Complications of regional anaesthesia - Wiley Online Library

Anaesthesia, 2010, 65 (Suppl. 1), pages 105–115 doi:10.1111/j.1365-2044.2009.06205.x .....................................................................................................................................................................................................................

Complications of regional anaesthesia J. Picard1 and T. Meek2 1 Consultant, Department of Anaesthesia, Charing Cross Hospital, London, UK 2 Consultant, Department of Anaesthesia, James Cook University Hospital, Middlesbrough, UK Summary

Regional anaesthesia can marvellously dull the pain (and limit some other complications) of trauma, surgery and childbirth. But like all powerful techniques, it may have complications. Here the complications of regional anaesthesia are reviewed. The risks, presentation and the management of these complications are discussed in turn. . ......................................................................................................

Correspondence to: Dr John Picard E-mail: [email protected]

Regional anaesthesia is a marvellous thing, but, like all of life’s greatest pleasures, it carries risk. This article is not a comprehensive review of these risks; rather, it is a partisan selection: it may serve as a salutary warning for the over enthusiastic and a reassurance for the excessively hesitant. In general, regional anaesthesia is extremely safe, which just occasionally makes things awkward: the incidence of complications can be estimated only from extremely large samples spread awkwardly through different hospitals or over a long period. Patients and their attendants often have distorted views of the risks involved and, according to recent headlines, they expect either complete safety or certain catastrophe. It also means that academic journals publish case reports of individual complications. These necessarily include a diagnosis and a proposed mechanism, rarefied as they may be. However, clinicians initially managing a complication face a syndrome and a diagnostic conundrum. Hence, the remaining paragraphs are arranged by syndrome. Cardiopulmonary collapse

Regional anaesthesia only rarely causes cardiopulmonary collapse. For example, in the Royal College of Anaesthetists’ 3rd National Audit Project, conducted in 2006– 7 in the UK, there were only five cases of cardiovascular collapse amongst an estimated 707 425 neuraxial blocks (0.35 in 50 000) [1]. A prospective study in France in 1998–9 found that regional anaesthesia led to cardiopulmonary resuscitation or assisted ventilation after only 17 anaesthetics amongst 158 083 cases (5.38 in 50 000) and in a Brazilian teaching hospital, 11 cardiac arrests were 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

attributable to regional anaesthesia amongst 21 019 neuraxial and plexus blocks between 1996 and 2005 (7.14 in 50 000) [2, 3]. An optimist might conclude that regional anaesthesia has become suddenly safer; differences in casemix and error in recording events are more likely to account for the variation. The differential diagnosis of a cardiovascular collapse associated with regional anaesthesia includes a number of causes. Local anaesthetic intoxication The incidence of local anaesthetic (LA) intoxication is unknown [4]. It may even pass unrecognised [5]. It can cause mild transitory symptoms (such as classic circumoral paraesthesia) or progress to cardiac arrest. It may occur immediately after injection of a substantial dose of LA (presumably because of an accidental intravascular injection) or approximately 10–60 min later through excess systemic absorption or slowed metabolism. If LA infusions are in use, and if it is possible to attach the line to an intravenous giving set rather than a perineural or epidural catheter, it may happen even days after surgery. Severe LA intoxication may be associated with tonic-clonic seizure, transitory hypertension, bradycardia, conduction block, tachyarrhythmia, electromechanical dissociation and asystole. If a patient suffers a cardiovascular collapse and a large dose of LA has recently been given, or if an infusion is underway, then LA intoxication is difficult immediately to exclude. Until recently LA intoxication has had a grim prognosis: cardiac arrest was particularly refractory to conventional resuscitation. More recently, evidence has gathered that lipid emulsion is an effective antidote. Of 105

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J. Picard and T. Meek Complications of regional anaesthesia Anaesthesia, 2010, 65 (Suppl. 1), pages 105–115 . ....................................................................................................................................................................................................................

