Spinal (intrathecal) anaesthesia

Overview

Spinal (intrathecal) anaesthesia is the injection of a small dose of local anaesthetic into the cerebrospinal fluid (CSF) of the subarachnoid space, producing a rapid, dense and predictable block of the sensory, motor and sympathetic nerve roots that the solution bathes. A typical surgical spinal uses twelve-and-a-half to fifteen milligrams of hyperbaric bupivacaine in two-and-a-half to three millilitres, takes effect within five to ten minutes, gives a surgical block for around two hours, and wears off with motor function returning before sensation. Because the drug is deposited directly among the nerve roots in the CSF, only a small dose is needed and the block is denser and faster than any epidural; the trade-off is that the height of the block, once injected, cannot be extended and the sympathetic block it produces is fixed for the duration of the local anaesthetic. [1]

Mastery of the technique rests on four bodies of knowledge. First, the anatomy of the layers the needle traverses, the safe interspace below the conus, and the surface landmarks that identify it. Second, the determinants of how high the block rises, of which the baricity of the solution and the patient's position are the most important. Third, the physiology of the sympathetic block — arteriolar and venous vasodilation below the block, the fall in systemic vascular resistance and venous return, and the Bezold-Jarisch reflex that can turn a routine spinal into an episode of severe bradycardia or asystole. Fourth, the prevention, recognition and management of the characteristic complications: spinal-induced hypotension, the post-dural puncture headache, the high or total spinal, and the rare but catastrophic epidural haematoma or abscess[1][7].

Indications

Spinal anaesthesia is indicated for surgery below the umbilicus where a block to the fourth thoracic dermatome suffices. The common indications are: [1]

• Lower-limb surgery — total hip and knee replacement, femur and tibial fixation, varicose vein and lower-limb vascular surgery, and foot and ankle surgery (where an ankle block is an alternative).
• Perineal and urological surgery — transurethral resection of the prostate (TURP), cystoscopy and bladder surgery, haemorrhoidectomy, fistula-in-ano and other perineal procedures. The TURP was historically the archetypal spinal operation because the awake patient can report transient dyspnoea and the signs of the TUR syndrome.
• Lower abdominal and groin surgery — inguinal hernia repair, open appendicectomy, and gynaecological procedures confined to the lower abdomen.
• Obstetric surgery — elective and urgent caesarean section, and repair of third- and fourth-degree perineal tears. The obstetric spinal is the most widely performed and most studied spinal anaesthetic in the world, and the one in which proactive vasopressor prophylaxis has become the standard of care.
• Adjunct to general anaesthesia — in major abdominal, thoracic and lower-limb surgery a spinal or epidural is added to blunt the stress response, reduce opioid consumption, improve gut recovery and provide postoperative analgesia. [1]

The advantages of spinal over general anaesthesia are a patent, spontaneously breathing airway; minimal drug transfer across the placenta; a reduced stress response; excellent early postoperative analgesia; a lower incidence of postoperative nausea and vomiting; reduced blood loss in lower-limb and pelvic surgery; a reduced risk of venous thromboembolism; and, in the obstetric patient, a conscious mother at the birth. The awake patient also serves as a monitor for the high spinal (numbness and weakness in the hands, dyspnoea) and for local anaesthetic systemic toxicity. [1]

Contraindications

The contraindications divide into absolute and relative, and the obstetric anticoagulation question is governed by published consensus. [1]

Absolute contraindications are few. They are: patient refusal (informed consent is the cornerstone of any neuraxial technique); true allergy to the local anaesthetic (extremely rare with amides); infection or sepsis at the intended puncture site (the risk of introducing infection into the subarachnoid space); and raised intracranial pressure (the risk of tonsillar herniation after CSF loss through the dural puncture). Undiagnosed raised intracranial pressure from a space-occupying lesion is the feared occult contraindication. [1]

Relative contraindications demand a judgement of risk against benefit. They are: [1]

• Coagulopathy and therapeutic anticoagulation. A spinal performed in an anticoagulated patient carries a small but catastrophic risk of an epidural haematoma that compresses the cord. The decision to proceed, and the timing of the procedure relative to the last dose, is governed by drug-specific interval guidelines. The Society for Obstetric Anesthesia and Perinatology consensus statement integrates the pharmacokinetics of the anticoagulants with the obstetric setting and is the practical reference for the anticoagulated parturient needing a neuraxial technique[8]. As a working rule, a spinal or neuraxial catheter removal should not be performed within the anticoagulant effect window, and a low platelet count or a coagulopathy (international normalised ratio above one point four, for example) is a contraindication.
• Fixed cardiac output states. Severe aortic or mitral stenosis, hypertrophic obstructive cardiomyopathy and severe pulmonary hypertension are poorly tolerated because the loss of systemic vascular resistance from the sympathetic block cannot be compensated by an increase in stroke volume or heart rate. These patients may suffer profound and refractory hypotension, and a spinal is generally avoided in favour of a carefully titrated epidural or a general anaesthetic.
• Hypovolaemia. The sympathetic block unmasks a volume deficit as profound hypotension; resuscitate first.
• Severe valvular disease and ischaemic heart disease. The tachycardia and vasopressor response needed to offset the block may provoke ischaemia; weigh the risks.
• Progressive or evolving neurological disease. A pre-existing progressive lesion (for example, demyelination) may be worsened by a neuraxial technique, and a new deficit after the block may be wrongly attributed to it; a documented preoperative neurological examination is essential.
• Back pathology preventing access — previous spinal surgery at the level, severe scoliosis, or infection over the site — make the technique difficult or impossible.

