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Complications of obstetric anaesthesia
ARTICLE IN PRESS Current Anaesthesia & Critical Care (2006) 17, 151–162
www.elsevier.com/locate/cacc
FOCUS ON: OBSTETRICS
Complications of obstetric anaesthesia Amanda Pinder Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
KEYWORDS Pregnancy; Obstetric anaesthesia; Obstetric analgesia; Complications
Summary The obstetric anaesthetist has an increasing role to play in the provision of anaesthesia and analgesia for the parturient. Both regional and general anaesthesia carry with them the potential for complications, some of which, although rare, may be serious, life threatening and/or permanently disabling. Careful attention to detail in our anaesthetic practice will play an important role in minimizing their incidence. Measures to prevent and manage the following complications will be discussed: intubation problems, aspiration, awareness, hypotension, local anaesthetic toxicity, dural puncture and post-dural puncture headache, high regional blocks and neurological damage. & 2006 Elsevier Ltd. All rights reserved.
Introduction The repertoire of obstetric anaesthesia has grown in recent years to include epidurals, spinals, combined spinal epidurals (CSE), spinal catheters and general anaesthesia. All of these may be associated with complications. Common ones, such as nausea and vomiting or a patchy epidural, may not be particularly serious but can nonetheless be very distressing for the patient. What may concern the anaesthetist more are the rare and serious complications that may be potentially life threatening or permanently disabling. The maternal confidential enquiries1 revealed there to be 30–50 maternal deaths per triennium from general anaesthesia until the 1980s. These deaths were mainly due to aspiration and failure of oxygenation during failed intubation. The imTel.: +44 113 3926672.
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plementation of recommendations from previous reports, supported by the various professional bodies, has led to a fall in anaesthesia–related maternal deaths since then. Improvements in training, staffing, supervision, monitoring and facilities have all contributed, as have increased use of regional anaesthetic techniques and measures to prevent aspiration of gastric contents. It is somewhat disheartening that general anaesthetic deaths from poor airway management have returned to haunt us. There had been no general anaesthetic deaths in the previous two reports, although there had been some questionable regional anaesthetic management. In 2000–2002 there were six UK maternal general anaesthetic deaths and one late death from hypoxic brain damage from unrecognized oesophageal intubation. Three of these six deaths were also associated with unrecognized oesophageal intubation, with capnography only being used in one case! The numbers of deaths are small and the report does state that it is too
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early to say whether the increase in anaesthetic deaths is a real cause for concern, but it does recommend that anaesthesia training must ensure competency in airway management, especially the recognition and management of oesophageal intubation. Despite this, it is still 30 times safer to have a general anaesthetic on labour ward nowadays than it was in the 1950s. Regional anaesthesia may be safer than general anaesthesia, despite the deaths in the previous two confidential enquiries, but concerns still remain about other serious complications. High blocks, neurological damage and sequelae of dural puncture may be rare but can be life threatening and leave the mother with permanent residual damage. This paper aims to review some of the complications associated with obstetric anaesthesia. These are listed in Tables 1 and 2.
Complications of general anaesthesia Although the proportion of general anaesthetics used in obstetric practice has plummeted over the last two decades, the actual number given for emergency Caesarean sections is largely unchanged2,3 because of the increased section rate. General anaesthesia is potentially indicated for
Table 1
Complications of general anaesthesia.
Difficult and failed intubation Aspiration Awareness Nausea and vomiting Post-operative pain Sore throat Drowsiness Delayed bonding and breast feeding
Table 2
Complications of regional anaesthesia.
Failure (unable to site, partial or complete failure to work) Hypotension Local anaesthetic toxicity Dural puncture and post dural puncture headache High block Neurological complications Shivering Opioid effects (urinary retention, pruritis, delayed gastric emptying, and the potential for maternal and neonatal respiratory depression)
most category 1 Caesarean sections and when regional anaesthesia is contraindicated or has failed. I will discuss three main hazards of general anaesthesia: failed intubation, aspiration and awareness.
Difficult and failed intubation Failed intubation is eight times more common in the pregnant (incidence 1 in 280) than the nonpregnant population (incidence 1 in 2230).4 There were three maternal deaths in the last maternal confidential enquiry attributed to failed intubation and unrecognized oesophageal intubation by junior anaesthetists working in isolation.1 Concerns have been raised about insufficient training opportunities for junior doctors in obstetric general anaesthesia.5,6 An audit of failed intubations in the South West Thames region revealed that, although its incidence remains unchanged, in half of the cases for which the notes could be examined there was a failure to follow an accepted protocol for failed tracheal intubation. These protocol violations included giving a second dose of suxamethonium or repeated attempts at tracheal intubation.7 Why is there such a high incidence of airway problems in obstetrics? Oft quoted reasons include large breasts and full dentition, but few anaesthetists consider these particularly worrying characteristics in the non-obstetric population. The main reasons are time, fear and inexperience. Time. Once apnoea occurs after induction, the obstetric patient desaturates rapidly despite pre-oxygenation because of the combination of reduced functional residual capacity of the lungs and high metabolic rate. Fear, outside of obstetrics, increasing hypoxia during intubation is managed by pausing to re-oxygenate the patient with bag and mask ventilation. This is considered to be extremely dangerous in UK obstetric teaching, because of the risk of gastric insufflation and resultant regurgitation and aspiration. Trainees are taught to fear this manoeuvre and to immediately enter a failed intubation drill. With the words failure and aspiration filling their minds, fear can negatively affect performance and decision making. Inexperience is often a contributor to cases of failed intubation, and appears to be an insoluble problem. Most general anaesthetics are used for emergency sections, two-thirds of which are bound to occur out of hours when no consultant is on site. The combination of the relative rarity of general anaesthesia and reduced working hours has limited
ARTICLE IN PRESS Complications of obstetric anaesthesia training opportunities, and ensured the relative inexperience of the trainee anaesthetists who deliver most of the obstetric general anaesthesia in the UK. Of course, there are genuine physical predictors for airway problems, one of which is obesity. As serious obesity becomes more and more common, we might expect an increase in the incidence of failed intubation. This is particularly true given the high incidence of obstetric intervention required in the obese population. This is one condition where careful antenatal assessment may reduce anaesthetic risk. An anaesthetic plan in the medical notes which advocates early epidural analgesia to avert the need for general anaesthesia and early contact with a senior anaesthetist may be all that is required to avert a major problem. However, it is unlikely that routine antenatal airway screening will eliminate all unexpected difficult intubations because of the unreliability of the available tests.8 Some suggestions for preventing failed intubation are shown in Table 3. Many failed intubation algorithms exist in the anaesthetic literature. Inevitably the more comprehensive they are, the more complicated they become. A simple example is suggested in Table 4. It is important that anaesthetists have a plan in their own minds of what do to if the failed intubation situation arises, and that they are intimately familiar with the airway equipment available to them. The commonest reason for using general anaesthesia is probably for the category 1 Caesarean section for severe fetal distress. Traditional anaesthetic teaching argues that the safety of the mother should not be compromised for the sake of the fetus. This would imply that the option of allowing surgery to continue after rescuing a failed intubation by, for example, inserting a laryngeal mask, is not acceptable. I do not support this view, as most couples would gladly accept personal risk in exchange for a healthy baby. It is a
Table 3
153 difficult decision, but (in very experienced hands) it can be appropriate to allow surgery to continue with a spontaneous breathing mask or laryngeal mask anaesthetic. In these circumstances, a senior surgeon should be summoned to expedite the procedure. A deep plane of anaesthesia should be maintained to reduce the risk of laryngospasm and vomiting. Sevoflurane is ideal under these circumstances as it is non-irritant and its low bloodgas solubility allows rapid deepening of anaesthesia. Unfortunately, it reduces uterine tone and oxytocin infusions may be necessary for troublesome atonic bleeding. Propofol infusions may be beneficial in patients at high risk of major haemorrhage as it has minimal effects on uterine tone. If the decision is made to wake the patient up, the anaesthetist is then faced with choosing one of several unattractive options. Repeat conventional general anaesthesia, general anaesthesia after an awake intubation, or regional anaesthesia in a patient recovering from anaesthesia and hypoxia. Whatever the experience level of the initial anaesthetists, the assistance of an experience, fresh, unstressed colleague is strongly recommended. Airway problems may also arise at the end of general anaesthesia. If intubation has been difficult and traumatic, the airway should be examined before awakening and a leak around the endotracheal tube confirmed. Aspiration is also a risk at emergence. Intraoperative antacid prophylaxis should be given, such as intravenous ranitidine, and the patient should be extubated awake, on her side and in the head-down positioning. Following a failed intubation, the patient should be closely monitored postoperatively, ideally in a high dependency environment, keeping a careful eye for any airway or respiratory complications. It is important to document events in the medical notes and inform the patient and her general practitioner.
Preventing failed intubation.
1. 2. 3. 4. 5.
Careful pre-operative assessment; if difficulty anticipated, avoid general anaesthesia or seek senior assistance Obsessional pre-induction positioning to achieve ‘‘sniffing the morning air’’ Obsessional pre-oxygenation to maximize safe intubation time Use your favourite laryngoscope from the start; you will never waste time asking for a second scope Guide the placement and force of your assistant’s cricoid pressure with your right hand as you visualize the airway 6. Always use a small endotracheal tube (6.5–7.0); you will never waste time asking for a smaller one 7. Incomplete view of the glottis; don ot waste time trying to intubate with the tube, pass a bougie This recipe brings you to the diagnosis of failed intubation quickly, hopefully before serious hypoxia has ensued.
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Table 4
Failed intubation drill.