course, there are no controlled trials of lipid in human cases of LA overdose; severe LA intoxication is too rare, too dangerous and too unpredictable to allow patients to be recruited ethically. But there are supportive animal studies and also a gathering series of case reports of lipid’s efficacy. The state of the art has recently been described [6, 7]. The Association of Anaesthetists of Great Britain & Ireland issued guidelines for the management of LA intoxication and recommended that a litre of 20% IntralipidTM (Fresenius Kabi Ltd, Runcorn, UK) be immediately available to all patients receiving potentially cardiotoxic doses of LA [8]. Overwhelming sympathetic block Regional anaesthesia is often associated with a sympathetic block. The extent of the sympatholysis depends upon the spread of the LA. It is most significant when both legs, the splanchnic circulation, or all three, are affected by a spinal or epidural block. Some patients are particularly intolerant of this decrease in systemic vascular resistance. Anaesthetic tradition identifies aortic stenosis and spinal anaesthesia as a particularly malignant combination. The facts are more complex. Patients with aortic stenosis may succumb after spinal anaesthesia, but also after epidural or even general anaesthesia [9]. Conversely, other pathologies may make patients intolerant of sudden changes in systemic vascular resistance. The Brazilian survey reports a cardiac arrest in a patient with mixed mitral valve disease after a spinal, for example [3]. Moreover, there are reports of patients with significant aortic stenosis undergoing successful neuraxial anaesthesia [10]. The patient’s homeostasis is perhaps best maintained when the sympatholysis is matched by exogenous vasoconstrictors. In practice, this often involves titrating an infusion of vasoconstrictor against beat-to-beat measurement of arterial blood pressure. The titration may be smoother if the onset of changes in vascular resistance is incremental, following injection of successive small doses through an epidural or intrathecal catheter, rather than a single-shot injection [11–13]. Vaso vagal reactions The development of extreme bradycardia, even asystole, in previously fit patients has been described after regional anaesthesia in two settings: in awake, sitting patients after an interscalene block; and after a spinal anaesthetic. In patients sitting awake after an interscalene block, bradycardia associated with significant hypotension occurs comparatively frequently. Reported series record incidences of 13–28% [14]. The Bezold-Jarisch reflex has been implicated: the combination of pre-operative star106

vation and the sitting position is purported to reduce ventricular filling; meanwhile, position, anxiety and any exogenous adrenaline absorbed systemically cause vigorous ventricular contraction. If the ventricular walls touch in systole, an overwhelming vagal outflow may follow, producing profound bradycardia or asystole [15]. Omission of adrenaline from the LA injectate has been suggested as a way to decrease the incidence of such reactions [16]. Patients receiving long-term beta blockade may (or may not) be protected, and acute prophylactic beta blockade with intravenous metoprolol has been proposed, apparently preventing more cases than by giving prophylactic glycopyrronium [14, 15, 17]. Such practice is not universal in the UK. Cardiac arrest has been reported sporadically after interscalene anaesthesia [18, 19]. However, there are several reports of cardiac arrest occurring after neuraxial anaesthesia in healthy individuals [20–23]. Some of these arrests may be attributable to excess sedation or to toxicity, but there are case series in which each of these potential mechanisms is apparently excluded, and in which an overwhelming vagal outflow is implicated instead. Fit young men are apparently most at risk, perhaps because their resting autonomic balance is more parasympathetic than others [24]. Correspondingly, there are fewer cases of peripartum women’s being affected than the popularity of neuraxial technique in obstetric anaesthesia might suggest, perhaps because resting heart rates are increased toward term. Total spinal anaesthesia There is no agreed definition of what a ‘total spinal’ means; it is perhaps useful to define it as subarachnoid placement of LA drugs, whether deliberate or accidental whose clinical effect extends to cause either respiratory impairment sufficient to require active management or unresponsiveness in the patient, or both. This definition usefully excludes the simple application of supplementary oxygen. It reminds us that an active airway intervention may be required in a patient who remains responsive and, importantly, that that patient may be unresponsive but still conscious. Total spinal anaesthesia implies incipient or actual anaesthesia of at least some of the brainstem. Doses of LA conventionally given intrathecally will struggle to reach this far; more commonly, an unintended excess of LA is delivered to the subarachnoid space. For example, a catheter intended to remain in the epidural space may accidentally be placed intrathecally or may migrate there. Careful aspiration before injecting will sometimes identify this situation. Another risky situation occurs in obstetric anaesthesia, when an existing epidural is topped up to provide 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

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Anaesthesia, 2010, 65 (Suppl. 1), pages 105–115 J. Picard and T. Meek Complications of regional anaesthesia . ....................................................................................................................................................................................................................

