Define pain, acute pain and chronic pain

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.

Acute painLess than 3 months

Sub-acute3-6 months

Chronic PainLonger than 6 months

Outline the elements of a basic pain history

Site of paino Primary locationo Radiation

Circumstances associated with pain onseto Detains of trauma or surgery

Character of paino Sensory description

Sharp Throbbing Aching Neuropathic

Intensity of paino At resto On movemento Temporal factors

Duration Current pain, during last week, highest level Continuous or intermittent

o Aggravating or relieving factors Associated symptoms Effect of pain on activities and sleep Treatment

o Current and previous medicationso Other treatmento Health professionals consulted

Relevant medical historyo Prior or existing pain conditions and treatment outcomeso Prior or coexisting medical conditions

Factors influencing the patients symptomatic treatmento Belief concerning the causes of paino Knowledge, expectations and preferences of pain managemento Expectations of outcome of pain treatmento Reduction in pain required for patient satisfaction or to resume reasonable activitieso Typical coping response for stress or pain including presence of anxiety or psychiatric disorderso Family expectations and beliefs about pain, stress and postoperative course

Outline the basic concepts of multimodal analgesia and pre- emptive analgesia

Multimodal analgesia

Pain involves multiple mechanisms that ideally require treatment using a multimodal (or ‘balanced’) analgesic technique with the aim of improving analgesia by combining analgesics with additive or synergistic effects.

Combines classes of drugs and techniques that target more than 1 pain mechanism (eg, opioids plus NSAIDs)

Provides a way to reduce doses—and adverse effects— of individual agents

Pre-emptive analgesia

Transmission of pain signals evoked by tissue damage leads to sensitization of the peripheral and central pain pathways. Pre-emptive analgesia is a treatment that is initiated before the surgical procedure in order to reduce this sensitization. Owing to this ‘protective’ effect on the nociceptive system, pre-emptive analgesia has the potential to be more effective than a similar analgesic treatment initiated after surgery.

Pain signals from damaged tissue are not transmitted to the central nervous system (CNS) through ‘hard-wired’ pathways.

In contrast, nociceptive signals, once initiated, will launch a cascade of alterations in the somatosensory system, including an increase in the responsiveness of both peripheral and central neurons.

These alterations will increase the response to subsequent stimuli and thus amplify pain

Pre-emptive analgesia is a treatment that is initiated before and is operational during the surgical procedure in order to reduce the physiological consequences of nociceptive transmission provoked by the procedure. Owing to this ‘protective’ effect on the nociceptive pathways, pre-emptive analgesia has the potential to be more effective than a similar analgesic treatment initiated after surgery. Consequently, immediate postoperative pain may be reduced and the development of chronic pain may be prevented.

Outline the basic pharmacology and clinical use of the following analgesic agents:

Opioids (morphine, fentanyl, oxycodone, codeine) Opiate – all naturally occurring substances with morphine like propertiesOpioid receptor agonistParticularly Mu

Mu 1o Supraspinal analgesiao Euphoriao Serenity

Mu 2o Respiratory depressiono Sedationo Vomitingo Pruritiso Dependenceo Urinary retentiono Anorexiao Prolactin releaseo Delayed GI transito Bradycardia

Opioids produce their effect by acting as agonists at opioid receptors, which are found in the brain, spinal cord and sites outside the central nervous system – urinary tract, GI tract, lung, peripheral nerve endings.

Mu, delta, kappa

Delta Analgesia

Kappa Analgesia Sedation Psychotomimetic effects Dysphoria Diuresis

OxycodoneA: 50- 87% bioavailability‐D: 2.6L/Kg, 45% protein bound, pKa = 8.9M: extensive hepatic metabolism via CYP 450 3A to nor oxycodone (active) and various other conjugation glucuronidesE: renal elimination 19% free drug, 64% conjugated drugElimination half life = 3hrsClearance = 800ml/min

MorphineA: 30% bioavailability, high hepatic extraction ratioD: 3-5L/Kg, 35% protein bound, pKa = 7.9M: conjugation with glucuronic acid in liver and kidneys80% metabolized to morphine-3-glucoronide (inactive)10% metabolized to morphine-6-glucoronide (active)5% is demethylated to normorphinesmall amount converted to codieneE: renal elimination 7-10% biliary excretion1-2% unchanged in urineElimination half life = 1.7-3.3hrsClearance = 23ml/min/kg

FentanylA: 100%D: high lipid solubility84% protein boundVd = 0.88-4L/KgM: most undergoes demethylation and hydroxylation in the liver

The drug acts in 2-5 minutes when administered intravenously; a small dose has a duration of action of 30-60 minutesFentanyl is more lipid soluble than morphine (x800) and thus crosses the blood-brain barrier more easily; it thus has a more rapid onset of action than morphine.

