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Conduct of epidural and subarachnoid blockade

Created: 18/3/2005


In 1898, the first subarachnoid blockade in man was performed by Karl August Bier using a cocaine solution. From 1930 to 1950, spinal techniques were used widely for anaesthesia, but subsequently declined in popularity, partly because of the fear of toxicity and partly owing to the improvements in general anaesthesia that occurred at the time. Epidural anaesthesia was described by Sicard and Cathelin in 1901, but did not become popular until after World War II with the introduction of amide local anaesthetic agents and catheters that allowed replenishment of the block. Since 1960, there has been a resurgence of these regional techniques and subarachnoid and epidural anaesthesia and analgesia are used widely in current clinical practice.

Indications, contraindications and complications for neuroaxial blockade

Indications – epidural and subarachnoid blockade are suitable techniques to provide anaesthesia for abdominal, pelvic and lower limb surgery. They are unsuitable for thoracic or upper limb anaesthesia because of the accompanying local anaesthetic effects on respiratory muscles and the sympathetic nerve supply to the heart. By selecting suitable drug combinations they can provide analgesia to the lower limbs, abdomen and thorax and have been used to control intra- and postoperative pain, the pain of labour and for the treatment of chronic and terminal pain. These regional blocks are also beneficial for patients undergoing surgery when they are used to ameliorate the stress response of surgery, facilitate the production of a ‘bloodless field’, reduce the risk of postoperative thromboembolism and reduce the use of opioids in the perioperative period (Figure 1).

Figure 1

Advantages of subarachnoid and epidural anaesthesia

Contraindications (Figure 2) an epidural or subarachnoid technique should be considered if the benefits it provides outweigh the risks of performing the procedure. When assessing risks, alternative ways of providing anaesthesia and the benefits of the treatment should be considered.

Complications – important complications are given in Figure 3.

Pharmacology of commonly used agents

The most common drugs used in epidural or intrathecal regimens are local anaesthetic agents and opioids. Many other drugs have been used in the past and others are being evaluated.

Local anaesthetics act by blocking sodium channels on the inside of the axonal membrane, preventing depolarization and conduction along the nerve. They affect all types of nerve fibres, but have a more pronounced effect on small and unmyelinated axons. In low doses they cause analgesia and peripheral vasodilatation by their effects on A-delta (pain, temperature and touch) and B (preganglionic autonomic) fibres, with less effect on somatic muscle activity mediated by large myelinated Aa (motor and proprioception) and A-gamma (motor to muscle spindle) fibres. In higher concentrations, local anaesthetic drugs block all nerve modalities.

Figures 2 and 3

Contraindications to subarachnoid and epidural blockade

Complications of subarachnoid and epidural blockade

The first local anaesthetics were esters (e.g. procaine, amethocaine), which caused vasodilatation. In the 1940s, amide local anaesthetics became available. These drugs either had little effect on vasomotor tone or tended to cause vasoconstriction at therapeutic doses. The earliest amide local anaesthetic drugs (e.g. lidocaine, mepivacaine) have relatively low lipid solubilities. This gives them a short duration of action (about 90 minutes) and lidocaine also demonstrates tachyphylaxis. These properties limit their usefulness. The introduction of bupivacaine in the 1960s, which has a longer duration of action and does not demonstrate tachyphylaxis, provided clear advantages. Bupivacaine is widely used despite its greater potential for cardiac toxicity when inadvertently given intravenously.

Many local anaesthetic drugs exist in more than one isomeric form, with different potencies and side-effect profiles for each isomer. Recently, single isomers of some drugs have become available that have a better toxicity profile than their parent mixture (e.g. levobupivacaine, the L isomer of bupivacaine).

Opioids – opioid receptors are present in many areas of the brainstem and spinal cord, predominantly in the substantia gelatinosa, lamina II and dorsal horn. Opioids tend to block transmission through C pain fibres preferentially and spare motor activity. When administered via the epidural or intrathecal route they are delivered to these receptors at a much higher concentration than when given systemically. Opioids have to penetrate the dura and arachnoid and enter the cerebrospinal fluid before diffusing into the spinal cord and producing analgesia. When administered intrathecally these barriers are bypassed, but opioids administered into the epidural space have to cross them. Most drugs rapidly cross the dura, but the rate of penetration across the arachnoid is determined by lipid solubility. Drugs with low lipophilicity (e.g. morphine) cross the arachnoid slowly and have a slow onset of action; they are cleared slowly, resulting in a long duration. Cephalad spread of drugs with low lipophilicity may result in delayed onset of nausea and respiratory depression. Drugs with higher lipid solubilities (e.g. fentanyl) have a faster onset, a shorter duration and are associated with fewer late-onset side-effects.

Other agents have been used intrathecally and in the epidural space.

