Hypotension is a common complication of neuraxial anaesthesia for caesarean delivery.

Its incidence may be as high as 80% after spinal anaesthesia.

The most widely accepted definition for maternal hypotension is a systolic blood pressure (SBP) lower than 100 mmHg or a decrease in SBP of more than 20% to 30% from baseline values [13]. Spinal anaesthesia-induced hypotension is principally related to a decrease in systemic vascular resistances rather than a decrease in cardiac output which is commonly increased [14]. In case of severe hypotension, the uteroplacental perfusion may be impaired, resulting in fetal hypoxia, acidosis and neonatal depression. In the parturient, hypotension may result in nausea and vomiting, altered consciousness, aspiration, apnoea and cardiac arrest. The severity of hypotension is related to the rate and extent of the sympathetic blockade [13]. Therefore, hypotension is less common with epidural anaesthesia than with spinal anaesthesia because of the slower onset of sympathetic blockade and the earlier recognition and treatment [15]. Although some physical methods (leg wrapping, thromboembolic stockings) and prevention of aorto-caval compression by left displacement of the uterus are useful, main prevention relies on two pharmacological methods, vasopressor therapy and intravascular fluid loading generally in combination [16]. Phenylephrine is now the vasopressor of choice since it has been demonstrated that as compared to ephedrine, phenylephrine decreases the risk of fetal acidosis [17]. Crystalloid preloading is ineffective and should be abandoned. Crystalloid coloading is more effective. Preloading or coloading with hydroxyethyl starch is equally effective. Combining phenylephrine infusion with hydroxyethyl starch preloading or with crystalloids coloading is the method of choice to prevent and reduce the severity of spinal hypotension during caesarean delivery [16].

It is not uncommon that a neuraxial blockade does not provide adequate anaesthesia to initiate or to complete a caesarean delivery. This can occur in up to 4% of the cases following spinal anaesthesia and 13% of the cases following epidural anaesthesia [18, 19].

In the UK, pain is the most common cause of litigation related to regional anaesthesia in obstetrics [20]. In the recent SCORE project of the SOAP, the incidence of failed neuraxial anaesthesia that required an alternate technique for caesarean delivery was 1.7% [11]. Initiation of surgery should be delayed until adequate level of thoracic and sacral sensory blockade has been achieved. Management of breakthrough pain begins with acknowledgement of patient’s discomfort and consideration of fetal, surgical and anaesthetic implications. In case of partial block in an elective procedure, a second neuraxial technique may be performed with caution. A second epidural after a failed epidural caries the risk of local anaesthetics toxicity. A second spinal after a partial but failed spinal or a spinal after a failed epidural is controversial because the intrathecal administration of a standard dose of bupivacaine in those settings may result in a high spinal block. Combined spinal-epidural anaesthesia (CSE) is recommended by many practitioners to allow a cautious titration of the rescue neuraxial anaesthesia [13]. If discomfort arises after the start of surgery and if an epidural catheter is in place, an additional dose of local anaesthetic with an opioid should be administered. Inhalation of nitrous oxide or intravenous administration of an opioid or ketamine in 5–10 mg increments, combined with small doses of midazolam, may be helpful. Care must be taken to avoid deep sedation and loss of consciousness given the risk of aspiration [13]. Finally, conversion to general anaesthesia may be necessary and should be offered to the patient in case of persisting pain or discomfort.

High neuraxial blockade can result from an excessive spread of spinal or epidural drugs or an accidental intrathecal or subdural administration of an “epidural dose”.

When a T2 sensory level is achieved, patient may complain of dyspnoea or the inability to cough. Impaired phonation, impaired ventilation, unconsciousness, bradycardia and hypotension are potential sequelae of high neuraxial blockade. Tracheal intubation and circulatory support are required in this setting [13].

In the SCORE project of the SOAP, high neuraxial block has been reported with an incidence of 1 in 4336 anaesthesia. Forty percent of the cases followed a spinal anaesthesia, 36% an epidural and 24% an unrecognized spinal catheter. Obesity and spinal technique after failed epidural were the most common associated risk factors.

No maternal death was reported as the consequence of high neuraxial block [11].

Similarly, in the last MBBRACE-UK report, no maternal death was related to a high neuraxial block [4]. It is recommended that anaesthetists remain vigilant for a potentially misplaced catheter. Aspiration of an epidural catheter for CSF or blood has a high sensitivity and specificity [21]. The routine use of a test dose in an epidural catheter to detect an inadvertent intrathecal placement is controversial and does not guarantee proper placement as the majority of epidural anaesthesia associated with high neuraxial block and maternal death can occur after an uneventful test dose [6].

Local anaesthetic toxicity (LAST) after epidural anaesthesia is a rare but potentially catastrophic complication with an incidence of 4 in 10,000 epidural procedures [22–24]. Clinical signs of LAST range from prodromal signs such as auditory change, metallic taste, and agitation to seizures, CNS depression and cardiovascular collapse. The incidence of LAST has decreased during the last decades due to the implementation of routine safety procedures such as catheter aspiration, test dose administration and slow injection of divided doses of local anaesthetics [22–24]. No maternal death related to LAST was reported in the SCORE project of the SOAP or in the last MBBRACE-UK report [4, 11]. The American Society of Regional Anesthesia and Pain Medicine (ASRA) and the Association of Aaesthesiologists of Great Britain and Ireland (AAGBI) have released recommendations for the treatment of LAST. They include prompt and effective airway management in order to prevent hypoxia and acidosis; treatment of seizures with benzodiazepine, propofol or thiopental; consideration of lipid emulsion administration at the first signs of LAST and modified ACLS (Advanced Cardiac Life Support) in the setting of cardiac arrest. The suggested modifications to ACLS include avoidance of high-dose epinephrine, vasopressin, calcium-channel and beta-adrenergic blockers and treatment of ventricular dysrhythmias with amiodarone instead of lidocaine. The currently recommended regimen for intravenous 20% lipid emulsion administration for LAST is an initial bolus of 1.5 mL/kg followed by an infusion of 0.25 mL/kg/min with a maximal dose of 10 mL/kg [25, 26].

Most of neurologic injuries after childbirth are related to obstetric rather than anaesthetic causes. However, in such circumstances, neuraxial anaesthesia is often wrongly considered as the cause of the neurologic deficit. In the SCORE project of the SOAP, the incidence of serious neurologic injury following obstetric anaesthesia was 1 for 35,923 [11].

When neurologic symptoms arise after childbirth, an accurate and prompt diagnosis is essential. History, clinical examination and other diagnostic tools such as radiology, electromyography and nerve conduction studies are paramount. They allow to localize the lesion and differentiate mononeuropathy or plexus lesions which are more likely obstetrical complications from radiculopathy or cord lesions, which are more likely related to neuraxial anaesthesia. The reported incidence of peripheral nerve palsy which has an obstetric cause ranges between 0.6 and 92/10,000. The most commonly reported lesions are: (a) compression of the lumbosacral trunks, (b) obturator nerve palsy, (c) femoral nerve palsy, (d) meralgia paresthetica, (e) sciatic nerve palsy, (f) peroneal nerve palsy. The complete description of these obstetric palsies are out of the scope of this chapter, but anaesthesiologists should have an adequate knowledge of segmental and peripheral sensory nerve distributions useful in the diagnosis of central and peripheral nerve lesions [27, 28].