CodeineA phenanthrene alkaloid which is a methylated morphine derivative.

Codeine has a very low affinity for opioid receptors; 10% of the drug is metabolised to morphine and the analgesic and constipating effects of the drug are probably mediated by opioid receptors. The antitussive effects of codeine appear to be mediated by specific, high affinity codeine receptors.

A: 60-70% bioavailabilityD: 7% protein boundVd = 5.4 L/KgM: 10% demethylated in liver to form morphineRemainder metabolised to norcodeine or conjugated to glucoronidesE: mostly in urine as free unconjugated codeine, norcodeine and morphine<17% excreted unchangedELH = 2.8hrsClearance = 98L/hr

Exhibits genetic polymorphism so that poor metabolizers may experience little pain relief (~10% of people)

NSAIDs

Analgesic Anti-inflammatory Antiplatelet Antipyretic

Cyclo-oxygenase inhibitors – synthesis of prostaglandins, prostacyclins, thromboxane A2 from arachidonic acid

Rapidly absorbed in upper GI tract Peak plasma levels reached after about 2hrs (PO administration) Metabolized in liver Excreted in kidney When used in combination enhance quality of analgesia Reduce opioid use – 20-40%

Side Effects Reduction of prostaglandins

o can lead to GI erosionso decreased RBF and ARFo Na, K and water retention

Aggregation of platelets depends on thromboxane A2 – reduced formation due to COX inhibition – prolonged bleeding times

Bronchospasm due to COX inhibition

COX 1 Present in most body tissues where prostaglandin production helps maintain normal organ function Inhibition is thought to be responsible for most of the adverse effects

COX 2 Is inducible Produced as a result of inflammation or tissue damage Inhibition will have mainly analgesic and anti-inflammatory effects

Tramadol

Atypical opioid agonist with high affinity to Mu receptor.Tramadol hydrochloride is an atypical central-acting opioid. The advantages of tramadol over traditional opioids are the minimal potential for tolerance, for addiction and for respiratory depressionIt also inhibits neuronal reuptake of noradrenaline and enhances serotonin (5-HT) release

A: 70% bioavaiability orallyD: 20% protein boundVd = 2-4L/KgM: 85% metabolized by demethylation in the liver to O-demethyl tramadol (active)E: 90% in urine10% in faecesClearance = 6-10ml/kg/minEHL = 4-7hrs

No clinically significant CVS effectsRespiratory rate essentially nchangedCNS – analgesic potency equivalent to pethadinePartially reversed by naloxone (30%)

Toxic side effectsNausea and vomiting, dizziness, sedation and diaphoresisCan minimize nausea by administering the drug slowly

Paracetamol

Inhibition of prostaglandin synthesis within the CNS Analgesic Antipyretic No anti-inflammatory effect Mostly excreted by the kidney after glucoronide and sulfate conjugation in liver Small amount metabolized to N-acetyl-benzoquinoneimine – hepatotoxic

o Normally inactivated by conjugation with hepatic glutathione (when depleted you get toxicity) Its antipyretic effect is due to prostaglandin inhibition in the thermoregulatory centre in the hypothalamus It acts peripherally by blocking impulse generation within the bradykinin-sensitive chemoreceptors

responsible for the generation of afferent nociceptive impulses. Paracetamol is a weak prostaglandin inhibitor 0-5% protein bound in the plasma; VD is 1 1/kg. Rapidly absorbed from the upper gastrointestinal tract; the bioavailability when administered by the oral

route is 70-90% due to first-pass metabolism.

