Complication of Regional Anesthesia

Anaesthesia / Volume 65, Issue s1 / p.
105-115
!Free Access
Complications of regional anaesthesia
J. Picard, T. Meek
First published: 08 March 2010

https://doi.org/10.1111/j.1365-2044.2009.06205.x
Citations: 20
" Correspondence to: Dr John Picard

E-mail: johnjpicard@googlemail.com
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.
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 di!erent 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, rare"ed 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 "ve 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 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; di!erences in
casemix and error in recording events are more likely to account for the variation. The
di!erential 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 su!ers a cardiovascular collapse and a large dose of
LA has recently been given, or if an infusion is underway, then LA intoxication is di#cult
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 e!ective antidote. Of 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 e#cacy. 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% Intralipid™ (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 signi"cant when both legs,
the splanchnic circulation, or all three, are a!ected by a spinal or epidural block. Some
patients are particularly intolerant of this decrease in systemic vascular resistance.
Anaesthetic tradition identi"es 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
signi"cant 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 "t 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 signi"cant hypotension occurs
comparatively frequently. Reported series record incidences of 13–28% [14]. The Bezold-
Jarisch re$ex has been implicated: the combination of pre-operative starvation and the
sitting position is purported to reduce ventricular "lling; meanwhile, position, anxiety and
any exogenous adrenaline absorbed systemically cause vigorous ventricular contraction.
If the ventricular walls touch in systole, an overwhelming vagal out$ow 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 out$ow 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 a!ected 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 de"nition of what a ‘total spinal’ means; it is perhaps useful to de"ne
it as subarachnoid placement of LA drugs, whether deliberate or accidental whose clinical
e!ect extends to cause either respiratory impairment su#cient to require active
management or unresponsiveness in the patient, or both. This de"nition 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 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’–
e!ectively 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
di#cult 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 $uid 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 $uids, vasopressors and, when indicated, an
antimuscarinic drug. The choice of vasopressor varies according to clinical circumstance:
an alpha-agonist is usually the "rst choice when peripheral vasodilatation is the
predominant problem; if bradycardia is also present, an antimuscarinic may be given "rst
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 identi"ed, 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
su#ce. Neuromuscular blocking drugs may rarely be required to facilitate tracheal
intubation. Maintenance of anaesthesia should not be forgotten. Unless LA intoxication
can be con"dently 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 insu#ciency 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
signi"cant 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 di#cult for others [32]. The other approach is simply to inject less
LA, exploiting the precision a!ording by ultrasound guidance [33].
Pneumothorax
Anatomy both favours and conspires against regional anaesthesia for upper limb surgery:
there is just one plexus to block, while the lower limb is innervated through two.
However, the brachial plexus’s narrowest point over the "rst rib is exquisitely close to the
pleura. So supraclavicular approaches to the brachial plexus that in principle o!er the
densest, most extensive block might also expose the patient to the greatest risk of
pneumothorax. This fear, apparently con"rmed by an early study, motivated innovators
to describe a $urry 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 signi"cant 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 di#cult
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 de"nition. However, it is useful to think of ‘high
spinal’ as deliberate or inadvertent subarachnoid placement of LA drugs whose clinical
e!ect extends su#ciently 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
su#cient 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 su#ce
provided patients are appropriately monitored and frequently 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 di!erential 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, pre-eclampsia 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 only a small
area of skin between the two, and the abdominal organs notoriously send some sensory
innervation along autonomic routes that are di#cult to block.
A regional anaesthetic may also disappoint if the injected LA does not reach the target
nerves. This may happen in di!erent 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 $ow 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 super"cial 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 di#culties 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 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 "nd widespread use [42].
Spinal
If a correct dose of LA is successfully placed into the cerebrospinal $uid (CSF), it is unusual
for it to fail completely. Possible confounders include mistaking subcutaneous lacunae of
recently injected LA for CSF and failing to insert the spinal needle su#ciently,
remembering that most atraumatic needle types have side ports and that a Sprotte
needle has its ori"ce positioned more proximally than a Whitacre needle. The possibility
exists of a syndrome of relative resistance to LA drugs; mutant sodium channels are one
explanation, but there appear few, concrete, published data [43]. Finally, the block must
be tested before surgery is allowed to start and tested appropriately: a knee replacement
requires a di!erent extent of block from a caesarean section. The test must also be able
adequately to predict anaesthesia for the duration of surgery, not just determine the
extent of block at time zero. For instance, it has been proposed that block to the fourth
thoracic dermatome (T4) to light touch predicts satisfactory spinal anaesthesia during
caesarean section, but that an equivalent block to cold does not [44]. Failure to test
appropriately is not the same as failure of block!
Management
Dogged belief in the e#cacy of a failing block undermines patients’ con"dence and
unnecessarily exposes them to pain. So if a patient complains of pain, it is important "rst
to believe and quickly clarify their symptoms, remembering that the operative site may
not be the source of pain. Involving patients in decisions that arise is also remarkably
analgesic; patients may prefer to tolerate discomfort if surgery is almost complete or a
tourniquet will soon be de$ated. If pain is intolerable, then options include: using more
LA (in"ltrated 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 anti-in$ammatory 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 unfortunate patient will su!er pain and, perhaps, the side
e!ects 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 e!ects that successful blocks
normally spare the patient.
Headache after neuraxial block