Anatomy of the neuraxial approach

A spinal needle is introduced in the midline, almost always at the L3/L4 or L4/L5 interspace, which lies safely below the termination of the spinal cord. The adult spinal cord ends as the conus medullaris at the lower border of the first lumbar vertebra (L1/L2), and below it the thecal sac contains the cauda equina — the lumbosacral nerve roots suspended in CSF. A puncture at L3/L4 or L4/L5 is therefore among freely mobile nerve roots that move away from the needle, the basis of the safety of lumbar neuraxial puncture. In the neonate and infant the cord ends lower, at about L3, so the safe interspace is L4/L5 or L5/S1. [1]

The surface landmark is Tuffier's (Tuffy's) line — a line joining the highest points of the two iliac crests, which crosses the spine at the L4 spinous process or the L4/L5 interspace. It is the cornerstone of identifying a safe interspace by palpation, though it is only an approximation: imaging studies show that the clinician's estimate of the interspace is often one or even two levels higher than intended, which is one argument for puncturing at L4/L5 rather than L3/L4 in the shorter or obese patient. [1]

The midline needle, advanced from the skin towards the canal, traverses the following structures in order[7]:

1. Skin and subcutaneous tissue, including the superficial fascia.
2. The supraspinous ligament, a strong fibrous cord joining the tips of the spinous processes from C7 to the sacrum, felt as a tough resistance in the midline.
3. The interspinous ligament, a thin sheet connecting the bodies of adjacent spinous processes, lying in the sagittal plane.
4. The ligamentum flavum — the keystone of the neuraxial approach. It is a thick, elastic, yellow ligament formed from the paired left and right leaves that run from the lamina of the vertebra above to the lamina below, and it is the structure whose elastic recoil gives the characteristic resistance, or 'pop', as the needle tip passes through it and enters the epidural space. The two leaves may fuse in the midline, giving a single pop, or remain separate, giving a double pop.
5. The epidural space, containing fat, the internal vertebral venous plexus, lymphatics and the spinal dural sac; the negative pressure here is used to confirm epidural catheter placement with the loss-of-resistance technique.
6. The dura mater — the tough outermost meningeal layer, continuous with the cranial dura; puncturing it gives the second, fainter 'pop' or 'give'.
7. The arachnoid mater — the delicate middle layer, adherent to the inner surface of the dura; the potential subdural space lies between them and is the site of the rare subdural injection.
8. The subarachnoid space — the actual target, containing CSF and the cauda equina nerve roots; the pia mater adheres to the cord and roots and is not crossed at this level. [1]

The free flow of clear CSF at the hub is the confirmation of the subarachnoid position before injection. Aspiration of CSF into the syringe and its gentle reinjection (a single barbotage) confirms the position, and the dose is then injected over five to ten seconds. [1]

Equipment: needles, gauge and design

The spinal needle is a fine, long needle with a stilette, introduced through a short wider introducer needle placed in the interspinous ligament to prevent the fine needle from deviating and to reduce skin contamination. The two key design choices are the gauge and the tip design, and both bear directly on the incidence of the post-dural puncture headache (PDPH). [1]

Cutting (Quincke) needles have a bevelled cutting tip that slices a clean, linear slit in the dura. Because the slit gapes as CSF leaks, they are associated with a higher incidence of PDPH and are now rarely used for spinal anaesthesia. Pencil-point (non-cutting) needles — the Whitacre and the Sprotte — have a solid, rounded, cone-shaped tip with the opening on the side; they part rather than cut the dural fibres, and the elastic recoil of the dura tends to close the puncture. They are the standard for modern spinal anaesthesia precisely because they lower the rate of PDPH[6].

Gauge matters in the same direction: the finer the needle, the smaller the dural defect and the lower the incidence of PDPH. A 25- or 27-gauge pencil-point needle is the common choice for adult spinal anaesthesia; finer needles (29-gauge) lower the PDPH rate further but are more difficult to place, more easily deviated, and give a slower CSF return that can delay confirmation. The orientation of a cutting-needle bevel — parallel to the longitudinal dural fibres, that is, with the bevel facing the ceiling or floor when the patient is in the lateral position — also reduces the leak by spreading rather than cutting the fibres, a detail that is irrelevant to the pencil-point needle but relevant if a Quincke is used. [1]

Pharmacology of intrathecal local anaesthetics

The standard agent for spinal anaesthesia is hyperbaric bupivacaine 0.5 percent in eight percent glucose (dextrose). The dose for a surgical block is in the range of seven-and-a-half to twenty milligrams, most commonly twelve-and-a-half to fifteen milligrams (two-and-a-half to three millilitres). Onset of sensory block is rapid (within two to five minutes), the surgical block lasts about two hours, and motor block recovers before sensory block. Bupivacaine is chosen for its long duration, its reliable dense block and its low cost. [1]

Baricity is the density of the local anaesthetic solution relative to CSF, and it is the single most important determinant of how the solution distributes in the subarachnoid column. CSF has a density of approximately one point zero zero zero six grams per millilitre. A hyperbaric solution (denser than CSF, as bupivacaine in dextrose is) sinks with gravity to the dependent part of the thecal column; an isobaric (plain) solution, of equal density to CSF, tends to stay where it is injected and spreads less predictably; and a hypobaric solution (lighter than CSF, for example bupivacaine diluted in sterile water) rises against gravity. Because a hyperbaric solution's behaviour with gravity is predictable, the patient's position after injection becomes a tool for shaping the block, which is why hyperbaric bupivacaine is the workhorse of spinal anaesthesia[9].

