Quality of Epidural Blockade Iii: Carbonated Local Anaesthetic Solutions

Bromage, Philip R.; Burfoot, M. F.; Crowell, D. E.; Truant, Aldo P.

doi:10.1093/bja/39.3.197

Cited by 40 publications

(14 citation statements)

References 0 publications

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“…Of particular practical importance is the markedly shortened time until full analgesia is obtained. While Bromage et al 2 found that the latency of carbonated solutions in extradural analgesia was shortened by one third as compared to the hydrochloride solutions, we saw the latency for full analgesia to pin prick cut by two thirds in brachial plexus to an average of 4-5 minutes. This rapidity of action with paraesthesia normally being experienced in less than one minute, allowed us to diagnose failure to block any one particular nerve at a much earlier time and to start supplementary blocking procedures.…”

Section: Discussioncontrasting

confidence: 64%

Carbon dioxide salts of lignocaine in brachial plexus block

Schulte-Steinberg

Hartmuth

1970

Anaesthesia

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Among the criticisms which are levelled against regional anaesthesia, the time spent waiting for the onset of analgesia and the need to accept a certain rate of failure are frequently cited.One of the authors had occasion in 1963, to observe the rapidity of action of carbonated local analgesic solutions (lignocaine and prilocaine) in extradural blockade as done by Bromage, who subsequently reported his findings 192. Compared with the conventional hydrochloride salts of local analgesics the carbonic salts shortened the latency of the agent by one third and produced a more intense sensory and motor blockade. There was a tendency to wider spread of analgesia even with a reduced total dose. The results were so impressive that they encouraged us to try these same solutions in peripheral nerve blocks. For our investigation we chose regional analgesia of the brachial plexus. Theory of carbonated local analgesic solutionsIt has been known for a long time that the hydrogen ion concentration is an important factor in the uptake of local analgesic agents. Bignon in 18923 mentioned cocaine with alkali added, and in 1910 Gros4 suggested how alkalinised solutions worked. The theory of carbonated local analgesics has been ably put forward by Bromagel. Carbonated solutions, in this case lignocaine carbonate, have a relatively high pH of 6.5 and are thus less demanding on the buffering capacity of the tissues (pH 7.4) than the commonly available local analgesics. Of these, the solutions containing vasoconstrictor agents have a pH of 4 and even those containing no vasoconstrictor are not higher than a pH of 6. In carbonated solutions the free base is liberated quickly due to rapid buffering, and the liberated carbon dioxide diffuses very rapidly causing a fall in the intracellular pH in the vicinity. Thus the analgesic base is brought closer to the nerve membrane in a higher concentration for combination with the receptor5.6. In addition carbon dioxide appears to have a direct effect on nerve fibres by stabilizing excitable tissue.

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Section: Discussioncontrasting

confidence: 64%

Carbon dioxide salts of lignocaine in brachial plexus block

Schulte-Steinberg

Hartmuth

1970

Anaesthesia

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“…The uptake of local anaesthetics into local tissues has been studied in dogs to a limited extent, following epidural injection of lignocaine and mepivacaine (Bromage et al 1963(Bromage et al , 1967 and subarachnoid administration of lignocaine and procaine (Cohen 1968). These studies showed extensive uptake into intradural spinal nerve roots and peripheral zones of the spinal cord, in particular the lateral and posterior columns.…”

Section: Tissue Concentrationsmentioning

confidence: 99%

“…Some investigators have reported that administration of carbonated solutions of lignocaine and prilocaine instead of the usual hydrochloride salt solutions produced earlier onset and improved the quality of the epidural block to a clinically useful degree, possibly by decreasing the intraneural pH and thereby increasing the fraction of active ionised drug (Bromage et al 1967;Cousins & Bromage 1971). These observations, obtained from open studies, were confirmed later by a double-blind study (Nickel et al 1986), although other doubleblind studies only partially confirmed the improved quality, and did not corroborate the faster onset (Cole et al 1985;Martin et al 1981;Morison 1981).…”

Section: Alkalisation and Carbonativnmentioning

confidence: 99%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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Epidural and spinal anaesthesia results from the interaction of local anaesthetics with nerve structures, primarily those located within the subarachnoid space. Local anaesthetics can reach the sites of action along various distribution pathways. Uptake into extraneural tissues (in particular epidural fat) and systemic absorption compete with neural tissue distribution and thereby affect the clinical potency and duration of action. Consequently, epidural doses must be much higher than spinal doses. The systemic absorption of lignocaine (lidocaine), bupivacaine and etidocaine following lumbar epidural administration has been shown to be biphasic, with a rapid initial absorption phase followed by a much slower absorption phase. Initial absorption rates of lignocaine and bupivacaine following subarachnoid injection are much slower, but the late absorption rates are similar to those after epidural administration. The tissue distribution characteristics of various amide-type agents are similar, because more extensive plasma binding offsets the greater tissue affinity of the more lipophilic compounds bupivacaine and etidocaine. The amide-type agents are predominantly eliminated by hepatic metabolism, except prilocaine, which is also metabolised elsewhere in the body. Ester-type agents are rapidly hydrolysed in blood and liver and are eliminated much faster than amide-type agents. The blood concentrations attained depend primarily upon the dose administered. The addition of adrenaline (epinephrine) reduces the peak plasma drug concentrations; similarly, the age of the patient, disease states and drug interactions may alter the pharmacokinetics to various extents. Because of the low dose requirements, systemic toxicity is not a problem during spinal anaesthesia. During epidural anaesthesia, however, the safety margin is relatively small, and systemic toxicity is very likely to occur after inadvertent intravascular injection of an epidural dose.

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“…Crawford (1964) has reported similar results from the epidural injection of local anaesthetic agents in man. Second, increasing the pH of the lignocaine solutions slightly shortened the onset and prolonged the duration of these responses as it does in man (Bromage et al, 1967). Third, the potentiating effect of adrenaline on the duration of lignocaine-induced epidural anaesthesia in man (Lund, 1966) was also seen in the cat.…”

Section: Discussionmentioning

confidence: 87%