After following Table 3, if it has been impossible to intubate with a bougie, activate the failed intubation drill. Dispatch someone to summon senior anaesthetic assistance 1. Achieve oxygenation by ascending through these options until successful a. Bag and mask ventilation with cricoid pressure maintained b. Try an oropharyngeal airway c. Ease off or remove cricoid pressure d. Insert a laryngeal mask airway (ProSealTM if experienced) e. Insert the cricothyroidotomy/tracheostomy device for which you have been trained 2. Allow the patient to wake up if a. you are not happy with oxygenation or security of the airway 3. Allow surgery to continue if a. you are happy with oxygenation and security of the airway b. there is life threatening maternal compromise or cardiac arrest
Do not be tempted to give a second dose of suxamethonium If regurgitation occurs with an unprotected airway, tilt head down and apply continuous suction to the pharyngx
After the incident, organize hazard warning, counselling, incident reporting
Aspiration The physiological changes of pregnancy put the parturient at risk of aspiration of gastric contents during anaesthesia. The progesteronemediated reduction in lower oesophageal sphincter tone, the enlarging uterus increasing intraabdominal pressure and higher gastric volumes and lower pH all contribute to this risk. Additionally, gastric emptying is delayed during labour, especially following the administration of opioids. Aspiration during obstetric anaesthesia was classically described by Mendelson in the 1940s.10 Deaths under deep ether anaesthesia were attributed to immediate asphyxiation from solid material and later respiratory failure from adult respiratory distress syndrome secondary to aspiration of liquid material. Mendelson concluded that the incidence of aspiration could be reduced by withholding oral feeding in labour and the wider use of regional anaesthesia. He also advocated the use of alkalization of stomach contents before anaesthesia to minimize the consequences of aspiration. Aspiration appears to be very rare in obstetric practice now, possibly because of the anti-aspiration strategies listed in Table 5. This has led to suggestions from some midwives and patient groups that we should be more liberal in our approach to allowing eating and drinking during labour. Prolonged labour can result in dehydration and ketosis, but there is little evidence that this adversely affects labour outcome. Scrutton et al.11 studied
Table 5
Anti-aspiration strategies.
Nil by mouth or clear fluid only policies in labour Antacid prophylaxis Rapid sequence induction using cricoid pressure and endotracheal intubation
Increased use of regional anaesthesia Improved anaesthetic training
the metabolic effects of feeding in early labour. They randomized parturients in early labour to receive either a light standardized low fat diet or water only. Feeding appeared to prevent the development of ketosis but gastric volumes measured by ultrasound were higher and greater volumes were vomited at delivery. The latter may increase the risk of pulmonary aspiration should a general anaesthetic be required. Another study12 looked at giving mothers in early labour isotonic sports drinks compared to water. This also appeared to prevent the development of ketosis but without increasing residual gastric volumes. It is not always easy to identify those women at low risk of needing anaesthesia during their labour. These women would probably be safe having a light diet. The majority of patients though, including those having opioid-containing epidurals, would be safer restricting their intake to water, and perhaps calories in the form of isotonic sports drinks rather than solid food.
ARTICLE IN PRESS Complications of obstetric anaesthesia Antacids, to reduce the volume and acidity of gastric contents, have a role to play in preventing aspiration or reducing its severity if it occurs. Gastric volumes of 0.4–0.8 mL/kg and pH of less than 2.5 are classically quoted as being the critical values concerned.13,14 Magnesium trisilicate was traditionally given during labour, and while it did reduce gastric acidity, its particulate nature caused problems if aspiration occurred. Sodium citrate, 30 mL 0.3 M, before induction of anaesthesia increases gastric pH but not volume. Histamine type 2 (H2) receptor antagonists, such as ranitidine 150 mg orally 1 h preoperatively, reduce gastric volume and acidity, especially in combination with sodium citrate. Ranitidine can also be given in an emergency intravenously at induction and will provide aspiration prophylaxis at emergence. Metoclopramide, a dopamine antagonist, increases lower oesophageal sphincter tone and gastric emptying. Proton pump inhibitors, such as omeprazole, increase gastric pH effectively but tend to be more expensive. The sentinel Caesarean section audit2 revealed that 99% of delivery suites in the United Kingdom routinely use drugs to reduce the gastric volume and acidity for elective Caesarean section and 98% for emergency. H2 receptor antagonists (ranitidine) and sodium citrate are the most commonly used agents. Only a minority of units used proton pump inhibitors, such as omeprazole. A postal survey of acid prophylaxis in obstetric anaesthetic units in the United Kingdom revealed similar results as regards the drugs used for acid aspiration prophylaxis, but additionally found that the number of units carrying out routine prophylaxis in active labour had fallen.15 The author’s unit uses ‘FasTab’ as an antacid prophylaxis. This is a fast acting oral preparation of lansoprazole, in a dose of 30 mg, which can be either be allowed to dissolve in the mouth, or swallowed with a small amount of water. Although it is easy to administer antacid prophylaxis to the parturient undergoing elective Caesarean section, it is easy to overlook it in an emergency. Increased use of regional anaesthesia has played a major role in the reduction of maternal deaths from aspiration, but it must be remembered that aspiration can occur with very high blocks and the loss of laryngeal reflexes. Rapid sequence induction also plays an important role, but introduces with it other risks such as failed intubation and oesophageal rupture if vomiting occurs. The management of aspiration during anaesthesia is outlined in Table 6. Just as intubation problems can complicate the termination of anaesthesia, so can aspiration. Some anaesthetists advocate attempts to empty the
155 Table 6 thesia. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Management of aspiration during anaes-
100% oxygen Head down position (+ turn to lateral) Suction oropharynx If no endotracheal tube in situ, apply cricoid pressure and intubate Suction and lavage tracheobronchial tree (preferably endoscopically) Bronchodilators for wheezing PEEP for hypoxaemia Post operative chest X-ray May need ventilation on ICU if severe Consider antibiotics if infected material aspirated
stomach with a large bore orogastric tube before emergence in all unfasted patients.
Awareness The spectrum of awareness under general anaesthesia ranges from dreaming, through recall of specific events, to the rare but very serious complication of full consciousness with total paralysis. It was a real concern for the obstetric anaesthetist in days gone by when minimal, or even no, volatile anaesthetic agent was given before delivery for fear of neonatal depression or uterine atony. Increased inspired oxygen concentrations, given at the expense of nitrous oxide to ensure optimal maternal and fetal oxygenation in the pre–saturation monitoring era, compounded this problem. The final straw was the avoidance of opioids until after delivery. Again, modern practice changes seem to have reduced the awareness problem. (Table 7). Anaesthetists now routinely give a reasonable induction dose of thiopentone (4–6 mg/kg) and maintain anaesthesia with at least one minimal alveolar concentration (MAC) of volatile anaesthetic agent, aided by end tidal anaesthetic gas monitoring. Modern volatile agents with low blood gas solubility, allow rapid progression to deep anaesthesia. Inspired oxygen can now be titrated against maternal saturation readings. It is rare to need more than 30%, so nitrous oxide need not be automatically restricted. Despite the above, awareness may still arise, especially in the emergency situation.16 Patients are anxious and unpremedicated. Opioid analgesia
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Table 7 Measures to reduce the incidence of awareness.
Adequate induction dose of thiopentone
(4–6 mg/kg) 0.3:0.7 oxygen: nitrous oxide mixture 1 MAC of low blood gas soluble volatile agent End tidal volatile agent monitoring Depth of anaesthesia monitoring in the future
is usually withheld until the baby is delivered. In the difficult intubation situation, oxygenation takes precedence and the patient may become aware as the induction agent wears off if inadequate volatile agent has been given. Concerns were raised by King et al.17 that the practice of allowing surgery to begin immediately after endotracheal intubation does not provide adequate depth of anaesthesia at the time of skin incision during Caesarean section. Again, modern low blood-gas soluable agents such as sevoflurane, especially with the use of ‘overpressure’ techniques, enable all these risks to be minimized. Awareness may also arise because of drug errors. The author is aware of two such cases of awareness at her institution; one followed inadvertent induction with saline and the other the antibiotic cefuroxime. Depth of anaesthesia monitoring is not widely available in most delivery suite theatres in the UK. Clinical signs tend to be unreliable. Most patients will be tachycardic, hypertensive and sweaty as they are usually very anxious pre-induction and are not given any analgesia until delivery. Various techniques for monitoring anaesthetic depth have been studied in clinical practice, including isolated forearm, lower oesophageal contractility and electroencephalographic bispectral monitoring (BIS).16–18 BIS values of less than 60 are required to ensure unconsciousness in the majority of patients. Chin determined that an end-tidal concentration of sevoflurane of 1.2–1.5% was required to minimize the risk of intraoperative awareness and subsequent recall during Caesarean section using this technique.18 It remains to be seen whether BIS monitoring will become a more widely used depth of anaesthesia monitor in the future.
Complications of regional anaesthesia The main complications of regional anaesthesia are listed in Table 2.
Hypotension Regional anaesthesia can cause significant hypotension due to blockade of sympathetic nerve fibres. The resultant lower body vasodilatation and venous pooling reduce cardiac output and hence blood pressure. Aortocaval compression and hypovolaemia may exacerbate these changes. Serious hypotension is now rare with modern lowdose epidural analgesia. Hawthorne et al.19 looked at the effect of fluid pre-loading on maternal haemodynamics for low-dose epidural analgesia in labour and found no difference in cardiac index or mean arterial pressure between patients given no fluid pre-load and those given a 7 mL/kg normal saline pre-load. Routine fluid preloading is not necessary before low-dose epidural analgesia and may in fact be hazardous to parturients with severe pre-eclampsia or cardiac disease, and can also inhibit uterine contractions. The anaesthetist may consider giving fluids to the parturient who is hypovolaemic from an antepartum haemorrhage or dehydrated from an excessively long labour, especially on a hot day. Management of hypotension following epidural analgesia is listed in Table 8. Remember that epidural top-ups with large volumes of high concentration of local anaesthetic agents for operative delivery may precipitate more severe hypotension. Hypotension is an inevitable consequence of high spinal anaesthesia in obstetrics if no preventative measures are used. The anaesthetic literature contains many systematic reviews of randomized controlled trials of interventions to reduce the incidence of hypotension during spinal anaesthesia including preload with crystalloid 20 mL/kg versus control, pre-emptive colloid versus crystalloid, ephedrine versus control and lower limb compression during control.20 Despite these measures hypotension was still a common problem, until recently. The answer to the problem of spinal anaestheticinduced hypotension may have been found with a change in vasoconstrictor practice. Traditional obstetric anaesthetic teaching recommended ephedrine, a combined a and b agonist, as the vasoconstrictor of choice. It increases blood pressure by a mediated activity increasing systemic vascular resistance and b mediated increases in cardiac output and heart rate and was thought to maintain uteroplacental blood flow better than other vasoconstrictors. This arose from studies in pregnant sheep in the 1970s given supranormal doses of vasoconstrictors but without regional anaesthesia.21 Uteroplacental perfusion was reduced with pure a agonists but was maintained
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 8 1. 2. 3. 4.
