receptors
• ? Mu
• ? Delta
• ? Kappa
• Mu most important for analgesic actions.
• Opioids problems
• Side-effects euphoria/dysphoria, constipation,
  respiratory depression, nausea/vomiting, urinary
  retention.
• Tolerance
• Definition A change in the dose-response
  relationship induced by exposure to the drug and
  manifest as a need for a higher dose to maintain
  an effect.
• Develops at different rates to varying effects
  respiratory depression, somnolence, nausea gtgt
  analgesia
• Analgesic tolerance is rarely a problem.
• Opioid doses remain relatively stable in the
  absence of worsening pathology and increased
  opioid requirements after stable periods is often
  a signal of disease progression.
• Dependence
• Definition The development of a withdrawal
  syndrome following dose reduction or
  administration of an antagonist.
• Often develops after only a few days of opioid
  therapy.
• Not a clinical problem if drug is tapered before
  discontinuation.
• Taper by no more than 50 of the dose/day.
• Addiction

5
Opioids MORPHINE
Administration Intravenous
Administration Subcutaneous (by continuous infusion or intermittent boluses)
Administration Intramuscular (not recommended).
Dosage IV Bolus 2-3 mg each 5-10 min, up to 0.1- 0.15 mg/kg.
Dosage SC 0.1- 0.15 mg/kg 4 - 6/h
Dosage IM 5-10 mg 3 - 4 hourly.
Monitoring Sedation, respiratory rate, nausea, vomiting, urinary retention.
Oral Strong Opiates

• No maximum dose for morphine
• No maximum dose for oxycodone alone
• Doses are limited with combination products.

Morphine Immediate Release MSIR Controlled
Release MS Contin
Oxycodone Combination product Percocet Controlle
d release Oxycontin
Transition From PCA To Orals

• Give 2/3 of previous 24 hour morphine
  requirements as OxyContin
• Oxycodone for breakthrough.

Opioids CODEINE
Administration Oral
Dosage 3 mg/kg/day (combined with Paracetamol)
Comments Analgesic action is likely to be due to conversion to morphine. Part of patients derive no benefit due to absence of the converting enzyme.
Equianalgesic Doses of Opioid Analgesics
PO / PR Analgesic SC / IV / IM
200 Codeine -
30 Morphine 10
20 Oxycodone -
- Fentanyl 0.1-0.25
6
Opioids TRAMADOL
Administration Intravenous
Administration Intramuscular
Administration Oral (as soon as possible).
Dosage 50-100 mg 6h
Mechanism of action reduces serotonin and norepinephrine reuptake and is a weak opioid agonist
Side effects nausea and vomiting
Comments 100 mg is equivalent to 5-15 mg Morphine 7 is "poor metabolizers.
Oxford Analgesic League Table (NNT)
Ibuprofen 800mg 1.6
Ketorolac 60mg IM 1.8
Diclofenac 100mg 1.9
Rofecoxib 50mg 1.9
Celecoxib 400mg 1.9
Paracetamol 1G Codeine 60mg 2.2
Pethidine 100mg IM 2.9
Morphine 10mg IM 2.9
Paracetamol 1000mg 3.8
Tramadol 100mg 4.8
Adjuvant Ketamine Magnesium Corticosteroids Clo
nidine - Normopresan Dexmedetomidine -
PRECEDEX Gabapentin - Neurontin Pregabaline
- Lyrica.
7

• Epidural Analgesia
• Dosage
• The response is not the same if the same dose is
  used but in a different volume and concentration.
  
• A higher volume of a low concentration of LA will
  result in a larger number of segments blocked but
  with less dense sensory block and less motor
  block.
• Local anesthetics in epidural space produce three
  types of blocks
• sympathetic
• sensory
• motor.
• The resulted block is concentration depended, the
  sympathetic block is been appearing first.
• Postdural puncture headache (PDPH).
• Results from the tension force applied to
  meningeal and vascular structures.
• May herald incipient cerebrovascular accident.
• Treatment
• simple analgesics
• bed rest
• fluid hydration
• an epidural blood patch after 24 hours.

• Peripheral nerve block
• PNB is induced by injecting LA near the course of
  nerves or plexuses.
• Cervical plexus
• Brachial plexus
• Lumbar plexus
• Sacral plexus.
• Cervical plexus
• The cervical plexus is formed from the first four
  cervical nerves (C1-C4).
• The most common clinical use for this block is
  for carotid endarterectomy.
• ? Phrenic Nerve from C3 C4 C5
• Brachial Plexus
• Interscalene
• Supraclavicular
• Infraclavicular
• Axillary.

8
Comparison of regional analgesia techniques
Advantages Disadvantages
Continuous Epidural Analgesia (CEA) Much experience Excellent pain control over an extended period Differential block with motor sparing is possible. Motor block and urinary retention may develop Requires regular clinical monitoring May risk a spinal haematoma or abscess.
Continuous Peripheral Nerve Blocks (CPNB) Better efficacy than parenteral opioids and comparable to epidural Lower incidence of side effects than with epidural Excellent pain control over an extended period. Slower learning curve Higher incidence of technical problems.

• Regional anesthesia COMPLICATIONS.
• Intravascular injection.
• Arterial injection direct injection into the
  vertebral or carotid artery immediately manifests
  as a seizure (most common with interscalene
  block).
• The convulsant dose after an unintentional
  arterial injection is 14.4 mg of lidocaine or 3.6
  mg of bupivicaine.
• Larger doses of anesthetic are tolerated from
  venous injection.
• Unintentional subarachnoid or epidural injection.
• LA intended for plexus block may spread to the
  neuraxis.
• Interscalene block in particular has been linked
  to unintended spinal and lumbar plexus block is
  prone to epidural spread.
• Nerve damage. Regional Anesthesia.
• Direct nerve damage
• 1 in 10,0001 in 30,000
• Significant permanent nerve damage
• less than 1 in 100,000
• Spinal haematoma
• 1 in 150,0001 in 220,000
• Spinal infection
• 1 in 100,0001 in 150,000
• Nerve Damage. Central Blocks
• Direct injury caused by the needle or the
  catheter