anaesthesia for caesarean section, but fails and the anaesthetist performs a spinal. Two likely mechanisms exist and both are likely to contribute in varying degrees. First, the hole in the dura mater allows an uncontrolled portion of the LA solution in the epidural space to leak into the subarachnoid space. Indeed, this phenomenon is exploited in the emerging technique of ‘dural-puncture epidurals’ – effectively a combined spinal-epidural in which no intrathecal drug is given, but the dural hole allows epidural drug to leech in [25]. Secondly, the thecal sac is compressed by the epidural space contents and this enhances the spread of any inrathecal drugs. Regardless of mechanism, the risk of high spinal anaesthesia in these circumstances can be decreased by avoiding topping up ‘unreliable’ epidurals. However, this is a notoriously difficult judgment. Where the clinical situation allows, a safe approach is to wait before the spinal is performed to allow dissipation of the epidural load of LA. Unfortunately, a ‘safe’ time period has not been experimentally determined but, given the ‘leakiness’ of the epidural space, perhaps 30 min is a reasonable target. If a delay of this duration is not possible, the patient should be suitably warned of the increased risk during the consent process, and the anaesthetist should retain a high index of suspicion during anaesthesia. A total spinal can also follow attempted peripheral blocks. Some argue that the posterior approach to the interscalene brachial plexus is particularly hazardous in this respect, but the posterior approach to the lumbar plexus has also been implicated [26, 27]. Recovery from a total spinal is usually fairly rapid, most often within a small number of hours. Recovery is also complete providing prompt recognition and action has prevented sustained periods of hypotension or hypoxia. Other causes Regional anaesthesia rarely occurs in isolation; typically it is associated with other manoeuvres that may themselves cause a cardiovascular collapse. Exposure to latex or to an intravenous colloid and consequent anaphylactic reaction, or an embolism of thrombus or amniotic fluid may coincide with placement of a regional anaesthetic; the resultant cardiovascular depression may initially be attributed to the block. Management The clinical management of cardiovascular collapse crystallises to simple ‘ABC’. Supplemental oxygen should be provided and the airway should be promptly secured as is clinically indicated; for example, tracheal intubation would be appropriate when there is a risk of aspiration. The lungs may be ventilated by whichever method is most suitable. Circulatory support is provided using 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

fluids, vasopressors and, when indicated, an antimuscarinic drug. The choice of vasopressor varies according to clinical circumstance: an alpha-agonist is usually the first choice when peripheral vasodilatation is the predominant problem; if bradycardia is also present, an antimuscarinic may be given first or an alternative such as ephedrine or adrenaline used. In pregnancy, hypotension can be compounded by aortocaval compression, which may be relieved by turning the patient out of a strictly supine position. If hypotension is severe, the full left lateral position may be required. When a precipitating cause can be identified, it should be eliminated. In apparent total spinal, it is important to remember that there are reports of patients’ remaining aware. Constant verbal reassurance should be given and consideration should be given to giving consciousness obtunding drugs before intubation, although a greatly decreased dose will suffice. Neuromuscular blocking drugs may rarely be required to facilitate tracheal intubation. Maintenance of anaesthesia should not be forgotten. Unless LA intoxication can be confidently excluded, treatment according to the current AAGBI guidelines [8] should be seriously considered. Respiratory embarrassment

Regional anaesthesia cannot be presumed to be entirely innocuous to the respiratory system, and its contribution to any respiratory insufficiency should be considered. There are a number of possible causes. Hemidiaphragmatic paresis All patients receiving interscalene blocks using conventional doses and volumes of LA also get a hemidiaphragmatic paresis [28]. Four out of eight volunteers receiving a supraclavicular block similarly lost half their diaphragmatic function [29]. Hemidiaphragmatic paresis has also been reported after infraclavicular blocks [30, 31]. Decreasing the amount of LA that spreads to the phrenic nerve will obviously decrease the risk and extent of its block. Recently, enthusiasts have taken two approaches to this end. One option is to direct the local anaesthesia slightly more distally, but before significant nerves leave the plexus. Bending the needle and directing it tangentially along the brachial plexus makes this easier for some, but may make appreciation of the needle’s position more difficult for others [32]. The other approach is simply to inject less LA, exploiting the precision affording by ultrasound guidance [33]. Pneumothorax Anatomy both favours and conspires against regional anaesthesia for upper limb surgery: there is just one plexus 107

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to block, while the lower limb is innervated through two. However, the brachial plexus’s narrowest point over the first rib is exquisitely close to the pleura. So supraclavicular approaches to the brachial plexus that in principle offer the densest, most extensive block might also expose the patient to the greatest risk of pneumothorax. This fear, apparently confirmed by an early study, motivated innovators to describe a flurry of approaches that were ostensibly safer [34]. In fact, even these approaches have been complicated by pneumothorax, as have paravertebral blocks [35]. Conversely, large series of paravascular supraclavicular block have been reported without clinically significant pneumothorax [36, 37]. The key to managing this risk lies in careful adaptation of anaesthetic technique to patient and surgery. In many patients, puncture of the pleura may be innocuous, so long as positive pressure ventilation and nitrous oxide are avoided. Without ultrasound guidance, if a patient with end-stage respiratory failure requires arm surgery, a difficult balance has to be struck between the risks of general anaesthesia, supraclavicular block (possible pneumothorax) or combined axillary and interscalene blocks (probable hemidiaphragmatic paresis). Whether ultrasound guidance substantially decreases the risk of pneumothorax during supraclavicular approaches remains to be seen. High spinal block As with total spinal, there is no agreed definition. However, it is useful to think of ‘high spinal’ as deliberate or inadvertent subarachnoid placement of LA drugs whose clinical effect extends sufficiently high to cause concern to the patient (by way of symptoms) or to the anaesthetist (by way of symptoms or signs) but without respiratory impairment sufficient to require active airway management or patient unresponsiveness. A high spinal most often arises in the course of a ‘normal’ spinal, with a ‘normal’ dose (in contrast with total spinal). Using too large a dose, or using hyperbaric solutions followed by head-down positioning may predispose. Pregnant women are particularly susceptible, and spinal anaesthesia after failed epidural anaesthesia is known to carry a further increased risk of a high spinal. It is sensible both to warn women in this position of this increased risk and to have to hand everything necessary to treat the problem. Management Subjective dyspnoea is very common in high spinal, and occasionally complicates brachial plexus blocks too. If patients can demonstrate an adequate inspiration and a reasonable cough, the familiar combination of supplemental oxygen and reassurance may suffice provided patients are appropriately monitored and frequently 108