157
Management of hypotension following epidural analgesia.
Left lateral positioning to relieve aortocaval compression Commence intravenous fluid infusion Consider vasoconstrictor e.g. 3–6 mg increments of ephedrine Exclude other causes e.g. subarachnoid epidural catheter placement, hypovolaemia, obstetric haemorrhage
with ephedrine, even at doses which increased the blood pressure by 50%. It was concluded, therefore, that ephedrine was the superior prophylactic vasoconstrictor and that pure a agonists should be avoided. Meta-analysis has revealed a higher incidence of fetal acidosis at delivery following spinal anaesthesia for Caesarean section than epidural or general anaesthesia.22 This may be due to spinalinduced hypotension or drugs used to correct this, usually ephedrine. Concerns have now been raised that doses of ephedrine large enough to maintain the blood pressure after induction of spinal anaesthesia may be detrimental to the fetus. Tachyphylaxis can occur with ephedrine and large amounts of drug may then be needed to maintain its effect. This can then cross the placenta and stimulate fetal metabolism via its b agonist activity, resulting in a metabolic acidosis. This effect may be even more significant in the compromised fetus. Phenylephrine is at least as effective as ephedrine in the prevention or treatment of spinal anaesthesia induced hypotension. In addition, it is associated with a lower incidence of fetal acidosis and maternal sickness.23 Given in doses that maintain normotension, phenylephrine does not cause clinically significant placental vasoconstriction or decreased perfusion.24 Audit data following a change in vasoconstrictor regimen at the author’s institution from an ephedrine (30 mg/1 L NSaline) to a phenylephrine infusion (1 g/1 L NSaline) commenced upon spinal injection has revealed a significant fall in the incidence of severe hypotension, with additional vasoconstrictor therapy only rarely being needed. Some authors state that the clinical situation must guide which vasopressor is appropriate for the patient, considering not only the blood pressure but the heart rate too.25 Because of its indirect stimulatory effect on heart rate, ephedrine may be the vasopressor of choice in a parturient who is hypotensive and bradycardic, while phenylephrine would be preferable in someone who is hypotensive and tachycardic, due to its reflex baroreceptor effect in slowing the heart rate. Bradycardia
occurring during phenylephrine use is better treated with glycopyrollate rather than atropine, as the former does not cross the placenta and has a more sustained effect. Whichever vasoconstrictor regimen is chosen, it must be remembered to take measures to avoid aortocaval compression, usually by left lateral tilt of the theatre table.
Local anaesthetic toxicity Local anaesthetic toxicity may be caused by inadvertent intravascular injection into a catheter which has been sited or migrated into an epidural vein. Theoretically, systemic toxicity can also follow from excessive epidural dosing. The safe maximum dose of bupivacaine is quoted as 2 mg/kg every 4 h. A standard epidural top-up for an emergency Caesarean section of 20 mL 0.5% plain bupivacaine, often following on from an infusion and several top-ups in labour, can easily reach this supposedly toxic level in small parturients. Toxicity from systemic absorption in these circumstances does however appear to be very rare, and the quoted maximum doses rather conservative for obstetric practice. Signs and symptoms of toxicity include numbness and tingling of the tongue and around the mouth, tinnitus and ear popping, funny taste sensations, light-headedness, confusion and slurred speech. Later, loss of consciousness, convulsions and cardiovascular collapse can ensue. Deaths have been attributed to bupivacaine-induced cardiotoxicity in the past. Racemic bupivacaine is a mixture of its R and S isomers. The latter is responsible for its physiological effects and the former its unwanted ones, especially cardiotoxicity. This prompted the development and marketing of single S isomer local anaesthetics. Levobupivacaine is the S-enantiomer of bupivacaine. It has been found to have an improved cardiovascular safety profile compared to racemic bupivacaine26 and only a slightly lower potency.27 Ropivacaine is the S-enantiomer of propivacaine.
ARTICLE IN PRESS 158 Table 9 city.
A. Pinder Management of local anaesthetic toxi-
1. 2. 3. 4. 5. 6.
Stop injection of local anaesthetic ABC and call for help Oxygen via face mask Left lateral positioning Support airway and ventilation if necessary Control fits with an intravenous benzodiazepine or thiopentone 7. Treat hypotension with fluids and vasopressors 8. Cardiac arrest as per standard guidelines. Refractory arrhythmias may be a problem with bupivacaine
This agent also has lower cardiotoxicity than racemic bupivacaine, although this may be partly related to its lower potency.28,29 Management of local anaesthetic toxicity begins with attempts at its prevention. Following a bloody tap at epidural insertion, the catheter should be withdrawn and flushed with saline. If the catheter fails to clear it should be resited. Test doses are advocated to detect intravenous injection. No test dose is 100% sensitive and specific and it is wise for the anaesthetist to consider ‘every dose a test dose’. Aspiration should be performed before injections, drugs should be given in small divided quantities and toxic doses should not be exceeded. If signs and symptoms of local anaesthetic toxicity develop, the management plan in Table 9 should be followed. Drug administration must be stopped, airway, breathing and circulation (ABC) attended to and then any neurological or cardiovascular complications treated. Bretylium was traditionally used to treat refractory bupivacaineinduced arrhythmias, but since its withdrawal, amiodarone or magnesium should be considered.
Accidental dural puncture and dural puncture headache The incidence of inadvertent dural puncture with an epidural needle varies widely between units, but is consistently around 0.6% in the author’s institution. Headache after spinal anaesthesia with 27 gauge pencil point needles is currently 0.25%, usually after repeated needle passes. Inadvertent dural puncture with an epidural needle is usually easily recognized by a rapid flow of CSF from the epidural needle, but a glancing dural puncture might produce a less convincing
flow. Some recommend testing the temperature and glucose content of the CSF to confirm the diagnosis, but both these tests produce false positive results. Some dural taps only become apparent on aspiration through the epidural catheter, or after the epidural test dose. Later on, some dural taps present as headache without any record of CSF leak at the time of insertion. One explanation for this is the epidural needle transfixing the dural sack at insertion, causing two dural punctures but no leak. The fact that not all dural punctures are spotted by the epiduralist makes it vital that anaesthetists and midwives are trained to identify the features of subarachnoid injection of epidural drugs, and post-dural puncture headache. The complications of accidental dural puncture include headache, high or total spinal anaesthesia, 6th cranial nerve palsy and subdural haemorrhage. The historical management of a recognized accidental dural puncture is to resite the epidural. This may be considered by some to be the safest approach as it is familiar practice. The epidural may prove difficult, another anaesthetist may need to be called to help and there is the risk of repeating the dural puncture. Theoretically, there is the risk of the epidural catheter or local anaesthetic solution passing through the dural puncture hole and unpredictable blocks. ‘Anaesthetist only’ top-ups may therefore be recommended. A better option is to thread the epidural catheter into the subarachnoid space if possible (Table 10). Intermittent ‘anaesthetist only’ top-ups given by this route usually provide excellent analgesia, albeit with tachyphylaxis developing after some time. The author’s institution uses the standard low-dose bupivacaine and fentanyl mixture in small increments titrated to analgesic effect. The catheter can be topped up with incremental hyperbaric bupivacaine if operative delivery is needed. Dural puncture headache, and hence the need for epidural blood patching, may also be less common if the catheter is left in situ for 24 h.30,31 This is thought to be due to an inflammatory reaction taking place around the catheter sealing the dural hole, although not all workers have confirmed this finding.32 Everyone must be aware that the catheter is in the intrathecal space to reduce the risk of inadvertent administration of an epidural local anaesthetic dose down it with the potential for a high or total spinal. A recent survey of the management of accidental dural puncture during labour epidural analgesia revealed the insertion of the epidural catheter intrathecally when accidental dural puncture was diagnosed to be the most
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 10 Management of accidental dural puncture: epidural or intrathecal catheter?. Epidural catheter Advantages Familiar practice Good analgesia
Disadvantages Possible higher headache rate Unpredictable blocks
Intrathecal catheter Excellent analgesia Top-ups possible for operative delivery Possible lower headache rate
159 Table 11
Epidural blood patch procedure.
