Studies of factors affecting PERIDURAL ANESTHESIA

Erdemir, Hamdi; Soper, Leslie E.; Sweet, Robert B.

doi:10.1213/00000539-196507000-00008

Cited by 31 publications

(7 citation statements)

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“…When the second injection through the catheter in the needle group is inadvertent, it is impossible to continue the epidural anesthesia. Moreover, the local anesthetic previously administered through the needle may conceal trauma to neural tissue during catheter placement16 • Erdemir et al 7 reported that fast injection (1 ml-secr "] was found to produce slightly higher analgesic levels (only 0.7 dermatome higher) than slow injection (0.33 ml-sect '}. However, they did not discuss the physical characteristics of the patients.…”

Section: Discussionmentioning

confidence: 99%

Epidural administration and analgesic spread: Comparison of injection with catheters and needles

1992

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This study was designed to investigate differences in epidural analgesic spread between catheter and needle injections in 48 patients with comparable physical characteristics. The spread of analgesia in the catheter injection group with a 0.24 ml.sec(-1) injection rate (n = 16) was 16.8 +/- 1.5 spinal segments and that in the needle injection group at the same injection rate (n = 16) was 12.5 +/- 1.8 spinal segments ( P < 0.01). Needle injection at the faster rate of 1.2 ml.sec(-1) (n = 16) produced a significantly greater spread of analgesia than with the 0.24 ml.sec(-1) rate through the needle (16.2 +/- 1.6 vs 12.5 +/- 1.8 spinal segments, P < 0.01). Thirteen of 16 patients receiving the fast needle injection complained of back compression or discomfort during the injection. The injection through an epidural catheter and the fast (1.2 ml.sec(-1)) injection through a needle produced extensive and equivalent epidural analgesic spread. However, because of patients discomfort with fast injection through the needle, the authors conclude that when using continuous epidural anesthesia, the initial injection of local anesthetic should be administered through the epidural catheter not the needle.

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Section: Discussionmentioning

confidence: 99%

Epidural administration and analgesic spread: Comparison of injection with catheters and needles

1992

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“…Although the injection of larger volumes may result in a more extensive analgesic spread (Erdemir et al 1965), the total dosage is probably a more important determinant of the spread of epidural and spinal anaesthesia than either the volume or concentration of local anaesthetic in the solution (Bromage 1962(Bromage , 1978Sheskey et al 1983). Within the clinically useful dose range, increases in the dose generally result in disproportionately smaller increases in the number of blocked segments (Grundy et al 1978;Park et al 1982;Sheskey et al 1983), and will, within limits, also speed the onset, enhance the intensity and prolong the duration of anaesthesia (Bridenbaugh et al 1973;Buckley et al 1978;Crawford 1964;Littlewood et al 1979;Lund 298 et al 1973;Park et al 1982;Scott et al 1980;Sheskey et al 1983).…”

Section: Dose and Concentrationmentioning

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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“…Slowing the speed of injection permits more time for redistribution of the dose to occur and may allow detection of an inadvertent intravenous injection before all of the dose is administered. Furthermore, peridural injections given within I minute are less comfortable for the patient and are accompanied by a greater incidence of incomplete analgesia (Erdemir et a\., 1966).…”

Section: Speed Of Injectionmentioning

confidence: 99%

Clinical Pharmacokinetics of Local Anaesthetics1

Tucker

Mather

1979

Clinical Pharmacokinetics

284

145

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The introduction of the new long acting local anaesthetics, bupivacaine and etidocaine, has stimulated an expansion of interest in regional anaesthesia, particularly for obstetrical applications and pain therapy. System toxicity following injection of local anesthetics occurs albeit infrequently, and tentative correlations have been made between the onset of CNS and cardiovascular effects and circulating drug concentrations in both adults and neonates. Amongst other factors, interpretation of these relationships depends upon blood distribution and plasma binding of the agents, sampling sites and acid-base balance. The disposition kinetics and placental transfer of the amide type agents have been well characterised. In adults their clearance is almost entirely hepatic but in neonates an increase in the renal component is, in part, a reflection of the immaturity of some of the enzymes responsible for their metabolism. Ester type agents are rapidly hydrolysed by plasma pseudocholinesterase and this has led to a preference for chloroprocaine in some obstetric procedures. Major determinants of the systemic absorption of the agents after perineural administration include their physicochemical and vasoactive properties, perfusion and tissue binding at the site of injection and whether or not adrenaline has been added. In respect of blood drug concentrations achieved after various regional anaesthetic procedures, the margin of systemic safety appears to favour bupivacaine and etidocaine compared to shorter acting analogues such as lignocaine and mepivacaine. The time course of local anaesthetic remaining at the site of injection has been calculated following intravenous regional anaesthesia and peridural block. This has allowed prediction of the local and systemic accumulation of the drugs following contined dosage. Blood concentrations of local anaesthetics after perineural injection are not closely related to age, weight or pregnancy but may be influenced by diseases associated with haemodynamic changes and by other drugs given at or around the time of regional blockade.

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Studies of factors affecting PERIDURAL ANESTHESIA

Cited by 31 publications

References 0 publications

Epidural administration and analgesic spread: Comparison of injection with catheters and needles

Epidural administration and analgesic spread: Comparison of injection with catheters and needles

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Clinical Pharmacokinetics of Local Anaesthetics1

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