NSAIDs are analgesic, anti-inflammatory and antipyretic. Act to inhibit cyclo-oxygenase in the spinal cord and periphery to decrease prostanoid synthesis and diminish post-injury hyperalgesia at these sites. NSAIDs reversibly inhibit cyclo-oxygenase to reduce prostaglandin and thromboxane synthesis (Fig. 10.4). Type 1 cyclo-oxygenase (COX-1) is present in gastric mucosa to produce protective prostaglandins and modulates renal function and platelet adhesiveness. Type 2 cyclo-oxygenase (COX-2) is responsible for inflammatory prostaglandins. Drugs which inhibit only COX-2 (rofecoxib, parecoxib) cause fewer gastric, renal and haemorrhagic side-effects. NSAIDs also inhibit neutrophil activation by inflammatory mediators and act centrally on the thermoregulatory centre. There is minimal protein binding with subsequent large volume of distribution.

Figure 10.4 Cyclo-oxygenase (COX) pathways.

Not generally as effective as opioids for acute pain, but reduce opioid requirements by 30–50%. May be useful in day-case surgery to avoid opioids.

Side-effects

• GI bleeding, fluid retention, asthma

• Renal failure (PGI₂ enhances Na⁺, Cl⁻ and water excretion; PGE₂ vasodilates to maintain GFR)

• Inhibit platelet function

• Blood dyscrasias

• Bowel enteropathy

• Pancreatitis

• Erythema multiforme

• Reye’s syndrome

• Anaphylaxis, urticaria

• Aseptic meningitis

• Delayed spontaneous labour.

There is no evidence that i.m. or rectal preparations reduce risk of side-effects. Advice from the Committee on Safety of Medicines recommends using the lowest possible doses to reduce the risk of GI complications.

Guidelines for the Use of Non-Steroidal Anti-Inflammatory Drugs in the Perioperative Period

Royal College of Anaesthetists 1998

Usage

NSAIDs are not sufficiently effective as the sole agent after major surgery in most patients, but are often effective after minor or moderate surgery. NSAIDs are the drug of choice after many day-case procedures.

NSAIDs often decrease opioid requirements and enhance the quality of opioid-based analgesia.

Gastrointestinal effects

GI bleeding or ulceration should be a prominent differential diagnosis in all patients receiving NSAIDs. NSAIDs should not be given to patients with a history of GI ulceration or bleeding.

Haematological effects

NSAIDs increase bleeding time and may increase blood loss. The clinical significance of a tendency to increased bleeding is unclear. It should not inhibit the use of NSAIDs in most cases if there are no specific contraindications. However, NSAIDs should not be given prior to surgery if there is an increased risk of intraoperative bleeding.

Renal effects

NSAIDs are contraindicated in renally compromised patients. Renal function should be monitored regularly in all patients taking NSAIDs after major surgery. Any increase in urea, creatinine or potassium or decreased urine output is an indication for discontinuing NSAIDs.

Other contraindications

NSAIDs are contraindicated in patients with hypovolaemia, pre-eclamptic toxaemia or uncontrolled hypertension. NSAIDs are contraindicated in aspirin-sensitive asthmatics and should be used with caution in other asthmatics. NSAIDs should be used with caution in the elderly, in patients with diabetes or vascular disease and after cardiac, hepatobiliary, renal or major vascular surgery.

Epidural anaesthesia

It is impossible to give meaningful recommendations on the safe use of NSAIDs with epidural anaesthesia.

Drug interactions

Patients taking NSAIDs should be monitored closely if they are also taking antihypertensive medication, ciclosporin (renal function) or lithium (lithium levels). NSAIDs used in the perioperative period have little clinical effect on warfarin, but INR should be checked after the start or withdrawal of treatment. Low-molecular-weight heparin may be affected by NSAIDs.

Opioids

• Narcotic – from Greek narco, meaning deaden/numb

• Morphine – from Greek Morpheus, god of dreams, son of the god of sleep.