1. Explain procedure to patient and obtain
informed consent 2. Full asepsis 3. Left lateral positioning for patient comfort 4. Interspace below previous dural puncture,
anaesthetist identifies epidural space 5. Colleague obtains 20 mL venous blood 6. Blood injected through Touhy needle into
epidural space 7. Patient advised to lay flat for 1–2 h and to avoid
Anaesthetist only topups Risk high block with inadvertant epidural doses
straining and lifting for several days 8. Follow up 9. May need to be repeated
Analgesia delay
significant change in practice, with only 1% of units doing this in 1993 but 59% in 2003.33 Whichever management option is taken, once the patient is comfortable, she should be informed of the complication and its implications. It should be documented in the medical notes and the patient closely followed up for the development of complications. In the past, elective forceps delivery used to be recommended to reduce straining during the second stage of labour, but not now. Headaches are common in all parturients following delivery. Fatigue and dehydration are common causes. Dural puncture may be unrecognized at the time of epidural insertion and may present as a postpartum headache. The classical dural puncture headache is postural, worse when sitting or standing, improved by lying flat, and begins within 48 h of delivery. It may be frontal or occipital and usually described as a severe aching or throbbing. Associated signs and symptoms include photophobia, neck stiffness, nausea, vomiting, cranial nerve palsies and, importantly for the mother, it interferes with her ability to care for the baby. The headache is caused by the leakage of cerebrospinal fluid through the dural hole, which results in traction on the pain sensitive meninges and compensatory vasodilatation. Management begins with measures to prevent accidental dural puncture happening in the first place by using a careful epidural technique and using loss of resistance to saline rather than air. Once dural puncture has occurred, measures to prevent headache from developing include leaving an intrathecal catheter in situ for at least 24 h, epidural saline infusions, prophylactic blood patching through an epidural catheter, keeping the
patient well hydrated and bed rest. None of these methods has been conclusively shown to work. Once a dural puncture headache has developed conservative measures such as regular analgesia and adequate hydration should be tried first as some headaches resolve spontaneously. Cerebral vasoconstrictors, such as caffeine and sumatriptan, have been tried, as have abdominal binders. Results are unconvincing. The definitive ‘gold standard’ treatment is the epidural blood patch. This involves the injection of about 20 mL of the patient’s blood into the epidural space under aseptic conditions (Table 11). Immediate relief is thought to be due to the mass effect of the blood compressing the dural sac and displacing cerebrospinal fluid into the cranium. Over the next few hours the blood clots and seals the dural hole. A single blood patch ‘cures’ the headache in about two thirds of cases, in the remainder a repeat blood patch may be necessary. Complications include repeating the dural puncture, transient nerve root pain and back pain.34
High blocks The incidence of high blocks is much less than that of failed intubations, but the actual number may be higher as far more regional anaesthetics are performed than general in the UK. It has been recommended that units have a high regional block drill, which is regularly reviewed and rehearsed like a failed intubation drill.35 Table 12 shows the circumstances and incidences of blocks that went high enough to require intubation during a 6 year period in the author’s unit.36 Performing spinal
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Table 12
High spinals in Leeds 1997–2003 (courtesy of M. Dresner).
Technique
Number of high blocks/total number of cases
Incidence (%)
Epidural analgesia CSE analgesia Spinal anaesthesia CSE anaesthesia Topped up epidural/CSE Spinal after an epidural
1/6796 0/2296 0/3784 0/222 1/995 5/342
0.01 0 0 0 0.1 1.46
Table 13 1. 2. 3. 4.
Management of high spinal.
Recognize early Reassure patient Call for help Symptomatic treatment a. Hypotension—relieve aortocaval compression, fluids, vasoconstrictors b. Bradycardia—glycopyrollate or atropine c. Inadequate respiration-100% oxygen, gentle bag and mask ventilation d. Loss of consciousness—consider anaesthesia and intubation
5. Consider urgent delivery of the baby
anaesthesia on women who have been receiving epidural analgesia seems to be the highest risk scenario. Management of high spinal blockade begins with early recognition (Table 13). Signs and symptoms usually develop rapidly, but may be late and insidious in onset. The patient may initially complain of numbness, weakness or tingling in her arms, difficulty in breathing and lightheadness. Her speech may become slurred or her voice hoarse. Hypotension and bradycardia are initially due to sympathetic blockade but later due to the effects of the local anaesthetic on the brain stem. The latter will also result in apnoea and loss of consciousness. Reassurance of the mother is very important as she will be terrified and hearing is late to disappear. Symptomatic treatment should follow as outlined in Table 13. Urgent delivery of the baby should be considered as this may cause the block to regress and the maternal condition to improve. However, one case in the author’s unit involved a woman who needed intubating for a high block caused by intrathecal injection of drugs via a misplaced epidural catheter that had been sited for pain relief. She was ventilated and sedated for
40 min, woken up, extubated, and then went on to have a normal delivery of a healthy baby with excellent analgesia from her unplanned spinal catheter.
Subdural block A subdural block may also be the cause of a high spinal. An epidural catheter may be sited in the potential space between the dura and arachnoid mater. The first epidural dose given through it produces as a slow onset high, patchy block with minimal motor block, sacral block or hypotension. Subsequent top up injections may then rupture through the arachnoid mater with intrathecal effects. If an epidural catheter is suspected to be subdural it should be re-sited. If not recognized, the resultant high spinal block should be managed as outlined above.
Neurological complications Any paper discussing the complications of obstetric anaesthesia would be incomplete without at least a mention of neurological sequelae (Table 14).37 These are the complications that we and patients all dread. How many of us have been asked during the anaesthetic visit ‘will it paralyse me, doctor?’. Despite our fears, neurological complications following obstetric anaesthesia are extremely rare, although the number of reported cases may increase as more regionals are performed. Neurological deficits, especially peripheral neuropathies, are more commonly caused by labour and delivery. We must also remember that spontaneous neurological insults can occur in the absence of regional analgesia or anaesthesia. Careful regional anaesthetic technique plays an important role in the prevention of neurological complications. This includes asepsis, inserting
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 14 Neurological complications associated with regional anaesthesia.37 Neuropathy Epidural abscess Epidural/spinal haematoma Meningitis Chronic adhesive arachnoiditis Subdural haematoma Cauda equina syndrome Anterior spinal artery syndrome Cranial nerve palsies
needles at the correct spinal level and not performing regionals in patients with contraindications, such as coagulopathies and infections. If neurological complications are suspected, prompt diagnosis and treatment, sometimes with neurosurgical intervention, are necessary to reduce or prevent long-term disability. Neuropathies are the commonest neurological complication. Nerve root damage may be caused by direct needle or catheter trauma or direct intraneural injection of local anaesthetic. Pain and/or parasthesia are usually noted during performance of the block, which should prompt the anaesthetist to withdraw the needle or catheter or to stop the local anaesthetic injection. They present as numbness in the dermatome supplied by the nerve root, sometimes with muscle weakness. Full recovery within months is usually to be expected. Spinal cord injury can occur during regional anaesthesia. Reynolds38 presented several cases of conus damage following spinal injection. These followed spinal or combined spinal-epidurals, and were associated with difficulty in siting the block and pain on needle insertion or drug injection. Interestingly the lesions were not consistent with the documented level of needle insertion, all being made at inappropriately high levels leading to direct damage to the spinal cord. She concluded that anaesthetists should not insert spinal needles above the third lumber vertebral space. In theory this is good advice, but it is well known that anaesthetists are very poor at correctly identifying the spinal level.39
Conclusion This paper reviews some of the complications associated with obstetric anaesthesia. While their potentially serious nature should be of significant
161 concern to every anaesthetist on delivery suite, one must also remember that these complications are rare. Careful attention to detail in our anaesthetic practice will play an important role in minimizing their incidence.
References 1. Confidential Enquiry into Maternal and Child Health. Why mothers die 2000–2: the sixth report of the confidential enquiries into maternal death in the United Kingdom. London: RCOG Press; 2004. 2. Royal College of Obstetricians and Gynaecologists. Clinical effectiveness support unit. The National Sentinel Caesarean Section audit report. London: RCOG Press; 2001. 3. Brown GW, Russell IF. A survey of anaesthesia for caesarean section. Int J Obstet Anesth 1995;4(4):214–8. 4. King TA, Adams AP. Failed tracheal intubation. Br J Anaesth 1990;65(3):400–14. 5. Johnson RV, Lyons GR, Wilson RC, Robinson AP. Training in obstetric general anaesthesia: a vanishing art? Anaesthesia 2000;55(2):179–83. 6. Hawthorne L, Wilson R, Lyons G, Dresner M. Failed intubation revisited: 17-yr experience in a teaching maternity unit. Br J Anaesth 1996;76(5):680–4. 7. Rahman K, Jenkins JG. Failed tracheal intubation in obstetrics: no more frequent but still managed badly. Anaesthesia 2005;60(2):168–71. 8. Yentis SM. Predicting difficult intubation—worthwhile exercise or pointless ritual? Anaesthesia 2002;57(2):105–9. 10. Mendelson CL. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol 1946;52:191–204. 11. Scrutton MJ, Metcalfe GA, Lowy C, Seed PT, O’Sullivan G. Eating in labour. A randomised controlled trial assessing the risks and benefits. Anaesthesia 1999;54(4):329–34. 12. Kubli M, Scrutton MJ, Seed PT, O’Sullivan G. An evaluation of isotonic ‘‘sport drinks’’ during labor. Anesth Analg 2002; 94(2):404–8 table of contents. 13. Roberts RB, Shirley MA. Reducing the risk of acid aspiration during cesarean section. Anesth Analg 1974;53(6):859–68. 14. Raidoo DM, Rocke DA, Brock-Utne JG, Marszalek A, Engelbrecht HE. Critical volume for pulmonary acid aspiration: reappraisal in a primate model. Br J Anaesth 1990; 65(2):248–50. 15. Greiff JM, Tordoff SG, Griffiths R, May AE. Acid aspiration prophylaxis in 202 obstetric anaesthetic units in the UK. Int J Obstet Anesth 1994;3(3):137–42. 16. Bogod DG, Orton JK, Yau HM, Oh TE. Detecting awareness during general anaesthetic caesarean section. An evaluation of two methods. Anaesthesia 1990;45(4):279–84. 17. King H, Ashley S, Brathwaite D, Decayette J, Wooten DJ. Adequacy of general anesthesia for cesarean section. Anesth Analg 1993;77(1):84–8. 18. Chin KJ, Yeo SW. A BIS-guided study of sevoflurane requirements for adequate depth of anaesthesia in Caesarean section. Anaesthesia 2004;59(11):1064–8. 19. Hawthorne L, Slaymaker A, Bamber J, Dresner M. Effect of fluid preload on maternal haemodynamics for low-dose epidural analgesia in labour. Int J Obstet Anesth 2001; 10(4):312–5. 20. Emmett RS, Cyna AM, Andrew M, Simmons SW. Techniques for preventing hypotension during spinal anaesthesia for
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caesarean section. Cochrane Database Syst Rev 2001(3): CD002251. Ralston DH, Shnider SM, DeLorimier AA. Effects of equipotent ephedrine, metaraminol, mephentermine, and methoxamine on uterine blood flow in the pregnant ewe. Anesthesiology 1974;40(4):354–70. Cooper DW, Carpenter M, Mowbray P, Desira WR, Ryall DM, Kokri MS. Fetal and maternal effects of phenylephrine and ephedrine during spinal anesthesia for cesarean delivery. Anesthesiology 2002;97(6):1582–90. Reynolds F, Seed PT. Anaesthesia for Caesarean section and neonatal acid-base status: a meta-analysis. Anaesthesia 2005;60(7):636–53. Riley ET. Editorial I: spinal anaesthesia for Caesarean delivery: keep the pressure up and don’t spare the vasoconstrictors. Br J Anaesth 2004;92(4):459–61 Erratum in: Br J Anaesth 2004;92(5):782. Vallejo MC, Ramanathan S. Should alpha-agonists be used as first line management of spinal hypotension? Int J Obstet Anesth 2003;12(4):243–5. Gristwood R, Bardsley H, Baker H, Dickens J. Reduced cardiotoxicity of laevobupivacaine compared with racemic bupivacaine (Marcain). Expert Opin Inv Drug 1994;3: 1209–12. Lyons G, Columb M, Wilson RC, Johnson RV. Epidural pain relief in labour: potencies of levobupivacaine and racemic bupivacaine. Br J Anaesth 1998;81(6):899–901 Erratum in: Br J Anaesth 1999;82(3):488. Caogna G, Celleno D, Lyons G, Columb M. Determination of the minimum local analgesic concentration (MLAC) of epidural ropivacaine in labour. Br J Anaesth 1998;80:148.