The alternatives have their niches. Levobupivacaine, the S-enantiomer of bupivacaine, is less cardiotoxic than the racemic drug on intravenous injection but is intrathecally equivalent in block quality and duration; it is used where a longer-acting, less toxic agent is preferred. Ropivacaine is another less cardiotoxic amide with a slightly shorter duration and a less dense motor block (the 'motor-sparing' advantage). Lidocaine was once the standard short-acting spinal agent but is now used cautiously because of transient neurological symptoms (TNS) — a transient back and leg pain after recovery — and concerns about cauda equina syndrome with the higher concentrations given intrathecally; 2 percent isobaric lidocaine is still used for short procedures, often with the patient informed of the TNS risk. Prilocaine (two percent hyperbaric) has gained a role for short ambulatory spinals because of its rapid recovery and low TNS rate. [1]

Determinants of block height

The height to which the block rises is governed by a hierarchy of factors. Knowing them is the key to producing a block of the right height and avoiding a high or inadequate block. [1]

The major determinant is the baricity of the solution, interacting with the patient's position[9]. A hyperbaric solution sinks with gravity, so its cephalad spread is shaped by where the dependent part of the thecal column lies. When the patient is turned supine after injection, the solution pools in the thoracic kyphosis (the natural forward curve of the upper thoracic spine) and the block rises cephalad; this is the basis of the caesarean spinal that aims for a T4 block. When the patient is kept sitting, the solution sinks to the lumbosacral sac and the block stays low, which suits a perineal or perianal operation. When the patient is kept in the lateral position with the operative side down, the solution sinks to the dependent side and a unilateral block results.

After baricity and position come the dose and volume of the local anaesthetic. A larger dose spreads higher; the relationship is roughly linear with the milligram dose, and the volume has an independent (smaller) effect by the bulk displacement of CSF. The site of injection also matters: a higher interspace gives a higher block because the solution starts higher in the column and has less distance to travel. [1]

A number of patient factors modify the spread. Pregnancy raises the block because the engorged epidural venous plexus compresses the thecal sac and reduces the CSF volume, so the same dose reaches higher; this is the reason the obstetric spinal needs a smaller dose than the non-pregnant adult. Age raises the block, partly through a smaller CSF volume and a less compliant theca. Patient height matters in the opposite direction: a tall patient has a longer column and a lower block for the same dose, while a short patient concentrates the solution. The speed and barbotage of injection have a smaller but real effect — a rapid injection or repeated barbotage (aspiration and reinjection of CSF with the dose) raises the block by turbulence, while a slow, smooth injection limits spread. Finally, raised intra-abdominal pressure (obesity, pregnancy, a large abdominal mass) and a high CSF pressure reduce spread by the same compression mechanism as pregnancy. [1]

The three concurrent blocks

A spinal produces three concurrent blocks whose cephalad extent differs by two to six segments, in the consistent order: the sympathetic block is highest, then the sensory block, then the motor block is lowest[1].

The sympathetic block interrupts the preganglionic sympathetic fibres that leave the cord from T1 to L2, travel in the lateral horn and the white rami, and supply the vasculature and viscera. A block of these fibres produces vasodilation below the level, with the loss of vasoconstrictor tone, and so the sympathetic block is the engine of the spinal's haemodynamic effects. Because the sympathetic fibres are thin and myelinated (small unmyelinated C and small myelinated B fibres), they are blocked first and highest — typically two to six segments above the sensory level. The corollary is that the haemodynamic consequences of a block to a given sensory dermatome extend higher than the sensory level itself. [1]

The sensory block interrupts the dorsal nerve roots, abolishing pain and temperature (the spinothalamic tract fibres) first, then light touch. It is the level that is assessed at the bedside with cold spray or pinprick. The motor block interrupts the anterior nerve roots and is the lowest of the three, assessed by the Bromage scale (below). The differential of two to six segments explains three classic clinical observations: a T4 sensory block carries a sympathetic block to T1/T2 with bradycardia from blockade of the cardiac accelerator fibres (T1 to T4); a motor block to the legs may coexist with a sensory block several segments higher; and sacral roots are the last to block and the first to recover (sacral sparing), which is why a block assessed as adequate at T10 for a hernia may yet fail to anaesthetise the perineum fully. [1]

Physiological effects of the block

The physiological effects of a spinal flow directly from the level of the three blocks, and the cardiovascular system dominates the clinical picture. [1]

Cardiovascular

The defining cardiovascular effect is spinal-induced hypotension. The sympathetic block below the level produces arteriolar vasodilation (a fall in systemic vascular resistance) and, more importantly, venodilation (a fall in venous return and preload). Cardiac output falls because the venous reservoir empties, and blood pressure falls with it. The incidence is high — up to seventy to ninety percent in obstetric spinals without prophylaxis, and around a third of non-obstetric spinals[1]. The risk factors are a high block, hypovolaemia, aortocaval compression in the obstetric patient, and the fixed cardiac output state (severe aortic or mitral stenosis). Because the venodilation is the dominant mechanism, the hypotension responds well to vasoconstriction (phenylephrine) and to volume, and poorly to head-up positioning (which worsens venous pooling).

A block to T4 and above adds bradycardia, because it interrupts the cardiac accelerator fibres (T1 to T4) that provide the sympathetic drive to the heart. Unopposed vagal tone then dominates, the heart rate falls, and a heart rate in the thirties or forties with hypotension is characteristic of the high spinal. A block to T1 also removes the sympathetic supply to the splanchnic vascular bed, siphoning further venous return. Bradycardia after a spinal is always a warning sign of important haemodynamic compromise and should be treated, not observed[1].