  • Epinephrine is used occasionally to produce vasospasm via its a1-receptor action and results in a slower clearance of other agents from the site. It may intensify and prolong the action of some agents.
  • Clonidine, a more selective a2-agonist, has been used to enhance analgesia with sparing of the motor and proprioception modalities and has the advantage over opioids of not causing respiratory depression, pruritus or nausea and vomiting. However, it can produce hypotension, bradycardia and sedation and has not established itself widely in clinical practice.

Differences between epidural and subarachnoid blockade

Factors influencing spread of blockade

Epidural blockade – local anaesthetics injected into the epidural space spread in cranial and caudal directions from the level at which they are administered. The drug bathes the nerve roots as they pass through the anterolateral epidural space, but roots above and below the limit of spread of local anaesthetic remain unaffected. This gives an epidural local anaesthetic block a top and a bottom level of effect, with the site of injection somewhere in between. There may be preferential spread of local anaesthetic to one side of the spinal canal, and when this occurs the level and intensity of blockade on each side of the body can be different. Occasionally single nerve roots are missed altogether resulting in a patchy block. Local anaesthetic solutions injected into the epidural space are influenced by gravity. With the patient in a sitting position the lower segments tend to be blocked, and when supine the block spreads higher. In the lateral position, the dependent side tends to block preferentially.

Subarachnoid block – intrathecal local anaesthetic acts directly on the spinal cord and all modalities below the upper limit of the block are affected. The subarachnoid block always blocks down to the sacral levels and more reliably affects both sides of the body. If the patient is seated, the local anaesthetic does not spread as far up the spinal canal and a saddle block, extending no higher than the upper lumbar levels, may develop. With this level of block it is possible to undertake pelvic operations, but not intra-abdominal operations, and much of the cardiovascular disturbance caused by blockade of the thoracic sympathetic outflow is avoided. In a supine position, local anaesthetic pools at about the level of the third thoracic vertebra, the lowest point of the thoracic kyphosis, providing reliable anaesthesia for most lower abdominal operations. When hyperbaric solutions of local anaesthetic are compared with isobaric solutions for spinal anaesthesia the mean height of block for any position is similar, but the variability of spread is greatest with isobaric solutions.

Intensity of blockade

Epidural anaesthesia – the intensity of the blockade is directly proportional to the concentration of local anaesthetic given. The addition of opioids to local anaesthetic solutions provides a greater degree of sensory blockade without enhancing motor block. If suitable mixtures of local anaesthetic and opioids are chosen this allows sensory blockade with sparing of the motor function.

Subarachnoid block – the intensity of the block is directly related to the dose of local anaesthetic administered. Large volumes of dilute local anaesthetic solutions have a similar effect to small volumes of concentrated solutions containing the same dose of local anaesthetic. In common with epidural mixtures, opioids added to local anaesthetic solutions have a motor-sparing effect.

Physiological effects of local anaesthetic blockade

Local anaesthetic drugs block conductance along all types of nerves with large, myelinated motor nerves being less sensitive than small, unmyelinated sensation and sympathetic nerves. Motor, sensory and autonomic nerves are all affected and the levels the local anaesthetic spreads across determines their effect. By considering the levels that become blocked, the effect can be predicted (Figure 4).

Figure 4: Physiological effect of spinal blockade at different levels

Effects of spinal blockade
Effects of spinal blockade 2

The effects of a ‘total spinal’: if a large volume of local anaesthetic is inadvertently injected intrathecally at the lumbar level it initially affects the lower limbs, but rapidly spreads cranially. Patients initially report a rapid onset of analgesia in their lower limbs and pelvis. At this time the small amount of arteriolar and venous dilatation in the legs results in a minor drop in blood pressure with a small compensatory tachycardia. Within about 30 seconds the block spreads up to the lower thoracic region and the patient may report minor difficulty breathing and, if monitored, the block may be seen to spread as a loss of sensation over the abdomen. When the mid-thoracic level is reached, the coeliac plexus becomes blocked, causing loss of sympathetic tone to the gastrointestinal tract, and the resulting arterial and venous dilatation causes severe hypotension with a marked compensatory tachycardia. As the block spreads to the upper thoracic region, the patient may complain of increasing shortness of breath and the height of the block will continue to rise up the chest wall. When the block reaches the sympathetic outflow to the heart, at the 3rd to 5th thoracic nerve roots, there is a loss of its positive chronotropic and inotropic effects. Unopposed vagal stimulation then results in bradycardia or asystole and cardiovascular collapse occurs.

As the block spreads to the lower cervical region the patient develops weakness in the arms, hands, shoulders and head with an associated Horner’s syndrome. The phrenic nerve becomes paralysed and the patient becomes apnoeic when the block reaches the upper cervical region. The anaesthetist should be aware that cardiovascular collapse occurs before respiratory failure, and that even after phrenic nerve paralysis the patient may remain aware, unless his conscious state is modified by drugs or inadvertent hypotension.

Copyright © 2004 The Medicine Publishing Company Ltd

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