Pharmacology. Protein binding is a major determinant of drug distribution. Albumin binds acidic drugs (e.g. morphine); α₁ acid glycoprotein (AAG) binds basic drugs (e.g. fentanyl, alfentanil, sufentanil). Neonatal albumin and AAG levels reach adult levels by 1 year.

Opioid receptors are found in high concentrations in the limbic system and spinal cord:

• μ (mu) – analgesia (μ₁), respiratory depression (μ₂), constipation

• δ (delta) – analgesia, respiratory depression, euphoria

• κ (kappa) – spinal analgesia, miosis, sedation, dysphoria, diuresis.

These opioid receptors have recently been reclassified by the International Union of Pharmacology (IUPHAR) as OP₁ (δ), OP₂ (κ) and OP₃ (μ).

Actions

• Cardiovascular: ↓ SNS drive, direct effect on vagal nucleus to ↓ HR, direct effect on SA node

• Respiratory: ↓ rate, dyscoordination, respiratory depression mediated by μ receptors. CO₂ response curve shifted to right. Depression of cough reflex

• Analgesia

• Anxiolysis (shift towards δ rhythm on EEG)

• Euphoria/dysphoria

• Histamine release via opioid receptors on mast cells. Blocked by naloxone

• GI: smooth muscle spasm, ↓ lower oesophageal sphincter tone, nausea and vomiting

• Miosis via opioid receptors on Edinger–Westphal nucleus

• Hormonal effects via D₂ receptors in hypothalamus: ↑ ADH, ↑ GH, ↑ prolactin; ↓ ACTH, ↓ FSH, ↓ LH

• Muscle rigidity via (?) opioid receptors in substantia nigra.

Routes of administration. Up to eightfold variation in minimum analgesic blood levels between patients. Therefore, no one regimen is suitable for all patients.

Oral. Delayed postoperative gastric emptying results in delayed absorption followed by large bolus absorbed when motility returns. May be of more use in the late postoperative period once bowel motility returns.

Nausea and vomiting prevent oral intake. Poor bioavailability because of first pass.

Sublingual. Systemic absorption avoids first pass. Dry mouth reduces absorption.

PR. Systemic absorption avoids first pass. Not affected by GI motility or nausea and vomiting. Slow absorption delays onset.

Transdermal. Rate of absorption ∝ lipid solubility. Reduced absorption with vasoconstriction.

Inhalational. Used for relieving symptoms of dyspnoea and postoperative pain. Some lost on expiration, widely variable absorption, nasal pruritis and cough limit its clinical application.

Intra-articular. Action via intra-articular opioid receptors.

Intranasal. Rapid onset of lipid-soluble drugs. Systemic absorption avoids first pass. Useful route for postoperative pain in children.

Subcutaneous. Useful for pain relief in children since small cannulae can be inserted with minimal distress. Use with continuous infusion or intermittent bolus.

Intramuscular. Pain of injection, erratic uptake if poor tissue perfusion, wide fluctuations in blood levels and thus degree of analgesia and side-effects. Often administered too infrequently if ‘prn’.

Intermittent intravenous injections. Avoids pain of injection but has similar problems to i.m. route. Needs 1:1 nursing care to monitor respiratory depression.

Continuous intravenous infusion. May need initial i.v. bolus dose since steady state takes five half-lives to establish. More stable blood levels, but risk of insidious onset of respiratory depression and obstructive apnoea greater than that with PCA.

Patient controlled analgesia (Fig. 10.5).

Figure 10.5 Patient controlled analgesia with intramucular morphine.