Ketamine

Wind up – spinal cord neurons show progressively greater response to repetitive but constant intensity stimuliNMDA receptor located in spinal cord are involved in wind up and involved in many types of pain – inflammatory, ischemic, neuropathic

NMDA receptor antagonistExcellent analgesia at sub anaesthetic doses

A: oral bioavailability = 20%D: 12% protein boundVD is 3 l/kg. Distribution half life = 11minsM: N-demethylation and hydroxylationE: conjugated metabolites excreted in urineClearance = 17ml/kg.minEHL = 2.5hrs

Side effectsCNSThe state of dissociative anaesthesia is produced by the drug. The cerebral blood flow, cerebral metabolic rate, intraocular pressure increased; amnesia is a marked feature.

Hallucinations, bad dreams

CVStachycardia, an increase in the blood pressure, central venous pressure and cardiac output secondary to an increase in sympathetic tone.

Outline clinical situations where the use of analgesic agents may be associated with increased risk to the patient and requires consultation with supervisors for the initiation of therapy

Patients with complex chronic pain issues Drug seekers Patients with severe OSA/obesity Patients with multiple allergies to analgesics Respiratory failure, serotonergic syndrome

Outline the principles of acute pain management and the assessment of analgesic efficacy and adverse effects as contained in the College professional document PS41 Guidelines on Acute Pain Managemen t

Pain is associated with negative outcomes, its treatment is humane, unrelieved pain increases risk of a chronic pain pathway becoming established. The use of protocols decreases risk and improves quality of treatment and min. sfx and cx therof. Groups at risk of pain/mismanagement/difficulty in management – pregnancy, paeds, opioid tolerant, disabled, frail/unwell, indigenous, non-english speaking, organ dysfunction

Adverse physiological and psychological effects may result from unrelieved severe acute pain. Effective treatment of postoperative pain may reduce the incidence of postoperative morbidity and facilitate earlier

discharge from hospital. Preventive treatment of postoperative pain may reduce the incidence of chronic pain. Effective management of acute pain requires tailoring of treatment regimens to the individual patient. Effective management of acute pain depends on close liaison with and education and training of all staff, and involvement

and education of the patient and their carers. Effective management of acute pain depends on formal protocols and guidelines covering acute pain management which

are relevant to each institution; and formal quality assurance programs to regularly evaluate the effectiveness of acute pain management.

The following groups of patients have special needs that require particular attention:o Childreno Pregnant patients.o Elderly patients. o Aboriginal and Torres Strait Islander People. o Maori. o Other ethnic groups and non-English speaking people. o Patients with obstructive sleep apnoea. o Patients with concurrent hepatic or renal disease. o Opioid-tolerant patients. o Patients with a substance abuse disorder. o Patients with cognitive behavioural and/or sensory impairments.

Outline a protocol for the management of pain in recovery

Multiple protocols existMorphine 10mg in 10mlsFentanyl 100mcg in 10ml Hydromorphone 1mg in 10mlOxycodone 10mg in 10mls

We commonly use fentanyl or oxycodone

Patient < 70yrs oldModerate Pain = give 1 ml Severe Pain = give 2 mls

Wait 3 minutes Assess pain and sedation scores Repeat until pain score ≤ 3

Patient ≥ 70yrs old Moderate Pain = give 0.5 mlSevere Pain = give 1 ml

Wait 5 minutes Assess pain and sedation scores Repeat until pain score ≤ 3

Pain Score ≤ 3 (up to 10mls administered) if yes can start regular analgesia if no review by anaesthetist may repeat protocol.

Outline a pain management plan for patients having day surgery procedures

Central neuraxial blockade and a range of regional anaesthetic techniques, including brachial plexus and paravertebral blocks, can be used effectively for day surgery

Analgesia is paramount and must be long acting but, as morbidity such as nausea and vomiting must be minimised, the indiscriminate use of opioids is discouraged (particularly morphine). Prophylactic oral analgesics with long-acting non-steroidal anti- inflammatory drugs (NSAIDs) should be given to all patients if not contraindicated. For certain procedures (e.g. laparoscopic cholecystectomy)there is evidence that standardised anaesthesia protocols or techniques improve outcome.

Multimodal approach with the indiscriminate use of opioids discouraged. Use NSAIDs, such as paracoxib, minimal fentanyl, regional techniques could be employed. Antiemetics are paramount in day cases as nausea will stop people from being discharged.