A. Pinder 29. Lyons G, Reynolds F. Toxicity and safety of epidural local anaesthetics. Int J Obstet Anesth 2001;10(4):259–62. 30. Dennehy KC, Rosaeg OP. Intrathecal catheter insertion during labour reduces the risk of post-dural puncture headache. Can J Anaesth 1998;45(1):42–5. 31. Ayad S, Demian Y, Narouze SN, Tetzlaff JE. Subarachnoid catheter placement after wet tap for analgesia in labor: influence on the risk of headache in obstetric patients. Reg Anesth Pain Med 2003;28(6):512–5. 32. Norris MC, Leighton BL. Continuous spinal anesthesia after unintentional dural puncture in parturients. Reg Anesth 1990;15(6):285–7. 33. Baraz R, Collis RE. The management of accidental dural puncture during labour epidural analgesia: a survey of UK practice. Anaesthesia 2005;60(7):673–9. 34. Cooper G. Epidural blood patch. Eur J Anaesthesiol 1999; 16(4):211–5. 35. Yentis SM, Dob DP. High regional block—the failed intubation of the new millennium? Int J Obstet Anesth 2001;10(3): 159–61. 36. Dresner M, Brennan A, Freeman J. Six year audit of high regional blocks in obstetric anaesthesia. Int J Obs Anesth 2003;12:202. 37. Loo CC, Dahlgren G, Irestedt L. Neurological complications in obstetric regional anaesthesia. Int J Obstet Anesth 2000;9(2):99–124. 38. Reynolds F. Damage to the conus medullaris following spinal anaesthesia. Anaesthesia 2001;56(3):238–47. 39. Broadbent CR, Maxwell WB, Ferrie R, Wilson DJ, Gawne-Cain M, Russell R. Ability of anaesthetists to identify a marked lumbar interspace. Anaesthesia 2000;55(11):1122–6.
www.elsevier.com/locate/cacc
FOCUS ON: OBSTETRICS
Complications of obstetric anaesthesia Amanda Pinder Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
KEYWORDS Pregnancy; Obstetric anaesthesia; Obstetric analgesia; Complications
Summary The obstetric anaesthetist has an increasing role to play in the provision of anaesthesia and analgesia for the parturient. Both regional and general anaesthesia carry with them the potential for complications, some of which, although rare, may be serious, life threatening and/or permanently disabling. Careful attention to detail in our anaesthetic practice will play an important role in minimizing their incidence. Measures to prevent and manage the following complications will be discussed: intubation problems, aspiration, awareness, hypotension, local anaesthetic toxicity, dural puncture and post-dural puncture headache, high regional blocks and neurological damage. & 2006 Elsevier Ltd. All rights reserved.
Introduction The repertoire of obstetric anaesthesia has grown in recent years to include epidurals, spinals, combined spinal epidurals (CSE), spinal catheters and general anaesthesia. All of these may be associated with complications. Common ones, such as nausea and vomiting or a patchy epidural, may not be particularly serious but can nonetheless be very distressing for the patient. What may concern the anaesthetist more are the rare and serious complications that may be potentially life threatening or permanently disabling. The maternal confidential enquiries1 revealed there to be 30–50 maternal deaths per triennium from general anaesthesia until the 1980s. These deaths were mainly due to aspiration and failure of oxygenation during failed intubation. The imTel.: +44 113 3926672.
E-mail address: [email protected].
plementation of recommendations from previous reports, supported by the various professional bodies, has led to a fall in anaesthesia–related maternal deaths since then. Improvements in training, staffing, supervision, monitoring and facilities have all contributed, as have increased use of regional anaesthetic techniques and measures to prevent aspiration of gastric contents. It is somewhat disheartening that general anaesthetic deaths from poor airway management have returned to haunt us. There had been no general anaesthetic deaths in the previous two reports, although there had been some questionable regional anaesthetic management. In 2000–2002 there were six UK maternal general anaesthetic deaths and one late death from hypoxic brain damage from unrecognized oesophageal intubation. Three of these six deaths were also associated with unrecognized oesophageal intubation, with capnography only being used in one case! The numbers of deaths are small and the report does state that it is too
0953-7112/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.cacc.2006.05.008
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early to say whether the increase in anaesthetic deaths is a real cause for concern, but it does recommend that anaesthesia training must ensure competency in airway management, especially the recognition and management of oesophageal intubation. Despite this, it is still 30 times safer to have a general anaesthetic on labour ward nowadays than it was in the 1950s. Regional anaesthesia may be safer than general anaesthesia, despite the deaths in the previous two confidential enquiries, but concerns still remain about other serious complications. High blocks, neurological damage and sequelae of dural puncture may be rare but can be life threatening and leave the mother with permanent residual damage. This paper aims to review some of the complications associated with obstetric anaesthesia. These are listed in Tables 1 and 2.
Complications of general anaesthesia Although the proportion of general anaesthetics used in obstetric practice has plummeted over the last two decades, the actual number given for emergency Caesarean sections is largely unchanged2,3 because of the increased section rate. General anaesthesia is potentially indicated for
Table 1
Complications of general anaesthesia.
Difficult and failed intubation Aspiration Awareness Nausea and vomiting Post-operative pain Sore throat Drowsiness Delayed bonding and breast feeding
Table 2
Complications of regional anaesthesia.
Failure (unable to site, partial or complete failure to work) Hypotension Local anaesthetic toxicity Dural puncture and post dural puncture headache High block Neurological complications Shivering Opioid effects (urinary retention, pruritis, delayed gastric emptying, and the potential for maternal and neonatal respiratory depression)
most category 1 Caesarean sections and when regional anaesthesia is contraindicated or has failed. I will discuss three main hazards of general anaesthesia: failed intubation, aspiration and awareness.
Difficult and failed intubation Failed intubation is eight times more common in the pregnant (incidence 1 in 280) than the nonpregnant population (incidence 1 in 2230).4 There were three maternal deaths in the last maternal confidential enquiry attributed to failed intubation and unrecognized oesophageal intubation by junior anaesthetists working in isolation.1 Concerns have been raised about insufficient training opportunities for junior doctors in obstetric general anaesthesia.5,6 An audit of failed intubations in the South West Thames region revealed that, although its incidence remains unchanged, in half of the cases for which the notes could be examined there was a failure to follow an accepted protocol for failed tracheal intubation. These protocol violations included giving a second dose of suxamethonium or repeated attempts at tracheal intubation.7 Why is there such a high incidence of airway problems in obstetrics? Oft quoted reasons include large breasts and full dentition, but few anaesthetists consider these particularly worrying characteristics in the non-obstetric population. The main reasons are time, fear and inexperience. Time. Once apnoea occurs after induction, the obstetric patient desaturates rapidly despite pre-oxygenation because of the combination of reduced functional residual capacity of the lungs and high metabolic rate. Fear, outside of obstetrics, increasing hypoxia during intubation is managed by pausing to re-oxygenate the patient with bag and mask ventilation. This is considered to be extremely dangerous in UK obstetric teaching, because of the risk of gastric insufflation and resultant regurgitation and aspiration. Trainees are taught to fear this manoeuvre and to immediately enter a failed intubation drill. With the words failure and aspiration filling their minds, fear can negatively affect performance and decision making. Inexperience is often a contributor to cases of failed intubation, and appears to be an insoluble problem. Most general anaesthetics are used for emergency sections, two-thirds of which are bound to occur out of hours when no consultant is on site. The combination of the relative rarity of general anaesthesia and reduced working hours has limited
ARTICLE IN PRESS Complications of obstetric anaesthesia training opportunities, and ensured the relative inexperience of the trainee anaesthetists who deliver most of the obstetric general anaesthesia in the UK. Of course, there are genuine physical predictors for airway problems, one of which is obesity. As serious obesity becomes more and more common, we might expect an increase in the incidence of failed intubation. This is particularly true given the high incidence of obstetric intervention required in the obese population. This is one condition where careful antenatal assessment may reduce anaesthetic risk. An anaesthetic plan in the medical notes which advocates early epidural analgesia to avert the need for general anaesthesia and early contact with a senior anaesthetist may be all that is required to avert a major problem. However, it is unlikely that routine antenatal airway screening will eliminate all unexpected difficult intubations because of the unreliability of the available tests.8 Some suggestions for preventing failed intubation are shown in Table 3. Many failed intubation algorithms exist in the anaesthetic literature. Inevitably the more comprehensive they are, the more complicated they become. A simple example is suggested in Table 4. It is important that anaesthetists have a plan in their own minds of what do to if the failed intubation situation arises, and that they are intimately familiar with the airway equipment available to them. The commonest reason for using general anaesthesia is probably for the category 1 Caesarean section for severe fetal distress. Traditional anaesthetic teaching argues that the safety of the mother should not be compromised for the sake of the fetus. This would imply that the option of allowing surgery to continue after rescuing a failed intubation by, for example, inserting a laryngeal mask, is not acceptable. I do not support this view, as most couples would gladly accept personal risk in exchange for a healthy baby. It is a
Table 3
153 difficult decision, but (in very experienced hands) it can be appropriate to allow surgery to continue with a spontaneous breathing mask or laryngeal mask anaesthetic. In these circumstances, a senior surgeon should be summoned to expedite the procedure. A deep plane of anaesthesia should be maintained to reduce the risk of laryngospasm and vomiting. Sevoflurane is ideal under these circumstances as it is non-irritant and its low bloodgas solubility allows rapid deepening of anaesthesia. Unfortunately, it reduces uterine tone and oxytocin infusions may be necessary for troublesome atonic bleeding. Propofol infusions may be beneficial in patients at high risk of major haemorrhage as it has minimal effects on uterine tone. If the decision is made to wake the patient up, the anaesthetist is then faced with choosing one of several unattractive options. Repeat conventional general anaesthesia, general anaesthesia after an awake intubation, or regional anaesthesia in a patient recovering from anaesthesia and hypoxia. Whatever the experience level of the initial anaesthetists, the assistance of an experience, fresh, unstressed colleague is strongly recommended. Airway problems may also arise at the end of general anaesthesia. If intubation has been difficult and traumatic, the airway should be examined before awakening and a leak around the endotracheal tube confirmed. Aspiration is also a risk at emergence. Intraoperative antacid prophylaxis should be given, such as intravenous ranitidine, and the patient should be extubated awake, on her side and in the head-down positioning. Following a failed intubation, the patient should be closely monitored postoperatively, ideally in a high dependency environment, keeping a careful eye for any airway or respiratory complications. It is important to document events in the medical notes and inform the patient and her general practitioner.