Route of choice. Less overall opioid requirements than other routes. Patient acts as feedback to prevent overdose. Patients do not have to wait after onset of pain to receive analgesia, and immediate administration gives patients a greater sense of control. Requires loading dose and correct settings of lockout time (5–10 min), dose per bolus (morphine 0.01–0.025 mg/kg) and maximum dose/hour. Suitable for most children over 5 years. Background dose increases risk of respiratory depression and does not affect total dose. Fentanyl PCA reduces pruritis compared with morphine and may also be more appropriate in renal failure. Less incidence of respiratory depression (0.1–0.8.%) when compared with i.m. opioid boluses (0.2–0.9%) or i.v. opioid infusion (1.7%). Patient concerns regarding addiction and overdose may limit effective use.

Intrathecal/extradural. Most effective when combined with local anaesthetics. Side-effects are common, especially pruritis. Respiratory depression up to 24 h.

Fentanyl Patches: Serious and Fatal Overdose from Dosing Errors, Accidental Exposure, and Inappropriate Use

MHRA Guidance 2007

• Healthcare professionals, particularly those who prescribe fentanyl patches, must fully inform patients and caregivers about directions for safe use:

– Follow the prescribed dose

– Follow the correct frequency of patch application

– Ensure that old patches are removed before applying a new one

– Patches must not be cut

– Avoid touching the adhesive side of patches and wash hands after application

– Follow instructions for safe storage and disposal of used or un-needed patches.

• Increased body temperature, exposure of patches to external heat sources, and concomitant use of CYP3A4 inhibitors may lead to potentially dangerous rises in serum fentanyl levels. Concomitant use of other CNS depressants might also potentiate adverse effects from fentanyl

• Healthcare professionals, particularly those who prescribe fentanyl patches, should ensure that patients and caregivers are aware of the signs and symptoms of fentanyl overdose, i.e. trouble breathing or shallow breathing; tiredness; extreme sleepiness or sedation; inability to think, walk, or talk normally; and feeling faint, dizzy, or confused. Patients and caregivers should be advised to seek medical attention immediately if overdose is suspected. Patients who experience serious adverse events should have the patches removed immediately and should be monitored for up to 24 h after patch removal.

α₂-Agonists (e.g. clonidine)

α₂-adrenergic receptors are located at peripheral (primary afferent terminals), spinal (neurones in the superficial laminae of the spinal cord) and brainstem sites (brainstem nuclei) where they are involved in nociceptive modulation. α₂ adrenoceptors are devoid of respiratory depressant and addictive effects, but sedation and hypotension are limiting their clinical use as an effective analgesic agent.

α₂-agonists have the following characteristics:

• Haemodynamic stabilizing properties decrease arrhythmias caused by halothane and reduce labetalol requirements in hypotensive anaesthesia

• Sedative and anxiolytic (via activation of postsynaptic α₂-adrenoceptors in the locus coeruleus of the brainstem)

• Analgesic – inhibit substance P release at dorsal root ganglia, enhance and prolong duration of epidural

• Reduced sympathetic tone (via activation of postsynaptic α₂-adrenoceptors in the nucleus tractus solitarius and locus coeruleus of the brainstem) and reduced cortisol release

• Decreased volatile and i.v. induction agent doses, decreased intraocular pressure and attenuated rise in IOP with intubation, decreased shivering.

NMDA receptor antagonists

NMDA receptors on the postsynaptic membrane of dorsal horn neurones are activated by glutamate to stimulate ascending pathways. Activation of NMDA receptors results in induction and maintenance of central sensitization during pain states. NMDA antagonists (especially those acting on the NR2β receptor subunit) may be useful in the treatment of chronic pain.

Ketamine blocks the open calcium channel of the NMDA receptor. Psychotomimetic side-effects, salivation and cardiac stimulation limit its use.

Gabapentin

Introduced for epilepsy in 1990s. High binding affinity for the α₂δ subunit of the presynaptic voltage-gated calcium channels, binding to which inhibits calcium influx and subsequent release of excitatory neurotransmitters in the pain pathways. At least as effective as morphine for postoperative analgesia and may also prevent opioid tolerance. May cause dizziness and somnolence.