The Bezold-Jarisch reflex

In the young, fit, hypovolaemic or obstetric patient, a spinal can produce a dramatic and paradoxical response: a sudden, profound bradycardia with hypotension, occasionally progressing to asystole, in the minutes after the block develops. This is the Bezold-Jarisch reflex, a cardioinhibitory reflex triggered by the sudden reduction in venous return to an under-filled, vigorously contracting ventricle[1]. Mechanoreceptors in the inferoposterior wall of the left ventricle (and to a lesser extent the right) sense the empty, hypercontractile chamber and fire through vagal afferents (the C fibres) to the medulla, which responds with a vagal efferent discharge that slows the heart, vasodilates and can arrest it. The reflex is the cardiac equivalent of the vasovagal faint, and it is precisely the under-filled, fit, vagotonic patient — the young athlete, the hypovolaemic obstetric patient with aortocaval compression, the patient who has been fasting — who is at risk. The treatment is to restore venous return (head-down tilt, leg elevation, fluid), give a vasopressor (phenylephrine or ephedrine) to restore the afterload and venous return, and give atropine for the bradycardia; refractory cases may need adrenaline or a brief period of cardiopulmonary resuscitation. Ondansetron (a 5-HT3 antagonist) has been shown to attenuate the reflex by blocking the serotonin-mediated afferent limb and is used by some as prophylaxis[1]. The key preventive measures are a volume co-load begun at the block, the avoidance of the head-up position, and a low threshold for vasopressor prophylaxis.

Respiratory

In the awake, spontaneously breathing patient a spinal to the thoracic dermatomes does not significantly impair gas exchange, because the diaphragm is spared (phrenic nerve, C3 to C5) and the intercostal contribution to ventilation is modest. A high spinal that reaches the cervical roots, however, paralyses the intercostals and then the diaphragm, producing respiratory distress, paradoxical breathing, and ultimately apnoea — this is the 'total spinal', the central emergency of the technique. Even a high thoracic block can produce a sensation of dyspnoea (from intercostal paralysis and the loss of chest wall proprioception) that is frightening to the patient; reassurance, supplemental oxygen, and watchful monitoring suffice unless the block ascends further. Vocalisation and hand grip are useful bedside monitors: if the patient cannot phonate or grip, the block is ascending towards the cervical roots. [1]

Gastrointestinal

The sympathetic block leaves the vagus unopposed, so the bowel becomes contracted and peristaltic — an ideal condition for bowel surgery, and the basis of the 'intestinal squeeze' that can cause nausea in the awake patient. Nausea after a spinal is most often a sign of hypotension (reduced cerebral and gut perfusion) rather than gut traction, and the first response is to check and treat the blood pressure before reaching for an antiemetic. [1]

Renal and urinary

A block to the sacral roots (S2 to S4, the supply to the detrusor and the sphincter) abolishes the bladder's sensation and the voiding reflex, producing urinary retention. The post-spinal patient may need a urinary catheter, particularly after an opioid or a long-acting block, and the inability to void is a leading cause of delayed discharge after ambulatory surgery. [1]

Thermoregulation

The redistribution of body heat from the core to the vasodilated periphery below the block causes core hypothermia in the first thirty minutes; shivering above the block, impaired thermoregulation below it, and the loss of the vasoconstrictor response all contribute. Active warming (forced-air blanket, warmed fluids) mitigates it. [1]

Spinal-induced hypotension: incidence, mechanism and risk

Because spinal-induced hypotension is the commonest significant complication of the technique and the gateway to all the cardiovascular emergencies that follow, it deserves its own treatment[1].

The mechanism, restated, is the sympathetic block below the level: arteriolar vasodilation lowers systemic vascular resistance, but the dominant effect is venodilation, which pools blood in the splanchnic and lower-limb venous reservoirs and reduces venous return, preload and cardiac output. The incidence is very high in obstetric spinals without prophylaxis (sixty to ninety percent), because the parturient additionally suffers aortocaval compression by the gravid uterus in the supine position (which reduces venous return through the vena cava and cardiac output through the aorta) and a reduced CSF volume (from the engorged epidural plexus) that raises the block for the same dose. In the non-obstetric adult the incidence is around a third. The risk factors are a high block, hypovolaemia, baseline hypertension, obesity, advanced age, the obstetric state, and any fixed cardiac output state. [1]

The clinical consequences of untreated hypotension are nausea, vomiting, dizziness, altered consciousness (in the awake patient), and, in the obstetric patient, reduced uteroplacental perfusion and fetal acidosis. The prevention and treatment are therefore proactive, not reactive: anticipate the hypotension, co-load with fluid, and start a vasopressor at the time of the block. [1]

Vasopressor and fluid prophylaxis

Hypotension is anticipated and managed proactively. The two pillars are fluid and a vasopressor, and the obstetric patient additionally needs left lateral tilt to relieve aortocaval compression. [1]

Fluid strategy. The older practice of a preload (a fluid bolus before the block) has largely given way to a co-load (a rapid bolus given with the block as the vasodilation develops), because co-loading is as effective and avoids the unnecessary fluid in the patient in whom the block turns out to be inadequate. A colloid (for example hydroxyethyl starch) is more effective than a crystalloid at the same volume because it stays in the intravascular space longer, but crystalloid co-loading is widely used and adequate if the rate of administration is fast enough (a bolus over five to ten minutes). The volume used is typically five hundred to a thousand millilitres of crystalloid or two hundred and fifty to five hundred millilitres of colloid[1].

Vasopressor strategy. The first-line vasopressor for spinal hypotension, and especially for the obstetric spinal, is phenylephrine, a pure alpha-1 agonist that restores the venous return and afterload without the fetal acidosis of ephedrine. It is given by infusion (twenty-five to one hundred micrograms per minute, titrated to the blood pressure) begun at the time of the block, or by boluses of fifty to one hundred micrograms as needed. Ephedrine, a mixed sympathomimetic with alpha and beta effects, is the traditional second-line agent; it crosses the placenta and, at higher doses, produces fetal tachycardia and a fall in fetal pH through its beta-adrenergic effect on fetal metabolism. Norepinephrine, with both alpha and some beta activity, has emerged as an effective alternative that may produce less bradycardia than phenylephrine; a prophylactic titrated infusion (starting at around two-and-a-half to five micrograms per minute) was shown to reduce the incidence of hypotension after obstetric spinal without detriment to the neonate[4]. Metaraminol and adrenaline are reserved for refractory cases.