reviewed. If pneumothorax is a possibility, the patient should be examined and a plain chest radiograph should be taken in end-expiration. Occasionally, drainage may be necessary. A high spinal block often disrupts other body systems too. It can cause sympatholysis and thence hypotension, which should be treated as described above. Transient somnolence is a common symptom, and the patient’s level of consciousness should be continually assessed. In particular, the risks of a full stomach must be remembered and assessed in parallel. Seizure or acutely changed cognitive function

Seizure is more commonly associated with regional anaesthesia when large doses of LA are injected. Conversely, seizure is rare after spinal injection of a small dose of LA. In the French prospective trial, the risk of seizure complicating a spinal block was 0.3 in 10 000, compared with 1.8 in 10 000 after an epidural and between 0.9 and 25.4 in 10 000 for peripheral nerve blocks [2]. Both regional anaesthesia and surgery can also be associated with acute changes in cognitive function that stop short of frank seizure [38]. The differential diagnosis is wide. If awake, patients may simply be confused by unfamiliar and stressful surroundings: disorientation may be paradoxically exacerbated by an amnesic benzodiazepine. Hypoglycaemia, fat embolism, bone cement implantation syndrome, preeclampsia or LA intoxication may be responsible, as may excess sedation and hypoxia. Once again, management is supportive: airway patency should be ensured and if necessary secured, and hypoxia avoided, blood pressure maintained, aspiration averted and seizures controlled – all in potentially challenging circumstances. If LA intoxication cannot be excluded, then a lipid infusion should be considered. Failure

A regional anaesthetic technique will fail to provide the intended analgesia or anaesthesia if the surgical stimulus surpasses the blocked area. During a caesarean section under neuraxial anaesthesia, for example, surgical attention to the paracolic gutters will often cause discomfort. Similarly, deltopectoral incisions toward the axilla will often escape an interscalene block at its caudad limit. More generally, it is important to know the sensory innervation of the periosteum and capsule in the case of bony operations or visceral organs in operations involving body cavities, which may be stimulated, rather than only the simple dermatomes of the planned incision; they often do not coincide. For example, the obturator nerve supplies both hip and knee joints, but classically supplies 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

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only a small area of skin between the two, and the abdominal organs notoriously send some sensory innervation along autonomic routes that are difficult to block. A regional anaesthetic may also disappoint if the injected LA does not reach the target nerves. This may happen in different ways according to the technique adopted. Peripheral If experience increases success with a nerve stimulator, it is because the experienced clinician knows better which elicited motor response to accept before injecting LA [39]. Conversely, if the wrong motor response is misinterpreted as the correct one, LA will be injected into the wrong place. For instance, twitches of sartorius and the rhomboids are easily misconstrued while attempting femoral nerve and interscalene brachial plexus blocks respectively. It is also possible to stimulate the correct nerve through a fascia that shields the nerve from any injectate. An experienced operator learns how much the motor response should change as the stimulating needle is moved. If the needle has to be held extremely precisely to elicit a motor response with a conventionally acceptable stimulus, it is likely that the needle is stimulating through a fascial plane that springs away from the nerve when the needle moves. Even if the correct nerve is directly stimulated, the injectate may not spread as desired. This may be particularly so in obese patients in whom even experts typically report lower success rates [36]. Ultrasound guidance in peripheral regional anaesthesia may increase success rates precisely because the flow of the injectate can be observed and the needle position adjusted if necessary. Epidural The local anatomy of the epidural space is notoriously variable, and this may underlie failure of epidural neuraxial blockade. It is possible to get a convincing but false loss-of-resistance within superficial tissues or within ligaments. Subdural placement of the catheter can lead to patchy or unexpectedly high block. If the epidural space is catheterised correctly, localised scarring may impede ‘normal’ spread of injectate. Such scarring may follow surgery, in which case difficulties may be anticipated, or after local pathological processes such as disc herniation, in which case it may not. Using air for loss-of-resistance may lead to incomplete spread of injectate by virtue of locules of air around nerve roots – one argument against use of this technique [40]. Incomplete block may be more common if ‘too much’ epidural catheter is inserted; 5 cm within the space has been recommended [41]. Consequently, improvement can sometimes be obtained if the catheter is withdrawn before giving a further top-up 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