Capsaicin receptor antagonists

Capsaicin is a vanilloid found in chilli peppers. Capsaicin activates the transient receptor potential ligand-gated ion channel family (TRPV1), as does heat, acidosis, cannabinoids and NADA (N-arachidonoyl-dopamine). Prolonged application of an agonist, e.g. capsaicin leads to release of central transmitters (glutamate and substance P) from nociceptive afferents and loss of function of the afferents due to exhaustion of neurotransmitters. This is the basis of the use of capsaicin cream where it has been shown to be of benefit in osteoarthritis, diabetic neuropathy, psoriasis and post-herpetic neuralgia.

The TRPV1 receptor may be upregulated in some disease states e.g. osteoarthritis, post-herpetic neuralgia, cancer-induced bone pain. TPRV1 antagonists may be an important new class of analgesic agents.

Transcutaneous electrical nerve stimulation (TENS)

May act through the gate control theory of pain and by release of endorphins. Usually applied at 70 Hz. May take several days of use to achieve maximal effect. Most effective with neurogenic pain, such as phantom limb pain, postherpetic neuralgia or nerve damage. Little evidence of efficacy in severe pain, e.g. childbirth.

Chronic pain

Defined as pain which persists past the time when healing is expected to be complete, usually more than 6 months.

Definition of pain terms

• Allodynia – pain due to a stimulus which does not normally cause pain

• Dysaesthesia – an unpleasant abnormal sensation, whether spontaneous or evoked

• Hyperpathia – a painful syndrome, characterized by increased reaction to a stimulus, as well as increased threshold

• Hyperalgesia – an increased response to a stimulus which is normally painful

Neuropathic pain is defined as: pain initiated or caused by a primary lesion or dysfunction in the nervous system. Covers a wide spectrum of clinical conditions:

• Trauma: spinal cord injury, phantom limb pain, reflex sympathetic dystrophy

• Ischaemic injury: painful diabetic neuropathy

• Infection/inflammation: post-herpetic neuralgia, reflex sympathetic dystrophy

• Cancer: invasion/compression of neuronal structures

• Drugs: vinca alkaloids

• Compression: sciatica, trigeminal neuralgia

• Unknown: trigeminal neuralgia, multiple sclerosis.

Reflex sympathetic dystrophy

Reflex sympathetic dystrophy (RSD) is now classified by the International Association for the Study of Pain as complex regional pain syndrome (CRPS) type I, and when associated with nerve injury (i.e. causalgia) it is known as CRPS type II.

CRPS type I (RSD). A syndrome that usually follows an initiating noxious event, with spontaneous pain or allodynia/hyperalgesia occurring in a regional distribution and not limited to the territory of a single peripheral nerve. Results in continuous pain in a portion of an extremity (not involving nerve damage), associated with sympathetic hyperactivity.

Characterized by:

1. Pain. Initial pain and burning become more diffuse and aching. Hyperalgesia and allodynia may be present.

2. Autonomic dysfunction. Abnormal skin blood flow causes both warm red skin and cold, cyanotic changes. Oedema occurs in 50% due to postcapillary vasoconstriction. Following nerve damage, C-polymodal nociceptors in the dorsal horn of the spinal cord develop increased sensitivity to sympathetic stimulation. Stimulation of these causes excess firing, which then causes increased pain and discharge of sympathetic neurones to the traumatized tissue. The increased sympathetic tone sensitizes peripheral chemoreceptors to such an extent that they fire without a stimulus, causing chronic sympathetically mediated pain. (This concept of central sensitization of the CNS may also be involved with mechanisms of pre-emptive analgesia.)

3. Trophic changes. Muscle wasting, thin shiny skin, coarse hair and thickened nails are late manifestations.

4. Motor impairment. Weakness and tremor (not necessary for diagnosis). Traditionally divided into three stages, but may not progress beyond the second:

• Acute stage – days to months after injury. Pain and oedema. Warm, dry red skin. Treatment most effective at this stage: physiotherapy, NSAIDs, antidepressants and sympathetic nerve block.