The phenylephrine versus ephedrine question is settled by two systematic reviews. Lee, Ngan Kee and Gin (2002) showed that phenylephrine and ephedrine were equally effective at preventing and treating maternal hypotension, but that women given phenylephrine had neonates with higher umbilical arterial pH values[2]. Veeser et al (2012), pooling twenty trials and over a thousand patients, found that the relative risk of true fetal acidosis was more than fivefold higher with ephedrine than with phenylephrine, and base excess values were lower after ephedrine, while there was no difference in the control of maternal blood pressure[3]. The mechanism of the fetal pH depression is a beta-adrenergic stimulation of fetal metabolism, not a CO2 effect. The practical conclusion — phenylephrine first-line, ephedrine second-line, and norepinephrine an effective modern alternative — is now the international standard[1][4].

Bradycardia from a high block (blockade of the cardiac accelerator fibres) or from the Bezold-Jarisch reflex is treated with atropine (three hundred to six hundred micrograms intravenously), and refractory bradycardia with a small dose of adrenaline. The combination of a vasopressor and atropine addresses the two limbs — the afterload/preload and the heart rate — of the spinal's cardiovascular insult. [1]

[1]

Technique, step by step

The technique is rehearsed here as it would be performed for an elective lower-limb or obstetric spinal; the same steps apply with modifications for the urgent or non-obstetric case. [1]

Preparation. Confirm consent, the absence of contraindications (anticoagulant history, platelet count, coagulation, infection at the site, valve disease), large-bore intravenous access, full monitoring (electrocardiogram, non-invasive blood pressure at one- to three-minute intervals, pulse oximetry), and the resuscitation drugs and airway equipment immediately to hand. Pre-oxygenate the obstetric patient and have the vasopressor infusion drawn up. [1]

Position. The patient is positioned sitting or lateral, with the back maximally flexed (knees drawn to the chest, chin on chest) to open the interspinous spaces. The sitting position gives the best midline for the obese or anatomically difficult patient and is the choice for a perineal block (where the hyperbaric solution is to stay low) and for the caesarean spinal in many units. The lateral position is preferred in the obstetric patient who cannot sit (for example, with a prolapsed cord) and for the unilateral spinal (operative side down). For an obstetric spinal, a wedge under the right hip or a left tilt of the table to fifteen degrees relieves aortocaval compression. [1]

Identify the interspace. Palpate Tuffier's line (the line between the iliac crests, crossing L4) and select L3/L4 or L4/L5. [1]

Asepsis. Wash, gown and glove; prepare the back with chlorhexidine or povidone-iodine, allowing it to dry (the chlorhexidine must dry before the needle passes through the field, to avoid neurotoxicity from carry-over); drape widely. [1]

Local infiltration. Raise a wheal of one percent lidocaine in the skin and infiltrate deeper into the interspinous ligament with a fine needle. [1]

Introducer and spinal needle. Place the introducer needle firmly in the interspinous ligament in the midline, aimed slightly cephalad (towards the umbilicus). Introduce the spinal needle (25- or 27-gauge pencil-point) through the introducer. Advance slowly, feeling the resistance of the supraspinous and interspinous ligaments, the firm elastic ligamentum flavum (the first, firm 'pop' as the needle enters the epidural space), and the fainter 'give' of the dura. If bone is encountered, withdraw to the subcutaneous tissue and redirect, slightly more cephalad or caudad. [1]

CSF and injection. Remove the stilette; clear CSF should appear at the hub, confirming the subarachnoid space. Attach the syringe, aspirate a little CSF to reconfirm (a single barbotage), and inject the dose over five to ten seconds without further barbotage. Replace the stilette and withdraw the needle and introducer together. [1]

Position for surgery and assess the block. For an obstetric spinal, turn the patient supine with a left wedge and start the vasopressor infusion. Assess the block height with cold spray or pinprick every two to three minutes until it stabilises at the target level, and assess the motor block with the Bromage scale. Confirm a T4 block (loss of cold sensation at the nipple line) before surgery for caesarean section; confirm the perineum is blocked before perineal surgery. [1]

Midline versus paramedian

The midline approach is the default. The paramedian approach enters one to one-and-a-half centimetres lateral to the midline, angled towards the midline and slightly cephalad, and is used when the midline is inaccessible (severe scoliosis, marked calcification of the supraspinous ligament in the elderly, the patient who cannot flex). It avoids the calcified interspinous ligament and enters the ligamentum flavum more laterally; the Taylor approach is the L5/S1 paramedian variant, used for sacral blocks. [1]

Assessing the block: the Bromage scale

The motor block is assessed with the modified Bromage scale: [1]

• Grade 0 — no block; full flexion of knees and feet.
• Grade 1 — unable to raise the extended leg (hip flexion blocked); able to flex the knees.
• Grade 2 — unable to flex the knees; able to flex the ankles.
• Grade 3 — unable to flex the ankles or feet (complete block of the lower limb). [1]

The sensory level is assessed with cold spray (ethyl chloride or a cold swab) or pinprick, mapping the bilateral dermatomes. The block is allowed to settle for five to ten minutes before surgery, and the level is rechecked before the incision and whenever the patient reports discomfort. [1]

Target block heights by surgery

The dose and the position are chosen to put the block at the height the operation demands: [1]

• T4 — caesarean section, to cover the visceral peritoneal traction that refers pain to T4 and to ensure the upper abdomen is anaesthetised if the uterus is exteriorised.
• T6 to T8 — upper abdominal surgery, open appendicectomy, open cholecystectomy (though a thoracic epidural or general anaesthesia is usually preferred here).
• T10 — lower abdominal and uterine surgery, inguinal hernia repair, transurethral resection of the prostate.
• T12 to L1 — hip and knee replacement and other lower-limb orthopaedics.
• S2 to S4 — perineal, perianal, vaginal and urological surgery; the saddle block, performed with the hyperbaric solution in the sitting position so it pools in the sacral curve. [1]

