Postpartum neurological lesions are often blamed on peripartum anaesthetic interventions, even though non-anaesthetic causes are much more likely. Obstetric anaesthetists may therefore find themselves involved in the assessment and management of these problems. There are many causes of spinal cord lesions (Table 54.1).
Problems and special considerations
The initial problem is one of diagnosis. Different lesions may present in different ways that may overlap with each other and with other conditions (Table 54.1). Spinal cord lesions are more commonly associated with spinals and combined spinal-epidurals, and it should be remembered that peripheral neuropathies may arise as a result of obstetric interventions, especially those involving the lithotomy position. Spontaneous epidural haematoma or abscess (without neuraxial interventions) may also occur. Although cord lesions generally present with upper motor neurone signs and sensory impairment below the level of injury, and peripheral nerve injuries present with lower motor neurone signs, it may be surprisingly difficult to distinguish them clinically (see Chapter 53, Peripheral nerve lesions following regional anaesthesia).
Table 54.1 Causes of postpartum spinalcord lesions
|
Mechanism |
Condition |
Comment |
|
Compression |
Epidural haematoma Epidural abscess Prolapsed disc Tumour |
Not associated with back pain Associated with back pain plus evidence of local and/or systemic infection; typically presents several days postpartum |
|
Ischaemia |
Severe hypotension Anomalous arterial blood supply plus prolonged labour and hypotension Normal vascular supply and normotension |
|
|
Neurotoxicity |
Injection of wrong solution |
|
|
Trauma |
Back injury Direct damage during regional anaesthesia |
Associated with back pain May be associated with back pain, although paraesthesia is more common |
Sinister signs such as pyrexia, severe back pain, bilateral distribution, or loss of bladder or bowel function are suggestive of a compressive lesion such as epidural or spinal haematoma or abscess. These conditions are very rare (< 1 in 100,000) but may cause major, irreversible damage unless relieved within hours of presentation. Any suspicion should prompt immediate referral for a neurosurgical opinion. In the case of early lesions, some effects of spinal or epidural blockade may persist for several hours, occasionally over 12 hours (up to 48 hours has been observed, with no apparent cause), obscuring the underlying pathology. Since regression of a block often occurs under observation by nonanaesthetic staff, there may be delay in requesting appropriate medical input. In the case of acute potentially reversible spinal cord damage, for example cord compression caused by haematoma, delay of more than 6-8 hours is associated with an increasing chance of permanent impairment
Similarly, problems that present later, such as epidural abscess, may be missed if associated back pain is dismissed as trivial.
Management options
Anaesthetic-related problems may be reduced by attention to details such as:
• Assessing the coagulation status and pre-existing neurological status before performing regional techniques.
• Aseptic technique and exercising caution to avoid the contamination of needles and catheters with antiseptic solutions.
• Determining appropriate anatomical landmarks during the procedure, and awareness of the existence of anatomical variants and the risk of inserting the needle too high. Ultrasound guidance may help the identification of the correct intervertebral level, particularly when landmarks are difficult to palpate.
• Removal of the needle or catheter if severe paraesthesia or pain is experienced during a regional block.
• Prevention and management of hypotension after anaesthesia.
Maternity units should have local protocols for monitoring recovery from neuraxial blockade, and both patients and clinical staff should be educated on the ‘red flag’ features that they need to report without delay (e.g. persistent/progressive bilateral sensory/motor deficit, urinary retention/incontinence, faecal incontinence, persistent severe back pain). Any unexpectedly dense or prolonged block should always be observed carefully, especially if other risk factors (e.g. heparin therapy or sepsis) are present. A careful history and examination, and knowledge of the relevant anatomy, are vital to distinguish the various lesions from less severe conditions, and neurological referral is always advisable if there is any suspicion.
Individual conditions are managed as for non-pregnant patients, e.g. surgical decompression for cord compression, plus antibiotics for abscess.
Key points
• Anaesthetists may be involved in the assessment and management of postpartum spinal cord lesions.
• Knowledge of the appropriate anatomy and variations is crucial.
• In acute spinal cord compression, delay in decompression beyond 6-8 hours may result in permanent disability.
Further reading
Chambers DJ, Howells ACL. Neurological complications in obstetric regional anaesthesia. Anaesth Intensive Care Med 2016; 17: 372-4.
Cook TM, Counsell D, Wildsmith JA; Royal College of Anaesthetists Third National Audit Project. Major complications of central neuraxial block: report on the 3rd National Audit Project of the Royal College of Anaesthetists. Br J Anaesth 2009; 102: 179-90.
Moen V, Irestedt L. Neurological complications following central neuraxial blockades in obstetrics. Curr Opin Anaesthesiol 2008; 21: 275-80.
Porter JR, Christie LE, Yentis SM, Durbridge J, Dob DP. Prolonged neurological deficit following neuraxial blockade for caesarean section. Int J Obstet Anesth 2011; 20: 271.
Wong CA. Nerve injuries after neuraxial anaesthesia and their medicolegal implications. Best Pract Res Clin Obstet Gynaecol 2010; 24: 367-81.