injection. A block that fails to go low enough (‘sacral sparing’) can be hard to remedy, and this is more often seen in epidurals for labour. When a block fails to ascend high enough, giving a larger volume of injectate may help. The place of ultrasound guidance in placing neuraxial blocks remains to be seen; despite positive guidance issued by the UK National Institute for Health and Clinical Excellence, the technique has yet to find widespread use [42]. Spinal If a correct dose of LA is successfully placed into the cerebrospinal fluid (CSF), it is unusual for it to fail completely. Possible confounders include mistaking subcutaneous lacunae of recently injected LA for CSF and failing to insert the spinal needle sufficiently, remembering that most atraumatic needle types have side ports and that a Sprotte needle has its orifice positioned more proximally than a Whitacre needle. The possibility exists of a syndrome of relative resistance to LA drugs; mutant sodium channels are one explanation, but there appear few, concrete, published data [43]. Finally, the block must be tested before surgery is allowed to start and tested appropriately: a knee replacement requires a different extent of block from a caesarean section. The test must also be able adequately to predict anaesthesia for the duration of surgery, not just determine the extent of block at time zero. For instance, it has been proposed that block to the fourth thoracic dermatome (T4) to light touch predicts satisfactory spinal anaesthesia during caesarean section, but that an equivalent block to cold does not [44]. Failure to test appropriately is not the same as failure of block! Management Dogged belief in the efficacy of a failing block undermines patients’ confidence and unnecessarily exposes them to pain. So if a patient complains of pain, it is important first to believe and quickly clarify their symptoms, remembering that the operative site may not be the source of pain. Involving patients in decisions that arise is also remarkably analgesic; patients may prefer to tolerate discomfort if surgery is almost complete or a tourniquet will soon be deflated. If pain is intolerable, then options include: using more LA (infiltrated by the surgeon, injected down a catheter – with or without prior manipulation, or even supplementary nerve blocks); inhaled nitrous oxide in oxygen (from the anaesthetic machine or cylinder); intravenous analgesia (paracetamol, non-steroidal antiinflammatory drug (NSAID), ketamine or opioid as clinically indicated); or conversion to general anaesthesia. It is prudent also to document such discussions and decisions fully. When regional anaesthesia disappoints, an 109

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unfortunate patient will suffer pain and, perhaps, the side effects of systemic analgesia. For the sake of regional anaesthesia’s reputation in a hospital and the anaesthetist’s morale, it may be useful to remind attending surgeons, nurses and anaesthetists that these are exactly the ill effects that successful blocks normally spare the patient. Headache after neuraxial block

Faced with headache after neuraxial anaesthesia, postdural puncture headache (PDPH) is clearly a tempting diagnosis. However, clinicians should always first consider the possibility of other diagnoses. Important exclusions include viral, chemical or bacterial meningitis, intracranial haemorrhage and, in obstetric anaesthesia, pre-eclampsia. Other less common but equally serious differential diagnoses include cerebral venous thrombosis, intracranial tumour, pituitary apoplexy, cerebral infarction and uncal herniation. Less common and less serious causes include sinus headache, migraine and drugs, including caffeine withdrawal. Anaesthetists are rarely trained or experienced in the confident diagnosis of these. If there is any doubt, the anaesthetist must be prepared to defer to other colleagues; urgent referral to a neurologist is often the most appropriate action. In the absence of any reliable diagnostic tests for PDPH, clinical suspicion and thus clinical experience must not be underestimated. The stereotypical sufferer of PDPH is ashen-faced, pale, nauseated, supine and bed-ridden. The similarity between these symptoms and the severest of post-alcoholic hangovers reflects their common aetiology: sagging of intracranial structures with resultant traction and vasodilation in the meninges. In PDPH the culprit is, of course, loss of CSF. Onset is typically within 2–3 days of the dural puncture, but it can occasionally be much sooner or later. Symptoms are classically a searing frontal or occipital headache, exacerbated by head movement and upright posture, and relieved by lying down. Also present may be neck stiffness, nausea, vomiting, hearing loss, tinnitus, vertigo, paraesthesia and visual disturbance. Symptoms can, however, be confusingly nebulous. Any patient can succumb to PDPH but obstetric anaesthesia is a particular risk area. The patients are young and female (both risk factors for PDPH) and there is a high rate of neuraxial techniques and, consequently, an experienced obstetric anaesthetist may be your local ‘expert’. The constellation of symptoms above inevitably impairs mobilisation and activity at the worst possible time: the patient has just had an operation and needs to mobilise, or the patient has a new baby to care for, or the patient simply wants to go home. Thus when PDPH is diagnosed, a structured treatment plan, enacted by an experienced anaesthetist, is essential. The only treatments 110