The dose is titrated to the height and the patient: a smaller dose (seven-and-a-half to ten milligrams) for a short, obstetric or high-spinal-risk patient; a larger dose (fifteen to twenty milligrams) for a tall patient or a longer operation. [1]

The caesarean spinal recipe

The elective caesarean spinal is the most rehearsed spinal in anaesthesia, and its recipe is the synthesis of everything above. A typical recipe is hyperbaric bupivacaine 0.5 percent, twelve-and-a-half to fifteen milligrams, plus fentanyl ten to twenty micrograms and morphine one hundred to one hundred and fifty micrograms, with a prophylactic phenylephrine infusion begun at the block and left lateral tilt to fifteen degrees to relieve aortocaval compression. The block is performed in the sitting or lateral position, the patient is then turned supine with a wedge, and the block is allowed to settle to T4 (loss of cold at the nipple line) before the incision. The vasopressor infusion is titrated to keep the systolic pressure near baseline, treating any fall proactively; norepinephrine is an effective modern alternative to phenylephrine[4]. The intrathecal morphine provides prolonged postoperative analgesia, with the caveat of delayed respiratory depression that warrants postoperative monitoring. The recipe delivers a dense, fast, opioid-sparing block with minimal drug transfer to the fetus — the cardinal obstetric advantages of the spinal.

Intrathecal adjuvants

Small doses of adjuvant drugs added to the local anaesthetic enhance the block or extend analgesia without raising the local anaesthetic dose[5].

Intrathecal opioids. Fentanyl (ten to twenty-five micrograms) is added for faster onset and improved intraoperative analgesia; it has a rapid onset and a short duration (two to four hours) and adds little respiratory risk. Morphine (one hundred to two hundred micrograms, hydrophilic) is added for prolonged postoperative analgesia lasting up to eighteen to twenty-four hours, particularly after caesarean section and major lower-limb surgery; the price is delayed respiratory depression (the hydrophilic morphine rostrally spreads in the CSF to the respiratory centres over hours), which warrants postoperative respiratory monitoring. The Palmer dose-response study (1999) established that, for post-caesarean analgesia, increasing the intrathecal morphine dose above one hundred micrograms (zero point one milligram) gave no additional analgesic benefit but did increase pruritus and the need for its treatment, so there is little justification for use of more than zero point one milligram[5]. Diamorphine (two hundred and fifty to four hundred micrograms) is used in the United Kingdom for the same purpose, with a similar duration. Sufentanil (two-and-a-half to ten micrograms) is a lipophilic opioid used in some centres.

Alpha-2 agonists. Clonidine (fifteen to seventy-five micrograms) and dexmedetomidine (two to ten micrograms) prolong the block and add analgesia by their action on the spinal alpha-2 receptors; the dose is balanced against their sedative and hypotensive effects. [1]

Adrenaline (one hundred to two hundred micrograms, zero point one to zero point two milligrams) prolongs the block by local vasoconstriction, slowing the washout of the local anaesthetic; it is most useful with shorter-acting agents. [1]

Positioning and the unilateral spinal

Because a hyperbaric solution sinks with gravity, the patient's position is the principal tool for shaping the block after the dose is in[9].

For a unilateral lower-limb block (for example, a single knee replacement), the patient is kept in the lateral position with the operative side down for fifteen to twenty minutes after a low dose (seven-and-a-half milligrams of hyperbaric bupivacaine), so the solution preferentially sinks to the dependent side and the contralateral limb is largely spared. The unilateral technique reduces the incidence of hypotension (the sympathetic block is unilateral), speeds motor recovery, and shortens time to discharge; it is a standard ambulatory technique. [1]

For a perineal or caesarean block, the patient is turned supine (with left tilt in obstetrics) after injection to let the solution pool in the thoracic kyphosis and rise cephalad to T4. For a block that must stay low (a perianal operation), the patient is kept sitting upright for five to ten minutes so the solution sinks to the sacral curve and stays there. The site of injection can be chosen to suit: a higher interspace (L2/L3) for a higher block, a lower interspace (L4/L5) for a lower block. [1]

Complications: an overview

The complications of spinal anaesthesia span the common and benign to the rare and catastrophic. The Third National Audit Project (NAP3) of the Royal College of Anaesthetists (2009) established the incidence of the serious complications of central neuraxial block in the United Kingdom: the incidence of permanent injury was approximately two to four per hundred thousand, and the incidence of paraplegia or death approximately one to two per hundred thousand, with two-thirds of initially disabling injuries resolving within six months[7]. The data are reassuring: spinal anaesthesia is, in competent hands, very safe — but the rare catastrophic complications demand vigilance.

The complications group as follows: [1]

• Common and expected: hypotension, bradycardia, backache, urinary retention, shivering.
• Common but preventable: the post-dural puncture headache (incidence one to five percent with a 25- or 27-gauge pencil-point needle).
• Rare and serious: the high or total spinal, neurological injury (cord or nerve root), epidural haematoma and epidural abscess, arachnoiditis, transient neurological symptoms, and infection (meningitis). [1]

The post-dural puncture headache (PDPH)

The PDPH is the characteristic headache of the dural puncture, and it is the complication that the choice of needle is most designed to prevent[6].