• Dystrophic stage – 3–6 months after onset of symptoms. Burning pain may spread to involve whole limb. Muscle wasting, pale cyanotic skin associated with increased sympathetic activity. Decreased hair and nail growth, muscle wasting and disuse osteoporosis.

• Atrophic stage – 6–12 months after onset of symptoms. Pain may diminish. Cool limb, contractures and severe osteoporosis. Physiotherapy is the most effective treatment at this stage.

CRPS type II (causalgia – Greek: kausis = burning; algos = pain). Similar to RSD but associated with traumatic nerve injury. Onset may be delayed for several months. Commonest nerves are median, sciatic, tibial and ulnar.

Postherpetic neuralgia

Pain in the area of acute herpes zoster for at least 1 month after the initial infection. Incidence increases with age; female > male. Pain intensity during acute herpes zoster predicts severity of post-herpetic neuralgia. Predilection for thoracic dermatomes and ophthalmic division of trigeminal nerve. Sharp, burning pain. Due to damage of large myelinated fibres which removes inhibition to nociceptive input. Central neurones also expand receptor fields to produce allodynia and hyperpathia.

Early aggressive treatment reduces incidence of pain. Use antidepressants, anticonvulsants, neuroleptics, TENS, sympathetic blocks and topical local anaesthetics. Capsaicin cream enhances release and prevents reaccumulation of substance P from central and peripheral nerve terminals and may be of benefit.

Trigeminal neuralgia

Usually a primary neuralgia, but 3% of cases are due to MS, tumours, vascular malformation or dental lesions. Paroxysmal lancing pain, triggered by tactile stimulation, lasting a few seconds. Increasing severity and frequency of attacks as disease progresses. Anticonvulsants such as carbamazepine block sodium channels to reduce neuronal firing. Phenytoin, sodium valproate and clonazepam may also be effective. Vascular decompression and radiofrequency ablation may benefit some patients.

Postoperative pain

In a UK study (Kuhn et al 1990), 93% of patients described their postoperative pain as moderate (53%) or very painful (40%). Attempts have therefore been made to improve pain services.

Anaesthesia Under Examination – The Efficiency and Effectiveness of Anaesthesia and Pain Relief Services in England and Wales

Audit Commission 1997

Findings

• Many patients still suffer postoperative pain and some hospitals are better at controlling it than others.

• Some hospitals do not have guidelines regarding postoperative pain management and those that do often do not follow them.

• The availability of PCA pumps varies between hospitals. The majority of patients are more satisfied with PCA than with conventional administration of analgesics. There are, however, significant numbers of patients using PCA experiencing poor analgesia or nausea and vomiting.

• The use of epidural analgesia for major abdominal and thoracic surgery is increasing, but its use is limited by inadequate numbers of nurses trained in its management.

• Patients’ analgesia is often changed too quickly from strong opioids to minor analgesics, allowing breakthrough of pain.

Recommendations

• Develop specific targets to reduce the number of patients in severe pain after an operation.

• Identify one doctor with specialist knowledge of pain relief techniques to promote good practice.

• Carry out regular audit of pain relief targets.

• Develop evidence-based guidelines on effective analgesic therapies.

• The acute pain team should provide written information and guidelines, coordinate and educate staff, and provide leadership and a focus for improved team working.

• Develop a programme of continuing education in pain management for trainee doctors and nurses.

Bibliography

www.aagbi.org/publications/guidelines/docs/epidanalg04.pdf. Reproduced with the kind permission of the Association of anaesthetists of Great Britain and Ireland.

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Epidural and spinal anaesthesia

Anatomy

Spinal dura is continuous with the meningeal layer of the dura mater of the brain. Vertebral canal periosteum is continuous with the outer layer of the cerebral dura.

Boundaries of the epidural space are:

• superior: foramen magnum

• inferior: sacrococcygeal membrane

• lateral: intervertebral foramina and pedicles

• anterior: posterior longitudinal ligament.