with a currently positive evidence base are the passage of time and an epidural blood patch. Many other treatments have been proposed but none has yet shown consistent and convincing results in trials. Ideally, the treatment plan should include an initial trial of maximum analgesia, typically paracetamol, an NSAID and a weak opioid for not less than 24 h. Failure of this regimen should prompt consideration of an epidural blood patch. In severe cases, proceeding straight to blood patch may be indicated. The pattern of symptoms may also influence timing: it may be acceptable to prolong the trial of conservative measures if symptoms are generally improving, and vice versa. The timing of a blood patch should not be too soon, preventing a trial of conservative measures, but neither should it be too late, causing unnecessary patient distress and debility and risking more serious sequelae; the best policy is to have the decision made by an anaesthetist experienced in the assessment and treatment of this condition, and to involve the patient in the decisionmaking process. The efficacy of a blood patch after patients return home has been questioned [45]. This reminds us that robust follow-up arrangements must be made, with clear and accessible channels of communication between patient and medical services. Failure of repeat blood patches to work is another indication for neurology referral. Occasionally, anaesthetists may be able to return the favour: when patients under the care of neurologists develop PDPH after diagnostic lumbar puncture, an epidural blood patch may be an appropriate treatment. Peculiar neurology following a block

Regional anaesthesia is intended to disrupt patients’ neurology. Yet neural damage, one of its most feared complications, also disrupts neurology. Little wonder then that the clinical challenges of a suspected case of nerve damage are often compounded by confusion, which also spreads to some of the pertinent literature. The confusion, in turn, can be exacerbated by medicolegal concerns and a competitive apportionment of blame. Mechanisms of neural damage All regional anaesthesia techniques involve a rigid needle and sometimes a catheter too. Fascial blocks aside, the needle is directed toward nervous tissue, while a catheter may be left adjacent to it. Direct mechanical trauma has thus long been presumed to be the usual cause of nerve damage associated with regional anaesthesia. The needle or catheter may also cause bleeding and, within a confined space such as the vertebral canal or psoas compartment, a haematoma or abscess may compress nerves, causing ischaemia and dysfunction. This has long 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

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been the conventional view. While its basic elements may be valid, the truth is probably more complex. It has become evident, for example, that injections can be made directly within the epineurium without apparent longterm ill effect [46, 47]. Conversely, nerve function can be disturbed by a conventional injectate without direct mechanical trauma or ischaemic compression [48]. How pre-existing neuropathy, microanatomy, inadvertent trauma, compression and injected agents conspire to cause or avoid neurologic deficits is unclear. Nerve damage and regional anaesthesia may also be causally related in a less direct way: an effective block may allow patients to sustain positions that normally would quickly become intolerable. Timing the detection of a neurological abnormality The ill effects of regional anaesthesia on nerves can present much later than might be expected. They may be detected in the first hours after a block is placed, even while the block is still effective [48]. They may become evident only after a block recedes. They may, indeed, stem from the removal of a catheter, and so arise only in the hours, or even days, after a continuous technique ends [49]. Most peculiarly, they may first be detected only weeks after a single-shot technique [50]. The important messages are that neurological observation distal to a catheter should continue in the hours after its removal and that neurological symptoms that arise even 2 weeks after a single-shot block should not be dismissed lightly. Risks of neurological abnormalities Estimates of the incidence of neurologic disturbance after regional anaesthesia vary widely. In part, this is because many deficits are mercifully transient, so the timing of any survey affects its results. For example, 10 days after shoulder surgery combined with an interscalene block, 14% of patients had paraesthesia, dysaesthesia or pain unrelated to surgery. However, by 9 months, the incidence had fallen to just one patient in 520 [50]. Similarly, in the Royal College of Anaesthetists’ 3rd National Audit Project, half of patients developing deficits attributable to nerve or cord injury after spinal anaesthesia made a complete recovery within 6 months [1]. It seems that the incidence of deficit after spinal anaesthesia may be decreasing. The same National Audit Project, covering an estimated 324 950 spinal anaesthetics in 2006–7, estimated the risk of neurological trauma at 0.92 in 100 000 spinals [1]. However, in 1998–9, the risk in non-obstetric patients in France was estimated a whole order of magnitude higher, at 3.3 in 10 000 [2]. Perhaps the gathering awareness of anaesthetists’ inaccuracy in estimating levels in the lumbar spine has led to more cautious, caudad practice? 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