Outline the risks associated with and the monitoring requirements for patients receiving patient-controlled analgesia (PCA), opioid infusions or continuous regional analgesia for acute pain management

PCARisksProblems that may occur with PCA include allergic reactions to the medications and adverse side effects such as nausea, a dangerous drop in the rate and effectiveness of breathing, and excessive sedation. The PCA device must be monitored frequently to prevent tampering. Even sophisticated devices that monitor themselves and sound an alarm should be checked often, since no machine is perfect. Ineffective pain control must be assessed to determine whether the problem stems from inadequate dosage or from inability, or unwillingness, of the patient to carry out his or her own pain management.

Monitoring requirementsSedation score

Respiratory rate should be greater than ?Total amount of opioid deliveredSide effects and treatmentsPain scoresVAS

These parameters should be monitored at regular intervals.

Opioid infusionsAim is to avoid problems associated with the peaks and troughs of intermittent administration.

RisksCan have a delay between alteration of the infusion rate and its subsequent effect – may have delayed onset of side effects such as respiratory depressionMonitoringVery close monitoring requiredShouldn’t be employed on the ward without close monitoring of sedation score and respiratory rate.Usually used in ICU but can have backgrounds on the ward

Continuous regional analgesia

Epidural - RisksVasodilation leading to hypotension – give continuous IV fluids and slow titration of local anaestheticDural puncture – post dural puncture headacheRespiratory depression – early within 2hrs, late 6-12hrsSedation, N & VPruritisUrinary retentionMotor/sensory block

MonitoringBromage score

Regional nerve cathetersRisksInfectionBleedingNerve damageMotor blockLocal anaesthestic toxicityfailure

Monitoring Muscle strengthSiteSigns of toxicity

Outline the problems in managing acute pain for patients with chronic prior exposure to opioids

Tolerance to the effects of postoperative opioids, resulting in unrelieved pain or opioid withdrawal reaction, may be a problem in patients who have been taking opioids for more than 2 weeks before surgery.

Physical dependence means that a postoperative baseline opioid requirement is necessary to prevent withdrawal reactions.

Postoperative opioid requirements may be more or less than preoperative levels, depending on the effect of surgery.

Use of adjuvant analgesic drugs and regional techniques will result in ‘opioid-sparing’ effects and a reduction in the postoperative baseline opioid requirement.

Tolerance - This is defined as ‘a phenomenon in which exposure to a drug results in the diminution of an effect or the need for a higher dose to maintain an effect’.Describe the assessment and adjustment of continuous regional techniques for acute pain control

The overall aim in both groups is to control pain while avoiding overdose and withdrawal symptoms; no attempt should be made to withdraw opioids during the perioperative period.

Tolerant patients may require higher doses of opioid than opioid naïve patients.Tolerance to N&V, cognitive impairment, sedation and respiratory depression occurs rapidly. To constipation and miosis develops very slowly if at all.

Opioid rotation – use of alternate opioids especially if inadequate analgesia and or side effects are seen with increased doses.

Aims of treatment Provision of analgesia Prevention of withdrawal Management of withdrawal from other drugs Involvement of multidisciplinary and/or other specialist teams and treatment of comorbidities (eg depression) as

needed Management of aberrant drug-taking behaviours

These patients may report higher pain scores so they may not be as reliable. Need to have objective assessment of function –

Functional activity score A – No limitation meaning the patient’s activity is unrestricted by painB – Mild limitation means the patient’s activity is mild to moderately restricted by painC - Severe limitation means the patient ability to perform the activity is severely limited by pain

Local anaesthetic blocksNSAIDsKetamine – NMDA receptor antagonist

Multidisciplinary team Palliative care Chronic pain Psychiatry Drug and alcohol

Describe the advantages and disadvantages of patient- controlled analgesia (PCA), continuous infusion and intermittent prescription of opioids for acute pain management

Advantages DisadvantagesPCA Patient is in control of

pain management Faster alleviation Dosage monitoring –

can be increased or decreased depending on use

No change in side effect compared to other methods

Possibility of underdosing and overdosing

Not good for people with little understanding/confusion

Poor dexterity can be an issue

Continuous infusion Provides the most rapid onset of analgesia

Provides a consistent level of analgesia

Helps in identifying opioid nonresponsive pain quickly so other pain control strategies can be considered early

Good for those unable to push the PCA button

Requires prolonged venous access via central or peripheral catheter

Local irritation of skin may occur

Intravenous catheters can lead to infection

Requires initial close supervision, and continuity of skilled medical and nursing care