Faced with headache after neuraxial anaesthesia, post-dural puncture headache (PDPH)
is clearly a tempting diagnosis. However, clinicians should always "rst 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 di!erential 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 ca!eine withdrawal. Anaesthetists are rarely trained or experienced in
the con"dent 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 su!erer of PDPH is ashen-faced, pale, nauseated, supine and bed-
ridden. The similarity between these symptoms and the severest of post-alcoholic
hangovers re$ects their common aetiology: sagging of intracranial structures with
resultant traction and vasodilation in the meninges. In PDPH the culprit is, of course, loss
of CSF. Onset is typically within 2–3 days of the dural puncture, but it can occasionally be
much sooner or later. Symptoms are classically a searing frontal or occipital headache,
exacerbated by head movement and upright posture, and relieved by lying down. Also
present may be neck sti!ness, nausea, vomiting, hearing loss, tinnitus, vertigo,
paraesthesia and visual disturbance. Symptoms can, however, be confusingly nebulous.
Any patient can succumb to PDPH but obstetric anaesthesia is a particular risk area. The
patients are young and female (both risk factors for PDPH) and there is a high rate of
neuraxial techniques and, consequently, an experienced obstetric anaesthetist may be
your local ‘expert’. The constellation of symptoms above inevitably impairs mobilisation
and activity at the worst possible time: the patient has just had an operation and needs to
mobilise, or the patient has a new baby to care for, or the patient simply wants to go
home. Thus when PDPH is diagnosed, a structured treatment plan, enacted by an
experienced anaesthetist, is essential. The only treatments with a currently positive
evidence base are the passage of time and an epidural blood patch. Many other
treatments have been proposed but none has yet shown consistent and convincing
results in trials. Ideally, the treatment plan should include an initial trial of maximum
analgesia, typically paracetamol, an NSAID and a weak opioid for not less than 24 h.
Failure of this regimen should prompt consideration of an epidural blood patch. In severe
cases, proceeding straight to blood patch may be indicated. The pattern of symptoms
may also in$uence 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 decision-making process. The e#cacy 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 con"ned space such as the vertebral canal or psoas
compartment, a haematoma or abscess may compress nerves, causing ischaemia and
dysfunction. This has long 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 long-term ill
e!ect [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 de"cits is unclear. Nerve damage and regional
anaesthesia may also be causally related in a less direct way: an e!ective block may allow
patients to sustain positions that normally would quickly become intolerable.
Timing the detection of a neurological abnormality