Epidural space contains dural sac, spinal nerve roots, spinal arteries, venous plexus, fat and lymphatics. It is widest in the mid-lumbar region (5–6 mm) and narrows cranially to 1.5–2 mm in the lower cervical spine. Veins are valveless; therefore fluid/air injected into vein passes to intracerebral vessels. Veins drain via azygous vein to IVC. Vena caval obstruction, e.g. pregnancy, distends veins. Intervertebral foramina smaller and calcified in the elderly; therefore smaller volumes of LA required.

Negative pressures in epidural space may be due to coning of the dura at the tip of the epidural needle, pressure transmitted from the thorax, drag of gut viscera on paravertebral spaces or differential growth of the subarachnoid space more than the spinal cord.

When supine, highest point on curve of spine is at L₃; lowest point is at T₆.

Indications for regional anaesthesia

Patient assessment

Allows assessment of mental state during surgery, e.g. TURP, carotid endarterectomy, diabetes. Avoids risks of aspiration and management of difficult airway.

Cardiac disease

Avoids haemodynamic response to intubation and hypotensive effects of induction and maintenance agents. Can therefore give greater haemodynamic stability than GA for patients with ischaemic heart disease or failure if managed carefully. May reduce early postoperative mortality compared with GA in high-risk patients. Not shown to reduce reinfarction rate compared with GA, but when used for general and vascular surgery, may reduce postoperative cardiac failure (Yeager et al 1987).

Decreased SVR increases cardiac output providing venous return is maintained. Reduced diastolic may reduce coronary artery perfusion pressure. Blockade of cardioaccelerator fibres (T₁–T₄) may cause bradycardia and impaired cardiovascular response to hypovolaemia.

Pregnant patients with severe cardiac disease, e.g. aortic stenosis, Fallot’s, Eisenmenger’s and pulmonary hypertension, require good analgesia during labour to prevent potentially dangerous hypertension and tachycardia. However, serious complications can occur following large decreases in systemic vascular resistance and cardiac output.

Respiratory disease

Epidurals produce longer analgesia and better respiratory function (FEV₁ and PEFR) than i.v. morphine. May reduce postoperative respiratory complications by avoiding effects of systemic opioids.

Gastrointestinal

For GI surgery, an epidural results in good operating conditions, reduces blood loss and gives good postoperative analgesia. However, any hypotension may reduce mesenteric blood flow, and sympathetic blockade may result in a relative increase in parasympathetic activity, causing anastomotic disruption.

Obesity

Regional anaesthesia avoids managing a difficult airway with risk of aspiration. Postoperative analgesia using epidural opioids provides earlier ambulation, fewer respiratory complications and earlier discharge compared with i.m. opioids.

Pregnancy

Avoids difficult airway, risk of aspiration and fetal depression with GA. Good postoperative analgesia avoids use of systemic opioids, which contaminate breast milk and impair maternal nursing (drowsiness, nausea and vomiting).

Malignant hyperthermia

Local anaesthetics do not trigger malignant hyperthermia. Use of epidural avoids triggering agents used for GA.

Muscle disease

Epidurals allow avoidance of muscle relaxants in myasthenia gravis, muscular dystrophy and myotonic dystrophy.

Other advantages of regional anaesthesia

• Decreases neuroendocrine stress response and postoperative negative nitrogen balance with less hyperglycaemia because of reduced catecholamine release

• Decreases blood loss

• Decreases incidence of DVT and avoids morbidity of general anaesthetic

• May have a role in pre-emptive analgesia

• Reduces incidence of phantom limb pain if established >3 days prior to limb amputation.

Yeager et al (1987) investigated 53 high-risk patients. One group had epidural with LA combined with light GA, while a second group had GA with high-dose fentanyl. Postoperative analgesia was given with i.m./i.v. opioids ± epidural. Those with epidural had significantly reduced postoperative complications, cardiovascular failure, infection and hospital costs.