For all this variation, there is a pattern: in published series, the risk of nerve injury is highest during peripheral nerve and plexus blocks. The spread of ultrasound techniques may affect this risk too. The risk attributable to spinal anaesthesia is intermediate, and may be falling, and the risk attached to epidural anaesthesia may be lower (1.02 in 100 000 in the UK recently, and 0 in 5561 non-obstetric epidurals in the earlier French survey [1, 2]. Management Management of a neurological deficit after a regional anaesthetic depends upon the nature of the deficit. A resolving paraesthesia can be managed conservatively, and the patient reassured that complete resolution over time is probable. At the other extreme, an acute loss of power or of sphincter control should prompt urgent action. A cooperative radiologist’s help should be enlisted to exclude a surgically remediable cause. Within the vertebral canal, magnetic resonance imaging (MRI) is best suited to the exclusion of a haematoma or abscess. Similarly, the lumbar and sacral plexuses and the deep nerves they form are probably best seen by MRI. The brachial plexus and nerves of the upper limb may be examined with ultrasound. Simultaneously, an expert neurologist’s examination should be sought. This will provide an objective record of the starting point as the signs and symptoms progress. Time is of the essence: reviews of spontaneous epidural haematomata suggest that the chances of full recovery are maximised if the cord is decompressed within 12 h of the onset of symptoms [51]. Peripheral nerves may be still more intolerant of compression: when the distal brachial plexus is compressed by a haematoma attributable to arteriography, decompression within 4 h maximises the chances of recovery [52]. Prompt investigation and, if necessary, transfer to a neurosurgical unit are essential, even in the middle of the night or weekend. The National Audit Project provides useful example management algorithms for peri-operative leg weakness [1]. If decompressive surgery is not immediately indicated, the next step is to arrange an electrophysiological examination. The arcane details of clinical electrophysiology elude most anaesthetists. Yet one fact is well known: after an acute nerve injury, the electrophysiological deficit will become clear after approximately 2 weeks. But this, paradoxically, is exactly why a baseline exam should be performed in the 48 h after an injury is suspected. The results may reveal preexisting deficits and clarify results of tests 2 weeks later [53]. For similar reasons, all tests should be performed bilaterally. 111

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The consequences of successful blocks

Bladder dysfunction Voluntary voiding of the bladder is usually prompted by the somatic sensation of fullness. The bladder also possesses autonomic reflexes that provide automatic voiding, based upon stretch. Neuraxial anaesthesia disrupts both, with the autonomic dysfunction outlasting the sensory blockade. Spinal anaesthesia appears to offer less risk than epidural, presumably because of its finite, shorter duration. Yet urinary catheterisation carries risks, both of urethral trauma and long-term sequelae, and also of causing bacteraemia. Surgeons placing implants are naturally concerned about this and their views must be taken into account, though not slavishly followed [54]. Bladder ultrasound is a useful assessment modality that is easily learned and can help avoid unnecessary bladder catheterisation. Instrumental delivery The effect of epidural analgesia in labour on uterine contraction is not easy to study directly. However, proxy measures exist: epidurals do not increase the rate of caesarean section, do slightly prolong the length of the second stage of labour and may slightly increase the likelihood of instrumental delivery [55, 56]. Delayed diagnosis of compartment syndrome In the vexed question of compartment syndrome, ignorance meets obduracy. The problems are many: if the perfusion pressure in a closed osseofascial compartment is inadequate, muscle and nerve quickly die; compartmental necrosis has been associated with all postoperative analgesic techniques, including regional anaesthesia, and reversible compartmental ischaemia cannot reliably be diagnosed by non-invasive means [57]. Meanwhile, many surgeons balk at the percutaneous insertion of continuous compartmental pressure measurement catheters, particularly if a prosthesis has been placed. They prefer to rely instead on symptoms that tend to be obscured by regional block, such as patients’ reports of pain, paraesthesia and paralysis, however unreliable these indicators are [58]. Until a practical, noninvasive monitor of compartmental perfusion is developed, the problem may remain largely intractable: the hideous sequelae of late diagnosis of compartment syndrome are all too easily ascribed to regional anaesthesia. Self-defence, rather than patient’s interests, may lead many anaesthetists to eschew regional techniques if late diagnosis of compartmental ischaemia is possible. Motor weakness and impaired proprioception Human anatomy allows some procedures under sensory block alone. Inguinal surgery provides an example. More 112

