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Epidural anesthesia has the potential to produce local anesthetic-induced systemic toxicity (see Chapter 14 ), primarily through the unintentional administration of drug into an epidural vein. Considerable research has been undertaken to define the ideal test dose for continuous epidural catheter use. The use of test doses should minimize
The toxic effects of local anesthetics primarily affect the CNS and cardiovascular systems, with the CNS affected at lower blood levels. For example, four to seven times the dose of local anesthetic necessary to produce convulsions in dogs is required to produce cardiovascular collapse.[164] The CNS stimulation is a result of local anesthetic-induced inhibition of the CNS. The initial excitatory phase of a reaction is caused by selective inhibition of inhibitory neurons in the cerebral cortex, allowing facilitatory neurons to discharge in an unopposed fashion.[165] After blood levels are high enough, inhibitory and facilitatory pathways are inhibited, leading to CNS depression.
Initially, the potential for local anesthetic-induced toxicity (CNS and cardiovascular) was thought to parallel anesthetic potency.[166] [167] Information suggests that bupivacaine and etidocaine may be proportionally more cardiotoxic than their anesthetic potency predicts. [168] [169] This relative increase in cardiotoxicity appears to result from more potent electrophysiologic effects of the long-acting amides because of their fast-in-slow-out sodium channel blockade. Ropivacaine and (S)-(-)-levobupivacaine, other long-acting amide local anesthetics, have a CNS-to-cardiotoxicity ratio intermediate between lidocaine and bupivacaine.[170] [171] The clinical importance of these observations about toxicity must be balanced against clinical studies showing limited cardiovascular depression in patients undergoing bupivacaine-induced seizures during regional anesthetics.[172]
If signs of CNS toxicity or frank convulsions occur, several steps must be followed if adverse outcomes are to be minimized (see Chapter 14 ). Early in local anesthetic-induced seizures hypoxemia, hypercarbia, and acidosis develop rapidly, and symptomatic treatment of the toxicity must involve treatment of these factors. Oxygen should be given by bag and mask, and tracheal intubation is not mandated unless ventilation is ineffective.[173] The next step in therapy remains controversial, with succinylcholine or anticonvulsant administered. Succinylcholine is often recommended because the local anesthetic-induced seizures are usually short lived, and the muscle relaxation obtained facilitates ventilation and decreases the magnitude of metabolic acidosis. Nevertheless, it does not decrease cerebral metabolism; CNS oxygen requirements remain increased. Others suggest that diazepam is effective in controlling local anesthetic-induced seizures, although 2 to 3 minutes is required to control seizures after administration. [174] [175]
The most effective method of treating toxic reactions is prevention. Administration of excessive doses of local anesthetics should be prevented, and test doses of local anesthetics should be used before the injection of therapeutic doses. If a toxic reaction does occur, it is imperative that oxygen, a method of administering it, succinylcholine, and anticonvulsant drugs are immediately available.
The adverse effects of unintentionally administering an epidural dose of local anesthetic into the spinal fluid are highlighted by the neurologic changes that followed subarachnoid injection of 2-chloroprocaine. However, most subarachnoid injections of epidural local anesthetics are less dramatic; rather, the issue is how the physician should treat the cardiopulmonary effects resulting from such an injection. As in any neuraxial block that reaches high levels, arterial blood pressure and heart rate should be supported. The Trendelenburg position should be instituted to maximize venous return. Intravenous atropine and ephedrine are often effective and provide the time to administer a more potent catecholamine, if needed. Ventilation should be supported, and if the entire dose (20 to 25 mL) of local anesthetic has been administered into the CSF, tracheal intubation and mechanical ventilation are indicated because patients may require approximately 1 to 2 hours to maintain adequate spontaneous ventilation consistently. After a large dose of local anesthetic into the CSF, patients develop dilated pupils, which may seem to indicate CNS injury if this phenomenon is not recognized for what it is. The pupils return to the baseline state as the high block recedes. Fortunately, the necessity for sedation during the period of tracheal intubation and mechanical ventilation is minimal. These patients usually do not recall such events.[176]
When an epidural block is performed and the higher-than-expected block develops only after a delay of 15 to 30 minutes, subdural placement of local anesthetic must be considered. Treatment is symptomatic; the most difficult aspect is recognizing the possibility of a subdural injection.
With the exception of the publicity surrounding the 2-chloroprocaine-induced adhesive arachnoiditis, uncomplicated epidural anesthesia has not been linked with neurologic injury more frequently than other anesthetics, regional or general.[112] [115] No particular local anesthetic, needle versus catheter technique, addition or omission of epinephrine, or location of epidural puncture seems to be associated with an increased incidence of neurologic injury. Despite this information, neurologic injury is often feared and epidural anesthesia avoided in patients in whom antiplatelet drugs or other anticoagulants have been used preoperatively. Is this justified?
There are no data on patients taking the antiplatelet drug, aspirin, showing that there is an increased incidence of neurologic injury caused by epidural bleeding (hematoma) when epidural anesthesia is used.[177] It is doubtful that a perceived lack of data indicates that the problem has been overlooked, because epidural anesthesia is frequently used in patients undergoing orthopedic procedures, in whom aspirin and nonsteroidal anti-inflammatory drug use is widespread. Nevertheless, there are isolated case reports of neurologic injury after epidural and spinal anesthesia in patients in whom antiplatelet drugs were used. It may be significant that in these case reports the initial neuraxial technique was abandoned after technical difficulties with needle placement.[178] [179] The appropriate place of neuraxial techniques with the newer and more potent antiplatelet drugs (e.g., abciximab, a glycoprotein (GP) IIb/IIIa receptor antagonist) remains undetermined, although significant caution probably is needed.
The use of epidural anesthesia for patients receiving anticoagulants is less clear because epidural anesthesia is often avoided in these patients. There are data from Odoom and Sih,[180] who used continuous epidural anesthesia in 1000 vascular operations for patients receiving preoperative oral anticoagulants, without problem. The acceptable magnitude of preoperative anticoagulation and risk-benefit ratio of performing epidural anesthesia remain undetermined and should be focused on specific patients and their clinical setting. Despite lacking data, the use of epidural techniques in patients receiving subcutaneous heparin therapy is probably acceptable if the block can be performed atraumatically, although the risk-benefit ratio must be determined for each patient.[181] Some speculate that proof of minimal systemic effect from the subcutaneous heparin (normal partial thromboplastin time) is necessary before neuraxial block.[180]
There is consensus that when LMWH (e.g., enoxaparin) is used perioperatively, neuraxial block techniques need to be managed differently.[182] There is an increased risk of neuraxial bleeding when LMWH and neuraxial techniques are combined if the following recommendations are not followed[9] :
It does seem that the issue of intraoperative anticoagulation after epidural catheter insertion is as settled as clinical data allow. Approximately 5000 patients have undergone epidural anesthesia for vascular surgery with intraoperative heparinization and without a neurologic injury attributable to epidural bleeding. [180] [183] [184] Despite minimal problems with epidural anesthesia and neurologic dysfunction related to anticoagulation, if a patient has neurologic symptoms consistent with neuraxial mass after regional block, immediate neurosurgical consultation is indicated because time is of the essence if permanent sequelae are to be prevented. If the patient appears to be at increased risk for neuraxial bleeding but the neuraxial technique remains indicated, it may be prudent to use a shorter-acting epidural local anesthetic, even if it means reinjecting more frequently so that the block will resolve as rapidly as possible after the surgical procedure.
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