Pathophysiology. A persistent leak of CSF through the dural puncture lowers the CSF pressure. When the patient stands, the reduced CSF volume no longer buoyantly supports the brain, which sags on the pain-sensitive intracranial structures (the dura, the blood vessels, the cranial nerves); traction on these structures produces the headache, and the low CSF pressure also triggers a reflex cerebral vasodilation that adds to the pain. The headache is therefore postural — worse on standing, relieved by lying flat — and may be frontal, occipital or in the neck, with associated neck stiffness, photophobia, tinnitus and, rarely, a cranial nerve palsy (most often the sixth, abducens). Onset is typically twenty-four to forty-eight hours after the puncture (the CSF has to leak for a while to drop the pressure). [1]

Incidence and risk factors. The incidence falls with finer needles and with pencil-point over cutting tips; it is higher in young patients, women, the obstetric population, and after an accidental dural puncture with a larger epidural needle (the 'wet tap', which carries a PDPH rate of fifty percent or more with a sixteen- or eighteen-gauge Tuohy needle)[6]. A 25- or 27-gauge pencil-point needle carries a PDPH rate of around one to five percent.

Diagnosis. The diagnosis is clinical: a postural headache within a week of a dural puncture, typically fronto-occipital, relieved by lying flat, with or without neck stiffness and auditory or visual symptoms. The differential diagnosis is broad (migraine, tension headache, meningitis, cortical vein thrombosis, pre-eclampsia in the obstetric patient, pneumocephalus, cerebral haemorrhage), and not every post-neuraxial headache is a CSF leak — but a postural headache after a dural puncture is one until proven otherwise. [1]

Management. Conservative measures come first: reassurance, lying flat, oral hydration, oral analgesia (paracetamol, an NSAID, caffeine), and time, since most PDPH resolve spontaneously within seven to ten days. Caffeine (oral or intravenous) gives temporary relief by cerebral vasoconstriction but does not address the leak. The epidural blood patch is the definitive treatment for a severe or persistent PDPH: under aseptic conditions, fifteen to twenty millilitres of the patient's own venous blood is injected into the epidural space at or near the level of the puncture, where it clots and seals the dural tear; it relieves the headache in sixty to ninety percent of cases, immediately, and can be repeated once if it fails. The theoretical risks (back pain, infection, a repeat dural puncture) are uncommon. An abdominal binder and theophylline are second-line options. [1]

The high and total spinal

A high spinal is a block that ascends higher than intended, typically above T4, and a total spinal is the extreme in which the block reaches the cervical roots and the brainstem. The causes are an excessive dose, an unintended high injection (too cephalad, or into a subdural space), a hyperbaric solution allowed to run cephalad by poor positioning, or, classically, an intrathecal injection of an epidural dose (a wrong-route error, when a dose meant for the epidural space is injected into the subarachnoid space through an unrecognised dural puncture). [1]

Clinical features. The block ascends: numbness and weakness progress to the hands and arms, the patient complains of dyspnoea and a lump in the throat, the voice weakens, bradycardia and profound hypotension develop, and — as the block reaches the cervical roots and the brainstem — consciousness is lost and apnoea supervenes. The pupils may dilate. The picture can mimic a cardiac arrest, but the cause is the ascending local anaesthetic on the brainstem, not a primary cardiac event. [1]

Management. Call for help. Secure the airway and ventilate with one hundred percent oxygen (the apnoea is central, so the patient must be intubated and ventilated); support the circulation with vasopressors (phenylephrine or ephedrine, titrated generously, with adrenaline in reserve) and fluid; give atropine for the bradycardia; relieve aortocaval compression; and support the patient until the block recedes (typically two to four hours for a bupivacaine spinal, longer for a wrong-route lidocaine or an epidural dose). Reassure the team that this is recoverable with support: as the local anaesthetic wears off the block descends and the patient recovers. The prevention is the meticulous avoidance of the wrong-route error (label every epidural dose, aspirate before each epidural top-up, treat any dural puncture with a catheter re-sited in another space) and the careful choice of dose and position. [1]

Epidural haematoma and abscess

The epidural haematoma and the epidural abscess are the rare but catastrophic complications of neuraxial block, and both present the same way: severe back pain with a new and progressive neurological deficit, demanding urgent imaging and surgical decompression[7].

The epidural haematoma is bleeding from the epidural venous plexus into the closed spinal canal, compressing the cord. The risk factors are coagulopathy, therapeutic anticoagulation outside the recommended intervals, trauma from a repeated or difficult needle insertion, and the indwelling epidural catheter in an anticoagulated patient. It presents, within hours to days of the block, with severe back pain (often worse at night, often radicular), followed by a progressive motor and sensory deficit and bowel and bladder dysfunction. Magnetic resonance imaging is the diagnostic test of choice, and urgent surgical decompression (laminectomy and evacuation) within eight to twelve hours gives the best chance of recovery; delay beyond that window worsens the outcome dramatically. The prevention is the strict observance of the anticoagulation intervals before the block and before catheter removal, and the avoidance of a traumatic or repeated insertion in a coagulopathic patient[8].

The epidural abscess is infection in the epidural space, from skin flora (Staphylococcus aureus) introduced by the needle or the catheter, or haematogenous. The risk factors are poor asepsis, an indwelling catheter for days, diabetes, immunosuppression, and injection through infected skin. It presents, days to weeks later, with back pain, fever, a raised inflammatory marker, and a progressive neurological deficit; the source may be unmasked by blood cultures. Magnetic resonance imaging is diagnostic; treatment is urgent surgical decompression and prolonged antibiotics. [1]

Arachnoiditis is a chronic adhesive inflammation of the arachnoid from chemical (the wrong solution injected intrathecally, preservatives, antiseptic carry-over) or physical (trauma, haematoma) injury; it presents weeks to months later with chronic pain and a progressive neurological deficit, and it is largely irreversible. Transient neurological symptoms (TNS) — back and leg pain resolving within days, with no deficit — are associated with intrathecal lidocaine (and less so with mepivacaine), and are the reason lidocaine is used cautiously intrathecally. [1]

Spinal versus epidural versus combined spinal-epidural

Spinal anaesthesia is one of three neuraxial techniques, and the choice between them is a familiar viva question[9].