Preventing failed intubation.
1. 2. 3. 4. 5.
Careful pre-operative assessment; if difficulty anticipated, avoid general anaesthesia or seek senior assistance Obsessional pre-induction positioning to achieve ‘‘sniffing the morning air’’ Obsessional pre-oxygenation to maximize safe intubation time Use your favourite laryngoscope from the start; you will never waste time asking for a second scope Guide the placement and force of your assistant’s cricoid pressure with your right hand as you visualize the airway 6. Always use a small endotracheal tube (6.5–7.0); you will never waste time asking for a smaller one 7. Incomplete view of the glottis; don ot waste time trying to intubate with the tube, pass a bougie This recipe brings you to the diagnosis of failed intubation quickly, hopefully before serious hypoxia has ensued.
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Table 4
Failed intubation drill.
After following Table 3, if it has been impossible to intubate with a bougie, activate the failed intubation drill. Dispatch someone to summon senior anaesthetic assistance 1. Achieve oxygenation by ascending through these options until successful a. Bag and mask ventilation with cricoid pressure maintained b. Try an oropharyngeal airway c. Ease off or remove cricoid pressure d. Insert a laryngeal mask airway (ProSealTM if experienced) e. Insert the cricothyroidotomy/tracheostomy device for which you have been trained 2. Allow the patient to wake up if a. you are not happy with oxygenation or security of the airway 3. Allow surgery to continue if a. you are happy with oxygenation and security of the airway b. there is life threatening maternal compromise or cardiac arrest
Do not be tempted to give a second dose of suxamethonium If regurgitation occurs with an unprotected airway, tilt head down and apply continuous suction to the pharyngx
After the incident, organize hazard warning, counselling, incident reporting
Aspiration The physiological changes of pregnancy put the parturient at risk of aspiration of gastric contents during anaesthesia. The progesteronemediated reduction in lower oesophageal sphincter tone, the enlarging uterus increasing intraabdominal pressure and higher gastric volumes and lower pH all contribute to this risk. Additionally, gastric emptying is delayed during labour, especially following the administration of opioids. Aspiration during obstetric anaesthesia was classically described by Mendelson in the 1940s.10 Deaths under deep ether anaesthesia were attributed to immediate asphyxiation from solid material and later respiratory failure from adult respiratory distress syndrome secondary to aspiration of liquid material. Mendelson concluded that the incidence of aspiration could be reduced by withholding oral feeding in labour and the wider use of regional anaesthesia. He also advocated the use of alkalization of stomach contents before anaesthesia to minimize the consequences of aspiration. Aspiration appears to be very rare in obstetric practice now, possibly because of the anti-aspiration strategies listed in Table 5. This has led to suggestions from some midwives and patient groups that we should be more liberal in our approach to allowing eating and drinking during labour. Prolonged labour can result in dehydration and ketosis, but there is little evidence that this adversely affects labour outcome. Scrutton et al.11 studied
Table 5
Anti-aspiration strategies.
Nil by mouth or clear fluid only policies in labour Antacid prophylaxis Rapid sequence induction using cricoid pressure and endotracheal intubation
Increased use of regional anaesthesia Improved anaesthetic training
the metabolic effects of feeding in early labour. They randomized parturients in early labour to receive either a light standardized low fat diet or water only. Feeding appeared to prevent the development of ketosis but gastric volumes measured by ultrasound were higher and greater volumes were vomited at delivery. The latter may increase the risk of pulmonary aspiration should a general anaesthetic be required. Another study12 looked at giving mothers in early labour isotonic sports drinks compared to water. This also appeared to prevent the development of ketosis but without increasing residual gastric volumes. It is not always easy to identify those women at low risk of needing anaesthesia during their labour. These women would probably be safe having a light diet. The majority of patients though, including those having opioid-containing epidurals, would be safer restricting their intake to water, and perhaps calories in the form of isotonic sports drinks rather than solid food.
ARTICLE IN PRESS Complications of obstetric anaesthesia Antacids, to reduce the volume and acidity of gastric contents, have a role to play in preventing aspiration or reducing its severity if it occurs. Gastric volumes of 0.4–0.8 mL/kg and pH of less than 2.5 are classically quoted as being the critical values concerned.13,14 Magnesium trisilicate was traditionally given during labour, and while it did reduce gastric acidity, its particulate nature caused problems if aspiration occurred. Sodium citrate, 30 mL 0.3 M, before induction of anaesthesia increases gastric pH but not volume. Histamine type 2 (H2) receptor antagonists, such as ranitidine 150 mg orally 1 h preoperatively, reduce gastric volume and acidity, especially in combination with sodium citrate. Ranitidine can also be given in an emergency intravenously at induction and will provide aspiration prophylaxis at emergence. Metoclopramide, a dopamine antagonist, increases lower oesophageal sphincter tone and gastric emptying. Proton pump inhibitors, such as omeprazole, increase gastric pH effectively but tend to be more expensive. The sentinel Caesarean section audit2 revealed that 99% of delivery suites in the United Kingdom routinely use drugs to reduce the gastric volume and acidity for elective Caesarean section and 98% for emergency. H2 receptor antagonists (ranitidine) and sodium citrate are the most commonly used agents. Only a minority of units used proton pump inhibitors, such as omeprazole. A postal survey of acid prophylaxis in obstetric anaesthetic units in the United Kingdom revealed similar results as regards the drugs used for acid aspiration prophylaxis, but additionally found that the number of units carrying out routine prophylaxis in active labour had fallen.15 The author’s unit uses ‘FasTab’ as an antacid prophylaxis. This is a fast acting oral preparation of lansoprazole, in a dose of 30 mg, which can be either be allowed to dissolve in the mouth, or swallowed with a small amount of water. Although it is easy to administer antacid prophylaxis to the parturient undergoing elective Caesarean section, it is easy to overlook it in an emergency. Increased use of regional anaesthesia has played a major role in the reduction of maternal deaths from aspiration, but it must be remembered that aspiration can occur with very high blocks and the loss of laryngeal reflexes. Rapid sequence induction also plays an important role, but introduces with it other risks such as failed intubation and oesophageal rupture if vomiting occurs. The management of aspiration during anaesthesia is outlined in Table 6. Just as intubation problems can complicate the termination of anaesthesia, so can aspiration. Some anaesthetists advocate attempts to empty the
155 Table 6 thesia. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Management of aspiration during anaes-
100% oxygen Head down position (+ turn to lateral) Suction oropharynx If no endotracheal tube in situ, apply cricoid pressure and intubate Suction and lavage tracheobronchial tree (preferably endoscopically) Bronchodilators for wheezing PEEP for hypoxaemia Post operative chest X-ray May need ventilation on ICU if severe Consider antibiotics if infected material aspirated
stomach with a large bore orogastric tube before emergence in all unfasted patients.
Awareness The spectrum of awareness under general anaesthesia ranges from dreaming, through recall of specific events, to the rare but very serious complication of full consciousness with total paralysis. It was a real concern for the obstetric anaesthetist in days gone by when minimal, or even no, volatile anaesthetic agent was given before delivery for fear of neonatal depression or uterine atony. Increased inspired oxygen concentrations, given at the expense of nitrous oxide to ensure optimal maternal and fetal oxygenation in the pre–saturation monitoring era, compounded this problem. The final straw was the avoidance of opioids until after delivery. Again, modern practice changes seem to have reduced the awareness problem. (Table 7). Anaesthetists now routinely give a reasonable induction dose of thiopentone (4–6 mg/kg) and maintain anaesthesia with at least one minimal alveolar concentration (MAC) of volatile anaesthetic agent, aided by end tidal anaesthetic gas monitoring. Modern volatile agents with low blood gas solubility, allow rapid progression to deep anaesthesia. Inspired oxygen can now be titrated against maternal saturation readings. It is rare to need more than 30%, so nitrous oxide need not be automatically restricted. Despite the above, awareness may still arise, especially in the emergency situation.16 Patients are anxious and unpremedicated. Opioid analgesia
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Table 7 Measures to reduce the incidence of awareness.
