2. Extradural Space

The epidural space posteriorly is an actual space whose posterior dimensions can be seen easily on any coronal CT or MR scan of the vertebral column.
This actual space is the area surrounding the dural sheath as it lies within the vertebral canal. It extends from the foramen magnum superiorly (where the dura is fused to the skull) to the sacral hiatus inferiorly . So, in contrast to a ‘total spinal’, a patient with a high cervical epidural block may stop breathing but will not be unconscious.

The space is traversed by the dural sheath, whose thickness in the lumbar region is about 0.3–0.5 mm, and which comprises the membranes of the dura and arachnoid maters, the subarachnoid space containing CSF, the spinal nerves of the cauda equina and the filum terminale. Anteriorly, the epidural space is bounded by the bodies of the vertebrae and by the intervertebral discs, over which lies the posterior longitudinal ligament. The anterior dura mater and the posterior longitudinal ligament are closely apposed, and so anteriorly the epidural space is ‘potential’. Laterally, the epidural space is bounded by the pedicles and the intervertebral foramina Posteriorly, it is bounded by the laminae of the neural arches.

Ligamenta flava: these are not continuous Each ligament extends from the lower part of the anterior surface of the lamina above to the posterior surface of, and upper margin of, the lamina below. Their fibres run in a perpendicular direction, but when viewed in the sagittal plane the ligaments are triangular in shape, with the apex of the triangle formed at the upper lamina.

At the level of a typical lumbar vertebra, for example L3, the space contains the spinal nerves, each of which is invested with a cuff of dura, with loosely packed fat, areolar connective tissue, lymphatics and blood vessels. These vessels include the rich valveless vertebral venous plexus of Batson. (The lack of valves means that they will engorge as intra-abdominal pressure increases, for example during a contraction in labour.)

The depth of the posterior epidural space (between the ligamenta flava and the dura) varies with the vertebral level. In the mid-cervical region it is only 1.0–1.5 mm wide, and at T6 it is deeper, at around 2.5–3.0 mm. The greatest depth is at the L2 interspace in men, in whom this is 5.0–6.0 mm.

These include inadvertent dural puncture and subsequent post-dural puncture headache (PDPH) (incidence of 0.5%); failure (1%); unilateral or patchy block (5–10%); inadvertent subdural block (0.1%); intravascular injection; retention of a fragment of needle or catheter; epidural haematoma. The risk of permanent neurological sequelae is very small. The incidence is quoted at 1 in 10–15,000 epidurals but many of these complications are relatively minor, comprising, for example, little more than a patch of residual numbness, and even this figure is likely to be too high because childbirth itself may cause permanent neurological deficit (1 in 2,000). In the NAP 3 report on complications of central neuraxial blockade in the UK (2009), the incidence of permanent harm, considering the ‘pessimistic’ interpretation, was 1 in 161,550. There is finally no evidence, despite much debate fueled by the lay press, that routine epidurals lead to chronic back pain.

These include hypotension owing to sympathetic block; high spinal block; evidence of systemic toxicity of local anaesthetic; urinary retention; pruritus, nausea and vomiting (usually associated with extradural opiate); respiratory depression. A total spinal may follow inadvertent intrathecal injection, depending on the epidural dose. There are many case reports of accidental injection of the wrong solution. Numerous substances have been administered in this way, including various antibiotics; solutions of total parenteral nutrition (which apparently provided good quality analgesia); chlorhexidine, with catastrophic sequelae; and thiopental. do not have any influence on caesarean section rates but do increase the likelihood of instrumental delivery by up to 14%.

Diagnosis: the incidence of inadvertent dural puncture should not exceed 0.5%, and the incidence is usually quoted at between 0.5% and 1.0%. The incidence of PDPH is highest in obstetric patients, more than 80% of whom will develop symptoms. These are probably caused by traction on intracranial pain-sensitive structures such as the tentorium and blood vessel, and by adenosine-mediated reflex intracerebral vasodilatation. The low-pressure headache results from the failure of the choroid plexus to produce sufficient CSF to compensate for the loss through the breach in the dura. The onset is variable, with the headache commonly starting after about 12–24 hours. It can occur earlier or later. The headache may be frontal or occipital rather than global, but typically it is postural and relieved by recumbency or abdominal pressure. It may also be associated with photophobia, visual disturbance, neck and shoulder stiffness, and tinnitus. If the patient also complains of anorexia, nausea and vomiting, this is an indication that there is significant sagging of intracranial contents, with pressure on the brain stem at the foramen magnum includes migraine, pre-eclampsia (which can present post-delivery), intracranial haemorrhage (associated with severe hypertension), meningitis and cortical vein thrombosis