often, peripheral blocks target mixed nerves. Similarly, neuraxial opioids may provide some analgesia alone, but they are more usually combined with LAs. The results are motor weakness and proprioceptive deficit. Indeed, even inguinal field blocks can cause unexpected motor block [59]. Sceptics attribute immense influence to these effects of regional anaesthesia: they are held responsible for delayed mobilisation, bedsores and even hospital budgetary deficits. The ensuing debate ranges over the fine detail of anaesthetic technique and relatively grosser aspects of hospital care. Enthusiasts have hoped to decrease the extent and duration of motor block by using adjuvants, shorteracting agents and lower concentrations and doses. So, for example, lidocaine was used in day surgery for spinal anaesthesia until fears of neuropathy led instead to trials of ultra-low doses of intrathecal bupivacaine [60, 61]. Similarly, for postoperative and labour analgesia, lower and lower concentrations of epidural LA have been advocated. Meanwhile, in peripheral blocks, LAs can be combined. Lidocaine can be injected around the brachial plexus to allow use of a tourniquet, and a few selected distal nerves blocked with a longer-acting agent to provide effective postoperative analgesia. After knee surgery, a femoral nerve sheath catheter causes only a unilateral block, and so may accelerate mobilisation compared with an epidural [62]. Local anaesthetic infused through a perineural catheter, combining a basal infusion with boluses controlled by patients, may yield equal analgesia with a smaller LA dose [63, 64]. However, the exact effect of concentration and volume are not yet clear [65, 66]. In practice, the effect of motor weakness on the patient’s clinical course depends largely on how it is managed. Women in labour may have abnormal balance even before any analgesia, and it may be further undermined even by low-dose techniques [67–69]. ‘Mobile epidurals’ may be safe provided expectant mothers have constantly available suitable assistants. Equally, effective postoperative analgesia should be exploited by physiotherapists and surgeons, rather than tolerated or dismissed. Indeed, some centres have gathering experience of sending patients home within 24 h of major orthopaedic surgery precisely because they are discharged with continuous blocks still working [70, 71]. In short, regional anaesthesia may indeed cause weakness, but discharge and mobilisation often need not be delayed. Conclusions

Regional anaesthesia can substantially decrease, even occasionally eliminate, the stress and pain of surgery and childbirth. It has risks, some common and mild, others 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

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rare and worse. Dispassionate review of these risks may reassure the sceptical and cautious (sparing their patients unnecessary pain), and kerb the excesses of the thoughtless fanatic (sparing other patients undue risk). Conflicts of interest

Drs Picard and Meek contributed to the establishment of the internet sites www.lipidresure.org and www.lipid registers.org. They have no financial interest in either site’s past, present or future. Neither site has had an income. Both doctors are enthusiastic regional anaesthetists. They have no other potential conflicts of interest to declare. References 1 Royal College of Anaesthetists. Report and findings of the 3rd National Audit Project of the Royal College of Anaesthetists. http://www.rcoa.ac.uk/docs/NAP3_ Section2.pdf (accessed 20 ⁄ 10 ⁄ 2008). 2 Auroy Y, Benhamou D, Bargues L, et al. Major complications of regional anesthesia in France: The SOS Regional Anesthesia Hotline Service. Anesthesiology 2002; 97: 1274–80. 3 Braz LG, Modolo NS, do Nascimento P, et al. Perioperative cardiac arrest: a study of 53,718 anaesthetics over 9 yr from a Brazilian teaching hospital. British Journal of Anaesthesia 2006; 96: 569–75. 4 Mulroy MF. Systemic toxicity and cardiotoxicity from local anesthetics: incidence and preventive measures. Regional Anesthesia and Pain Medicine 2002; 27: 556–61. 5 Schwartz D, VadeBoncouer T, Weinberg G. Was case report a case of unrecognized local anesthetic toxicity? Anesthesia & Analgesia 2003; 96: 1844–5. 6 Rowlingson JC. Lipid rescue: a step forward in patient safety? Likely so! Anesthesia & Analgesia 2008; 106: 1333–6. 7 Picard J, Harrop-Griffiths W. Lipid emulsion to treat drug overdose: past, present and future. Anaesthesia 2009; 64: 119–21. 8 AAGBI. Guidelines for the management of severe local anaesthetic toxicity. http://www.aagbi.org/publications/ guidelines.htm (accessed 20 ⁄ 10 ⁄ 2008). 9 National Confidential Enquiry into Perioperative Deaths. Changing the Way We Operate: The 2001 Report of the National Confidential Enquiry into Perioperative Deaths. London: NCEPOD, 2001. 10 McDonald SB. Is neuraxial blockade contraindicated in the patient with aortic stenosis? Regional Anesthesia and Pain Medicine 2004; 29: 496–502. 11 Pittard A, Vucevic M. Regional anaesthesia with a subarachnoid microcatheter for caesarean section in a parturient with aortic stenosis. Anaesthesia 1998; 53: 169–73. 12 Fuzier R, Murat O, Gilbert ML, Magues JP, Fourcade O. Continuous spinal anesthesia for femoral fracture in two patients with severe aortic stenosis. Annales Françaises d’Anesthe´sie et de Reánimation 2006; 25: 528–31. 2010 The Authors Journal compilation 2010 The Association of Anaesthetists of Great Britain and Ireland

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