[1]

The spinal wins on speed, density and reliability, and needs only a small dose, but its height is fixed once injected and it cannot be extended. The epidural wins on flexibility (a catheter allows titration over hours or days) and on the lower PDPH rate, but needs a larger dose, has a slower and less dense onset, and can produce a patchy or unilateral block. The combined spinal-epidural (CSE) combines the rapid, dense onset of the spinal with the flexibility of an epidural catheter, at the price of a slightly higher PDPH rate than a pure epidural and the theoretical risk of the wrong-route error through the dural puncture; it is the choice for long surgery needing a fast onset, and for labour analgesia where rapid onset is desired. [1]

Special situations

The obstetric patient

The obstetric spinal differs from the non-obstetric in four ways: the engorged epidural venous plexus reduces the CSF volume and raises the block for the same dose (so a smaller dose is used); aortocaval compression by the gravid uterus in the supine position demands left lateral tilt; the high incidence of hypotension demands a prophylactic vasopressor infusion; and the addition of intrathecal morphine for post-caesarean analgesia (with postoperative respiratory monitoring). The obstetric spinal is one of the most rewarding techniques in anaesthesia: a dense, fast, opioid-sparing block with minimal drug transfer to the fetus, provided the haemodynamics are managed proactively[2][4].

The elderly patient

The elderly patient has a reduced CSF volume, a less compliant theca, and a higher baseline sympathetic tone, all of which raise the block for the same dose; the dose is reduced. The cardiovascular reserve is less, so the hypotension is less well tolerated and the vasopressor prophylaxis more important. The slower motor recovery raises the fall risk and the need for postoperative supervision. [1]

The paediatric and neonatal patient

In the neonate the cord ends at L3, so the safe interspace is L4/L5 or L5/S1; a caudal or lumbar spinal is performed under heavy sedation or general anaesthesia (the awake neonate cannot cooperate). The block is used for lower abdominal and lower-limb surgery, and there is interest in its use to reduce the general anaesthetic exposure of the developing brain. [1]

The ambulatory patient

For ambulatory surgery the priorities are a fast onset, a predictable height, and a fast motor recovery to allow discharge. The choice is a low dose of hyperbaric bupivacaine (seven-and-a-half to ten milligrams) or prilocaine for short procedures, often as a unilateral spinal, with attention to the prevention of urinary retention (the leading cause of delayed discharge). [1]

Red flags and key facts

[1] [1]

Summary

Spinal anaesthesia is a precise, reproducible and rewarding technique that gives a dense, fast and opioid-sparing block for surgery below the umbilicus and for caesarean section. Its mastery rests on four foundations: the anatomy of the layers the needle traverses and the safe interspace below the conus; the determinants of block height, of which the baricity of the solution and the patient's position are the levers you can use at the time; the physiology of the sympathetic block and its hypotension, the cardiac accelerator fibres and the bradycardia of the high block, and the Bezold-Jarisch reflex that can turn a routine spinal into a cardiac emergency; and the prevention, recognition and management of the complications — the hypotension and bradycardia, the post-dural puncture headache (prevented by the fine pencil-point needle), the high and total spinal, and the rare but catastrophic epidural haematoma and abscess. The proactive management of the haemodynamics — a fluid co-load, a prophylactic phenylephrine infusion, left lateral tilt in the obstetric patient, and a low threshold for atropine — is the difference between a smooth spinal and a difficult one, and it is the standard of care[1][2][4][7].

References

1. [1]Ferre F, Martin C, Bosch L, Kurrek M, Lairez O, Minville V Control of Spinal Anesthesia-Induced Hypotension in Adults Local Reg Anesth, 2020.PMID 32581577
2. [2]Lee A, Ngan Kee WD, Gin T A quantitative, systematic review of randomized controlled trials of ephedrine versus phenylephrine for the management of hypotension during spinal anesthesia for cesarean delivery Anesth Analg, 2002.PMID 11916798
3. [3]Veeser M, Hofmann T, Roth R, Klohr S, Rossaint R, Heesen M Vasopressors for the management of hypotension after spinal anesthesia for elective caesarean section. Systematic review and cumulative meta-analysis Acta Anaesthesiol Scand, 2012.PMID 22313496
4. [4]Ngan Kee WD, Lee SWY, Ng FF, Khaw KS Prophylactic Norepinephrine Infusion for Preventing Hypotension During Spinal Anesthesia for Cesarean Delivery Anesth Analg, 2018.PMID 28678073
5. [5]Palmer CM, Emerson S, Volgoropolous D, Alves D Dose-response relationship of intrathecal morphine for postcesarean analgesia Anesthesiology, 1999.PMID 9952150
6. [6]Sachs A, Smiley R Post-dural puncture headache: the worst common complication in obstetric anesthesia Semin Perinatol, 2014.PMID 25146108
7. [7]Cook TM, Counsell D, Wildsmith JA; Royal College of Anaesthetists Third National Audit Project Major complications of central neuraxial block: report on the Third National Audit Project of the Royal College of Anaesthetists Br J Anaesth, 2009.PMID 19139027
8. [8]Leffert L, Butwick A, Carvalho B, et al The Society for Obstetric Anesthesia and Perinatology Consensus Statement on the Anesthetic Management of Pregnant and Postpartum Women Receiving Thromboprophylaxis or Higher Dose Anticoagulants Anesth Analg, 2018.PMID 29099429
9. [9]Uppal V, Shanthanna H, Prabhakar C, McKeen DM Intrathecal hyperbaric versus isobaric bupivacaine for adult non-caesarean-section surgery: systematic review protocol BMJ Open, 2016.PMID 27194318