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Chapter 43 - Spinal, Epidural, and Caudal Anesthesia ^*

David L. Brown

Spinal, epidural, and caudal neuraxial blocks result in sympathetic block, sensory analgesia, and motor block, depending on dose, concentration, or volume of local anesthetic, after insertion of a needle in the plane of the neuraxis. Despite these similarities, there are significant physiologic and pharmacologic differences. Spinal anesthesia requires a small mass (i.e., volume) of drug, virtually devoid of systemic pharmacologic effect, to produce profound, reproducible sensory analgesia. In contrast, epidural anesthesia necessitates use of a large mass of local anesthetic that produces pharmacologically active systemic blood levels, which may be associated with side effects and complications unknown with spinal anesthesia. The introduction of combined spinal and epidural techniques blurs some of these differences but also adds flexibility to clinical care.

The blurring of differences between spinal and epidural anesthesia began early, when Corning^[1] reported on spinal anesthesia and local medications of the cord (see Chapter 1 ). It remains unclear whether his injection of cocaine "between spinous processes" produced spinal or epidural anesthesia. Bier understood he was producing spinal anesthesia in 1898, and through self-investigation of spinal anesthesia, he had personal knowledge of the symptoms of postdural puncture headache. These early years were principally involved with the advancement of spinal rather than epidural anesthesia for at least three reasons. First, the only practical local anesthetic available until 1904 (when procaine was synthesized) was cocaine, which was more suited to spinal than epidural anesthesia because of systemic side effects at doses required for each. Second, the equipment available for neuraxial blocks favored spinal anesthesia because the end point of cerebrospinal fluid (CSF) return was well defined and did not demand sophisticated glass syringes and needles required for epidural anesthesia. Third, muscle relaxants had not been introduced, and spinal anesthesia produced superb skeletal muscle relaxation, facilitating surgical exposure.

These advantages of spinal anesthesia historically created many enthusiastic clinicians. Morton^[2] promoted high spinal anesthesia for surgical procedures carried out on the head and neck, whereas Koster^[3] used total spinal blockade for thoracic and intracranial procedures. Spinal anesthesia was not limited to surgical conditions but was touted for the treatment of medical conditions (e.g., pulmonary edema) by taking advantage of its venodilatory effect. However, a number of impediments prevented more widespread use of spinal and epidural blocks.

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Despite the many advantages and safety of spinal anesthesia, Kennedy and colleagues^[4] described "grave spinal cord paralysis" accompanying the use of spinal anesthesia in 1950; this report was followed by one in 1954 detailing the well-publicized Woolley and Roe trial in England.^[5] In the latter instance, two patients, Woolley and Roe, had neurologic injury after receiving their spinal anesthetics, which were administered in the same hospital, on the same day, and by the same anesthetist in 1947. The exact cause of their neurologic dysfunction remains cloudy. Was it contaminated ampules or a toxic substance administered into the subarachnoid space by mistake?^[6]

Anesthesiologists continue to face confusion about balancing the risks and benefits of spinal anesthesia, specifically those involving continuous spinal anesthesia or the use of 5% lidocaine. The U.S. Food and Drug Administration (FDA) withdrew some spinal catheters in 1992 because of concerns about a perceived association between the small-bore catheters and development of cauda equina syndrome. ^[7] This decision appears to have been made with as many political implications as scientific ones. Since that time, attention turned to the questions about the appropriate uses of intrathecal 5% lidocaine^[8] and how to minimize risks of neuraxial anesthesia with concomitant use of low-molecular-weight heparin (LMWH).^[9]

Other impediments to the effective use of neuraxial blocks are the predictable decreases in arterial blood pressure and heart rate through the accompanying sympathectomy with its attendant vasodilation and blockade of cardioaccelerator fibers. Maintaining arterial blood pressure and heart rate at normal values during these blocks often requires administration of vasoactive drugs and intravenous fluids. The extent to which these steps are necessary is discussed later.

Another clinically important impediment to successful use of these blocks is the idea that the "blocks should do it all." It seems unreasonable to expect a single injection of local anesthetic into the subarachnoid or epidural space to provide ideal conditions for all patients undergoing various surgical procedures, even in the face of an adequate block. It seems likely that far more spinal and epidural anesthetics have failed because of inadequate intravenous sedation and anxiolysis than technically flawed blocks.

Evidence is accumulating that the use of neuraxial blocks, principally continuous epidural techniques to provide postoperative analgesia, may be able to decrease perioperative morbidity. These techniques may also decrease length of hospital stay and allow more efficient use of our increasingly stretched health care monies. ^{[10] [11]} To gain maximum benefit and minimize complications from these blocks, attention to technique and anatomy is essential, and the blocks should be used when the risk-benefit equation for the block is favorable.^{[12] [13]}