Adequate induction dose of thiopentone
(4–6 mg/kg) 0.3:0.7 oxygen: nitrous oxide mixture 1 MAC of low blood gas soluble volatile agent End tidal volatile agent monitoring Depth of anaesthesia monitoring in the future
is usually withheld until the baby is delivered. In the difficult intubation situation, oxygenation takes precedence and the patient may become aware as the induction agent wears off if inadequate volatile agent has been given. Concerns were raised by King et al.17 that the practice of allowing surgery to begin immediately after endotracheal intubation does not provide adequate depth of anaesthesia at the time of skin incision during Caesarean section. Again, modern low blood-gas soluable agents such as sevoflurane, especially with the use of ‘overpressure’ techniques, enable all these risks to be minimized. Awareness may also arise because of drug errors. The author is aware of two such cases of awareness at her institution; one followed inadvertent induction with saline and the other the antibiotic cefuroxime. Depth of anaesthesia monitoring is not widely available in most delivery suite theatres in the UK. Clinical signs tend to be unreliable. Most patients will be tachycardic, hypertensive and sweaty as they are usually very anxious pre-induction and are not given any analgesia until delivery. Various techniques for monitoring anaesthetic depth have been studied in clinical practice, including isolated forearm, lower oesophageal contractility and electroencephalographic bispectral monitoring (BIS).16–18 BIS values of less than 60 are required to ensure unconsciousness in the majority of patients. Chin determined that an end-tidal concentration of sevoflurane of 1.2–1.5% was required to minimize the risk of intraoperative awareness and subsequent recall during Caesarean section using this technique.18 It remains to be seen whether BIS monitoring will become a more widely used depth of anaesthesia monitor in the future.
Complications of regional anaesthesia The main complications of regional anaesthesia are listed in Table 2.
Hypotension Regional anaesthesia can cause significant hypotension due to blockade of sympathetic nerve fibres. The resultant lower body vasodilatation and venous pooling reduce cardiac output and hence blood pressure. Aortocaval compression and hypovolaemia may exacerbate these changes. Serious hypotension is now rare with modern lowdose epidural analgesia. Hawthorne et al.19 looked at the effect of fluid pre-loading on maternal haemodynamics for low-dose epidural analgesia in labour and found no difference in cardiac index or mean arterial pressure between patients given no fluid pre-load and those given a 7 mL/kg normal saline pre-load. Routine fluid preloading is not necessary before low-dose epidural analgesia and may in fact be hazardous to parturients with severe pre-eclampsia or cardiac disease, and can also inhibit uterine contractions. The anaesthetist may consider giving fluids to the parturient who is hypovolaemic from an antepartum haemorrhage or dehydrated from an excessively long labour, especially on a hot day. Management of hypotension following epidural analgesia is listed in Table 8. Remember that epidural top-ups with large volumes of high concentration of local anaesthetic agents for operative delivery may precipitate more severe hypotension. Hypotension is an inevitable consequence of high spinal anaesthesia in obstetrics if no preventative measures are used. The anaesthetic literature contains many systematic reviews of randomized controlled trials of interventions to reduce the incidence of hypotension during spinal anaesthesia including preload with crystalloid 20 mL/kg versus control, pre-emptive colloid versus crystalloid, ephedrine versus control and lower limb compression during control.20 Despite these measures hypotension was still a common problem, until recently. The answer to the problem of spinal anaestheticinduced hypotension may have been found with a change in vasoconstrictor practice. Traditional obstetric anaesthetic teaching recommended ephedrine, a combined a and b agonist, as the vasoconstrictor of choice. It increases blood pressure by a mediated activity increasing systemic vascular resistance and b mediated increases in cardiac output and heart rate and was thought to maintain uteroplacental blood flow better than other vasoconstrictors. This arose from studies in pregnant sheep in the 1970s given supranormal doses of vasoconstrictors but without regional anaesthesia.21 Uteroplacental perfusion was reduced with pure a agonists but was maintained
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 8 1. 2. 3. 4.
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Management of hypotension following epidural analgesia.
Left lateral positioning to relieve aortocaval compression Commence intravenous fluid infusion Consider vasoconstrictor e.g. 3–6 mg increments of ephedrine Exclude other causes e.g. subarachnoid epidural catheter placement, hypovolaemia, obstetric haemorrhage
with ephedrine, even at doses which increased the blood pressure by 50%. It was concluded, therefore, that ephedrine was the superior prophylactic vasoconstrictor and that pure a agonists should be avoided. Meta-analysis has revealed a higher incidence of fetal acidosis at delivery following spinal anaesthesia for Caesarean section than epidural or general anaesthesia.22 This may be due to spinalinduced hypotension or drugs used to correct this, usually ephedrine. Concerns have now been raised that doses of ephedrine large enough to maintain the blood pressure after induction of spinal anaesthesia may be detrimental to the fetus. Tachyphylaxis can occur with ephedrine and large amounts of drug may then be needed to maintain its effect. This can then cross the placenta and stimulate fetal metabolism via its b agonist activity, resulting in a metabolic acidosis. This effect may be even more significant in the compromised fetus. Phenylephrine is at least as effective as ephedrine in the prevention or treatment of spinal anaesthesia induced hypotension. In addition, it is associated with a lower incidence of fetal acidosis and maternal sickness.23 Given in doses that maintain normotension, phenylephrine does not cause clinically significant placental vasoconstriction or decreased perfusion.24 Audit data following a change in vasoconstrictor regimen at the author’s institution from an ephedrine (30 mg/1 L NSaline) to a phenylephrine infusion (1 g/1 L NSaline) commenced upon spinal injection has revealed a significant fall in the incidence of severe hypotension, with additional vasoconstrictor therapy only rarely being needed. Some authors state that the clinical situation must guide which vasopressor is appropriate for the patient, considering not only the blood pressure but the heart rate too.25 Because of its indirect stimulatory effect on heart rate, ephedrine may be the vasopressor of choice in a parturient who is hypotensive and bradycardic, while phenylephrine would be preferable in someone who is hypotensive and tachycardic, due to its reflex baroreceptor effect in slowing the heart rate. Bradycardia
occurring during phenylephrine use is better treated with glycopyrollate rather than atropine, as the former does not cross the placenta and has a more sustained effect. Whichever vasoconstrictor regimen is chosen, it must be remembered to take measures to avoid aortocaval compression, usually by left lateral tilt of the theatre table.
Local anaesthetic toxicity Local anaesthetic toxicity may be caused by inadvertent intravascular injection into a catheter which has been sited or migrated into an epidural vein. Theoretically, systemic toxicity can also follow from excessive epidural dosing. The safe maximum dose of bupivacaine is quoted as 2 mg/kg every 4 h. A standard epidural top-up for an emergency Caesarean section of 20 mL 0.5% plain bupivacaine, often following on from an infusion and several top-ups in labour, can easily reach this supposedly toxic level in small parturients. Toxicity from systemic absorption in these circumstances does however appear to be very rare, and the quoted maximum doses rather conservative for obstetric practice. Signs and symptoms of toxicity include numbness and tingling of the tongue and around the mouth, tinnitus and ear popping, funny taste sensations, light-headedness, confusion and slurred speech. Later, loss of consciousness, convulsions and cardiovascular collapse can ensue. Deaths have been attributed to bupivacaine-induced cardiotoxicity in the past. Racemic bupivacaine is a mixture of its R and S isomers. The latter is responsible for its physiological effects and the former its unwanted ones, especially cardiotoxicity. This prompted the development and marketing of single S isomer local anaesthetics. Levobupivacaine is the S-enantiomer of bupivacaine. It has been found to have an improved cardiovascular safety profile compared to racemic bupivacaine26 and only a slightly lower potency.27 Ropivacaine is the S-enantiomer of propivacaine.
ARTICLE IN PRESS 158 Table 9 city.
A. Pinder Management of local anaesthetic toxi-
1. 2. 3. 4. 5. 6.
Stop injection of local anaesthetic ABC and call for help Oxygen via face mask Left lateral positioning Support airway and ventilation if necessary Control fits with an intravenous benzodiazepine or thiopentone 7. Treat hypotension with fluids and vasopressors 8. Cardiac arrest as per standard guidelines. Refractory arrhythmias may be a problem with bupivacaine
This agent also has lower cardiotoxicity than racemic bupivacaine, although this may be partly related to its lower potency.28,29 Management of local anaesthetic toxicity begins with attempts at its prevention. Following a bloody tap at epidural insertion, the catheter should be withdrawn and flushed with saline. If the catheter fails to clear it should be resited. Test doses are advocated to detect intravenous injection. No test dose is 100% sensitive and specific and it is wise for the anaesthetist to consider ‘every dose a test dose’. Aspiration should be performed before injections, drugs should be given in small divided quantities and toxic doses should not be exceeded. If signs and symptoms of local anaesthetic toxicity develop, the management plan in Table 9 should be followed. Drug administration must be stopped, airway, breathing and circulation (ABC) attended to and then any neurological or cardiovascular complications treated. Bretylium was traditionally used to treat refractory bupivacaineinduced arrhythmias, but since its withdrawal, amiodarone or magnesium should be considered.