Management of severe PDPH: assuming the failure of initial conservative treatment, advising recumbence when headache supervenes and simple analgesia, management may move on to other treatment Cerebral vasoconstrictors such as caffeine and sumatriptan may improve symptoms, but they will not address the cause corticosteroids, and accordingly there is some evidence to support the administration of ACTH analogues such as tetracosactrin (Synacthen), which stimulate glucocorticoid release small. The only technique that is likely to provide immediate relief is an extradural blood patch (EBP). This will abolish symptoms in almost all patients, but in at least 30% of mothers the procedure will need to be repeated. EBP has been associated with the development of chronic low back pain, and this risk must be weighed against those of persistent long-term headache or of neurological disaster (such as subdural haemorrhage), of which there are numerous reports in the literature

catheter or needle may deposit solution in the subdural space between the dura and arachnoid mater. Radiologists maintain that during myelography there is a 1% incidence of subdural injection. It is much less commonly diagnosed in clinical anaesthesia. Some authorities cite an incidence of 1 in 1,000. Subdural block is often patchy; it may be extensive and unilateral, may extend very high (the subdural space extends into the cranium) and it often spares the sacral roots. The dura and arachnoid are more densely adherent to each other anteriorly, and so there may be a relative sparing of motor fibres. Sympathetic block may be minimal, and analgesia may be delayed. Horner’s syndrome may be apparent. The use of a multi-holed catheter may further confuse the picture, because it is theoretically possible for the catheter to lie partly within the epidural and partly within the subdural space. Slow injection will favour emergence of the solution from the proximal epidural holes; more vigorous injection will favour dispersal through the distal subdural hole

A high block or developing total spinal is characterized by the development of paraesthesia and weakness of the upper limbs, respiratory embarrassment owing to intercostal paralysis, a weak voice and cough, and sensory loss over the skin of the neck and eventually the jaw. If the block is a total spinal then apnoea and unconsciousness will supervene. Pupils dilate. It is usually asserted that a high sympathetic block will lead to hypotension and bradycardia because of local anaesthetic effects on the cardiac accelerator fibres (T1–T4). In practice, the cardiovascular changes are by no means always so predictable. High blocks regress quickly, whereas it might be some hours before a total spinal has worn off to the point at which comfortable respiration will be possible. Until this happens, anaesthesia must be maintained to prevent awareness.

angled downwards and overlap such that the process of one thoracic vertebra is opposite the transverse process of the one below. This means that if a midline approach to the epidural space is used, the advancing needle will have to be at an angle of at least 45 to the spinal column, depending on which interspace is being used. For this reason, many anaesthetists prefer the paramedian approach thoracic epidural can provide effective analgesia following thoracic and major abdominal surgery, can attenuate the stress response to surgery and decreases adverse peri-operative cardiac events.

The conclusions of a systematic review and meta-analysis of 125 trials comparing epidural with systemic opioid analgesia and published in 2014 were unequivocal decreased the risks of death, of atrial fibrillation and other supraventricular tachycardias, of deep venous thrombosis, respiratory depression, atelectasis and pneumonia, and post-operative nausea and vomiting. It also decreased ileus and accelerated the recovery of bowel function Predictably the technique increased the risk of arterial hypotension, pruritus, urinary retention and motor block, but these complications, some of which are readily manageable, would not seem to outweigh the substantial advantage

A sound knowledge of epidural anatomy is essential for clinicians to perform safe and effective regional anaesthesia.
The anatomy of individual vertebrae varies according to their level.
The ligamentum flavum fuses in the midline. Areas of absent fusion may account for failure to recognise loss of resistance.
Surface landmarks are useful but not reliable for identifying spinal levels accurately.
Ultrasound may be used to help identify access to the epidural space and for orientation in cases of altered anatomy.