Increased risk of complication if unmonitored ie respiratory depression

Intermittent opioids Medication given when it is needed

If titrated properly provides flexibility needed to cover the changes in pain stimulus

Often delay in receiving medication

Peaks and troughs Periods of inadequate

pain relief Increased risk of

inadvertent overdose and complications

Outline the management of hypotension associated with a central neuraxial block

Severe hypotension may be the result of vasodilatation, bradycardia, and decreased contractility. Volume loading the patient with 10-20 ml/kg of crystalloid fluid or appropriate amount of colloid immediately prior and during the administration of a spinal anesthetic may be helpful. The patient’s cardiac function and medical history should be taken into account prior to this measure. Left uterine displacement is essential for the parturient. Trendelenburg position may help increase blood pressure by autotransfusion. Care must be taken not to extend the neuraxial blockade even higher.Hypotension should be treated with metaraminol, a direct acting alpha adrenergic agonist, which increases venous tone and causes arterial constriction.Ephedrine has a direct beta adrenergic effect, increasing heart rate and contractility as well as some indirect vasoconstriction (α).

Pre loading with fluid Trendelenberg position if possible

o Care to not extend the blockade even higher Treat with metaraminol

o Direct and indirect acting sympathomimetic agent that has agonist effects at both alpha and beta adrenoreceptors

o Alpha agonist activity predominateso Peripheral vasoconstriction

Increases SVR Increases preload

Ephedrine can also be usedo Ephedrine acts both indirectly (by causing release of noradrenaline from sympathetic nerve terminals) and

directly by stimulation of alpha- and beta -adrenoreceptors.

Phenylephrine is a direct- acting sympathomimetic agent that has agonist effects at alpha- adrenoceptors. The dose that stimulates alpha1 receptors is far less than the dose needed to stimulate alpha2 receptors. Clinically, phenylephrine mimics the effects of noradrenaline, but is less potent and longer lasting

Outline the management of ‘high spinal’ block (also refer to the Regional and local anaesthesia and resuscitation, trauma and crisis management clinical fundamentals)

High neural blockade can occur with either epidural or spinal anesthesia. This complication may be due to the administration of excessive doses of local anesthetic, failure to reduce doses in patients susceptible to excessive spread (i.e. elderly, pregnant, obese, or short patients), increased sensitivity, and excessive spread. When dosing a spinal or epidural, it is important to monitor the patients’ vital signs and block level.

Incremental dosing of epidurals allows the anesthesia provider to determine if the block is progressing more rapidly than anticipated. With hyperbaric spinal techniques, changing the patients’ position may slow down excessive spread. Prevention is based on careful consideration in the dosing of the neuraxial block, anticipation of potential complications, and continual monitoring of the blocks progression.

Cardioaccelerator fibres found in T1 to T4. This leaves unopposed vagal tone to the heart.

Initial symptoms include the following: dyspnoea numbness or weakness of the upper extremities (i.e. tingling in the fingers) nausea will usually precede hypotension (hypoperfusion of the brain is responsible for nausea) mild to moderate hypotension

Management is supportive and dependent on the degree and height of the block. Early recognition is important to stop block progression – reverse Trendelenberg/head raised. Serious cardio-respiratory compromise can be avoided.

Outline a plan to transition patients with acute pain from parenteral to oral analgesic therapies (in low complexity cases)

Assess 24hr usage of opioid and determine whether it is possible to change to oral medication. If tolerating oral intake it is good to change to orals as soon as possible.

IV morphine to IV oxycodone 10mg = 10mg

IV fentanyl to IV oxycodone150mcg = 10mg300mcg = 20mg

IV oxycodone to PO oxycodone10mg = 20mg

eg. 1300mcg of fentanyl 1300/150 x 10 = 86.67mg of IV oxycodone86.87 x 2 = 173.3mg of PO oxycodone in 24hrs

Halve this and divide by six to get mid range hrly PRN dose

173.3/2 = 86.67mg/6 = 14mg

Therefore give range of 10-20mg 1hrly PRN

Need to make sure this is age appropriate – if elderly, may not be able to tolerate large doses of PRN opioid therefore care should be taken.

Outline the contribution of psychosocial factors to the patient’s experience of pain