Accidental dural puncture and dural puncture headache The incidence of inadvertent dural puncture with an epidural needle varies widely between units, but is consistently around 0.6% in the author’s institution. Headache after spinal anaesthesia with 27 gauge pencil point needles is currently 0.25%, usually after repeated needle passes. Inadvertent dural puncture with an epidural needle is usually easily recognized by a rapid flow of CSF from the epidural needle, but a glancing dural puncture might produce a less convincing
flow. Some recommend testing the temperature and glucose content of the CSF to confirm the diagnosis, but both these tests produce false positive results. Some dural taps only become apparent on aspiration through the epidural catheter, or after the epidural test dose. Later on, some dural taps present as headache without any record of CSF leak at the time of insertion. One explanation for this is the epidural needle transfixing the dural sack at insertion, causing two dural punctures but no leak. The fact that not all dural punctures are spotted by the epiduralist makes it vital that anaesthetists and midwives are trained to identify the features of subarachnoid injection of epidural drugs, and post-dural puncture headache. The complications of accidental dural puncture include headache, high or total spinal anaesthesia, 6th cranial nerve palsy and subdural haemorrhage. The historical management of a recognized accidental dural puncture is to resite the epidural. This may be considered by some to be the safest approach as it is familiar practice. The epidural may prove difficult, another anaesthetist may need to be called to help and there is the risk of repeating the dural puncture. Theoretically, there is the risk of the epidural catheter or local anaesthetic solution passing through the dural puncture hole and unpredictable blocks. ‘Anaesthetist only’ top-ups may therefore be recommended. A better option is to thread the epidural catheter into the subarachnoid space if possible (Table 10). Intermittent ‘anaesthetist only’ top-ups given by this route usually provide excellent analgesia, albeit with tachyphylaxis developing after some time. The author’s institution uses the standard low-dose bupivacaine and fentanyl mixture in small increments titrated to analgesic effect. The catheter can be topped up with incremental hyperbaric bupivacaine if operative delivery is needed. Dural puncture headache, and hence the need for epidural blood patching, may also be less common if the catheter is left in situ for 24 h.30,31 This is thought to be due to an inflammatory reaction taking place around the catheter sealing the dural hole, although not all workers have confirmed this finding.32 Everyone must be aware that the catheter is in the intrathecal space to reduce the risk of inadvertent administration of an epidural local anaesthetic dose down it with the potential for a high or total spinal. A recent survey of the management of accidental dural puncture during labour epidural analgesia revealed the insertion of the epidural catheter intrathecally when accidental dural puncture was diagnosed to be the most
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 10 Management of accidental dural puncture: epidural or intrathecal catheter?. Epidural catheter Advantages Familiar practice Good analgesia
Disadvantages Possible higher headache rate Unpredictable blocks
Intrathecal catheter Excellent analgesia Top-ups possible for operative delivery Possible lower headache rate
159 Table 11
Epidural blood patch procedure.
1. Explain procedure to patient and obtain
informed consent 2. Full asepsis 3. Left lateral positioning for patient comfort 4. Interspace below previous dural puncture,
anaesthetist identifies epidural space 5. Colleague obtains 20 mL venous blood 6. Blood injected through Touhy needle into
epidural space 7. Patient advised to lay flat for 1–2 h and to avoid
Anaesthetist only topups Risk high block with inadvertant epidural doses
straining and lifting for several days 8. Follow up 9. May need to be repeated
Analgesia delay
significant change in practice, with only 1% of units doing this in 1993 but 59% in 2003.33 Whichever management option is taken, once the patient is comfortable, she should be informed of the complication and its implications. It should be documented in the medical notes and the patient closely followed up for the development of complications. In the past, elective forceps delivery used to be recommended to reduce straining during the second stage of labour, but not now. Headaches are common in all parturients following delivery. Fatigue and dehydration are common causes. Dural puncture may be unrecognized at the time of epidural insertion and may present as a postpartum headache. The classical dural puncture headache is postural, worse when sitting or standing, improved by lying flat, and begins within 48 h of delivery. It may be frontal or occipital and usually described as a severe aching or throbbing. Associated signs and symptoms include photophobia, neck stiffness, nausea, vomiting, cranial nerve palsies and, importantly for the mother, it interferes with her ability to care for the baby. The headache is caused by the leakage of cerebrospinal fluid through the dural hole, which results in traction on the pain sensitive meninges and compensatory vasodilatation. Management begins with measures to prevent accidental dural puncture happening in the first place by using a careful epidural technique and using loss of resistance to saline rather than air. Once dural puncture has occurred, measures to prevent headache from developing include leaving an intrathecal catheter in situ for at least 24 h, epidural saline infusions, prophylactic blood patching through an epidural catheter, keeping the
patient well hydrated and bed rest. None of these methods has been conclusively shown to work. Once a dural puncture headache has developed conservative measures such as regular analgesia and adequate hydration should be tried first as some headaches resolve spontaneously. Cerebral vasoconstrictors, such as caffeine and sumatriptan, have been tried, as have abdominal binders. Results are unconvincing. The definitive ‘gold standard’ treatment is the epidural blood patch. This involves the injection of about 20 mL of the patient’s blood into the epidural space under aseptic conditions (Table 11). Immediate relief is thought to be due to the mass effect of the blood compressing the dural sac and displacing cerebrospinal fluid into the cranium. Over the next few hours the blood clots and seals the dural hole. A single blood patch ‘cures’ the headache in about two thirds of cases, in the remainder a repeat blood patch may be necessary. Complications include repeating the dural puncture, transient nerve root pain and back pain.34
High blocks The incidence of high blocks is much less than that of failed intubations, but the actual number may be higher as far more regional anaesthetics are performed than general in the UK. It has been recommended that units have a high regional block drill, which is regularly reviewed and rehearsed like a failed intubation drill.35 Table 12 shows the circumstances and incidences of blocks that went high enough to require intubation during a 6 year period in the author’s unit.36 Performing spinal
ARTICLE IN PRESS 160
A. Pinder
Table 12
High spinals in Leeds 1997–2003 (courtesy of M. Dresner).
Technique
Number of high blocks/total number of cases
Incidence (%)
Epidural analgesia CSE analgesia Spinal anaesthesia CSE anaesthesia Topped up epidural/CSE Spinal after an epidural
1/6796 0/2296 0/3784 0/222 1/995 5/342
0.01 0 0 0 0.1 1.46
Table 13 1. 2. 3. 4.
Management of high spinal.
Recognize early Reassure patient Call for help Symptomatic treatment a. Hypotension—relieve aortocaval compression, fluids, vasoconstrictors b. Bradycardia—glycopyrollate or atropine c. Inadequate respiration-100% oxygen, gentle bag and mask ventilation d. Loss of consciousness—consider anaesthesia and intubation
5. Consider urgent delivery of the baby
anaesthesia on women who have been receiving epidural analgesia seems to be the highest risk scenario. Management of high spinal blockade begins with early recognition (Table 13). Signs and symptoms usually develop rapidly, but may be late and insidious in onset. The patient may initially complain of numbness, weakness or tingling in her arms, difficulty in breathing and lightheadness. Her speech may become slurred or her voice hoarse. Hypotension and bradycardia are initially due to sympathetic blockade but later due to the effects of the local anaesthetic on the brain stem. The latter will also result in apnoea and loss of consciousness. Reassurance of the mother is very important as she will be terrified and hearing is late to disappear. Symptomatic treatment should follow as outlined in Table 13. Urgent delivery of the baby should be considered as this may cause the block to regress and the maternal condition to improve. However, one case in the author’s unit involved a woman who needed intubating for a high block caused by intrathecal injection of drugs via a misplaced epidural catheter that had been sited for pain relief. She was ventilated and sedated for
40 min, woken up, extubated, and then went on to have a normal delivery of a healthy baby with excellent analgesia from her unplanned spinal catheter.
Subdural block A subdural block may also be the cause of a high spinal. An epidural catheter may be sited in the potential space between the dura and arachnoid mater. The first epidural dose given through it produces as a slow onset high, patchy block with minimal motor block, sacral block or hypotension. Subsequent top up injections may then rupture through the arachnoid mater with intrathecal effects. If an epidural catheter is suspected to be subdural it should be re-sited. If not recognized, the resultant high spinal block should be managed as outlined above.
Neurological complications Any paper discussing the complications of obstetric anaesthesia would be incomplete without at least a mention of neurological sequelae (Table 14).37 These are the complications that we and patients all dread. How many of us have been asked during the anaesthetic visit ‘will it paralyse me, doctor?’. Despite our fears, neurological complications following obstetric anaesthesia are extremely rare, although the number of reported cases may increase as more regionals are performed. Neurological deficits, especially peripheral neuropathies, are more commonly caused by labour and delivery. We must also remember that spontaneous neurological insults can occur in the absence of regional analgesia or anaesthesia. Careful regional anaesthetic technique plays an important role in the prevention of neurological complications. This includes asepsis, inserting
ARTICLE IN PRESS Complications of obstetric anaesthesia Table 14 Neurological complications associated with regional anaesthesia.37 Neuropathy Epidural abscess Epidural/spinal haematoma Meningitis Chronic adhesive arachnoiditis Subdural haematoma Cauda equina syndrome Anterior spinal artery syndrome Cranial nerve palsies
needles at the correct spinal level and not performing regionals in patients with contraindications, such as coagulopathies and infections. If neurological complications are suspected, prompt diagnosis and treatment, sometimes with neurosurgical intervention, are necessary to reduce or prevent long-term disability. Neuropathies are the commonest neurological complication. Nerve root damage may be caused by direct needle or catheter trauma or direct intraneural injection of local anaesthetic. Pain and/or parasthesia are usually noted during performance of the block, which should prompt the anaesthetist to withdraw the needle or catheter or to stop the local anaesthetic injection. They present as numbness in the dermatome supplied by the nerve root, sometimes with muscle weakness. Full recovery within months is usually to be expected. Spinal cord injury can occur during regional anaesthesia. Reynolds38 presented several cases of conus damage following spinal injection. These followed spinal or combined spinal-epidurals, and were associated with difficulty in siting the block and pain on needle insertion or drug injection. Interestingly the lesions were not consistent with the documented level of needle insertion, all being made at inappropriately high levels leading to direct damage to the spinal cord. She concluded that anaesthetists should not insert spinal needles above the third lumber vertebral space. In theory this is good advice, but it is well known that anaesthetists are very poor at correctly identifying the spinal level.39
Conclusion This paper reviews some of the complications associated with obstetric anaesthesia. While their potentially serious nature should be of significant
161 concern to every anaesthetist on delivery suite, one must also remember that these complications are rare. Careful attention to detail in our anaesthetic practice will play an important role in minimizing their incidence.
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