The ill e!ects of regional anaesthesia on nerves can present much later than might be
expected. They may be detected in the "rst hours after a block is placed, even while the
block is still e!ective [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 "rst 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 de"cits are mercifully transient, so the timing of any
survey a!ects 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 de"cits attributable to nerve or cord injury after spinal anaesthesia made a
complete recovery within 6 months [1].
It seems that the incidence of de"cit 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?
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 a!ect 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 de"cit after a regional anaesthetic depends upon the
nature of the de"cit. 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 co-
operative 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 de"cit 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 pre-existing de"cits and clarify results of tests
2 weeks later [53]. For similar reasons, all tests should be performed bilaterally.
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 re$exes that provide automatic voiding, based
upon stretch. Neuraxial anaesthesia disrupts both, with the autonomic dysfunction
outlasting the sensory blockade. Spinal anaesthesia appears to o!er less risk than
epidural, presumably because of its "nite, 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 e!ect 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, non-invasive 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 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 de"cit. Indeed, even
inguinal "eld blocks can cause unexpected motor block [59]. Sceptics attribute immense
in$uence to these e!ects of regional anaesthesia: they are held responsible for delayed
mobilisation, bedsores and even hospital budgetary de"cits. The ensuing debate ranges
over the "ne 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, shorter-acting 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 e!ective 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
e!ect of concentration and volume are not yet clear [65, 66].
In practice, the e!ect 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, e!ective 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 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).
Con!icts of interest
Drs Picard and Meek contributed to the establishment of the internet sites
www.lipidresure.org and www.lipidregisters.org. They have no "nancial 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 con$icts of interest to
declare.
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Anaesthesia / Volume 65, Issue s1 / p.

Complications of regional anaesthesia

First published: 08 March 2010

" Correspondence to: Dr John Picard

Local anaesthetic intoxication

Severe LA intoxication may be associated with tonic-clonic seizure, transitory

Overwhelming sympathetic block

The patient’s homeostasis is perhaps best maintained when the sympatholysis is

Vaso vagal reactions

Total spinal anaesthesia

Another risky situation occurs in obstetric anaesthesia, when an existing epidural is

When a precipitating cause can be identi"ed, it should be eliminated. In apparent total

High spinal block

Seizure or acutely changed cognitive function

Once again, management is supportive: airway patency should be ensured and if

Ultrasound guidance in peripheral regional anaesthesia may increase success rates

Headache after neuraxial block

Peculiar neurology following a block

Mechanisms of neural damage

Timing the detection of a neurological abnormality

Risks of neurological abnormalities

If decompressive surgery is not immediately indicated, the next step is to arrange an

The consequences of successful blocks

Delayed diagnosis of compartment syndrome

Motor weakness and impaired proprioception

2 Auroy Y, Benhamou D, Bargues L, et al. Major complications of regional anesthesia in

5 Schwartz D, VadeBoncouer T, Weinberg G. Was case report a case of unrecognized local

8 AAGBI. Guidelines for the management of severe local anaesthetic toxicity.

19 Turker G, Demirag B, Ozturk C, Uckunkaya N. Cardiac arrest after interscalene brachial

34 Brand L, Papper E. A comparison of supraclavicular and axillary techniques for brachial

42 National Institute for Health and Clinical Excellence. Ultrasound-guided catheterisation of

45 Eustace N, Hennessy A, Gardiner J. The management of dural puncture in obstetrics and

46 Russon K, Blanco R. Accidental intraneural injection into the musculocutaneous nerve

49 Sandhu H, Morley-Forster P, Spadafora S. Epidural hematoma following epidural analgesia

50 Borgeat A, Ekatodramis G, Kalberer F, Benz C. Acute and nonacute complications

51 Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-

59 Lipp AK, Woodcock J, Hensman B, Wilkinson K. Leg weakness is a complication of ilio-

60 Zaric D, Christiansen C, Pace NL, Punjasawadwong Y. Transient neurologic symptoms after

67 Davies J, Fernando R, McLeod A, Verma S, Found P. Postural stability following ambulatory

68 Pickering AE, Parry MG, Ousta B, Fernando R. E!ect of combined spinal-epidural

69 Buggy D, Hughes N, Gardiner J. Posterior column sensory impairment during ambulatory

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Explore this article's citation statements on scite.ai

© 2022 Association of Anaesthetists

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