Neuraxial anesthesia involves the placement of local anesthetics and/or opioids into the intrathecal (subarachnoid) or epidural space (Fig. 4.2), either by a single injection or by a continuous infusion catheter technique. The medications act directly on the spinal cord and, for epidurals, also on the spinal roots. This results in decreased transmission of impulses through the various nerves (Table 4.1).
Some local anesthetics have differential effects on various nerve types. For most applications, we would prefer to block only the pain impulses, but no agent is quite that specific. Bupivacaine blocks sensory more than motor fibers and is the agent of choice for labor analgesia where we desire maintenance of maternal mobility (“Push! Push!”).
The dermatomal level (Fig. 4.3) achieved depends on several factors (Table4.2). Consider a Cesarean delivery, for which we require a T4 sensory level tominimize discomfort with uterine manipulation.
For an epidural, we select a local anesthetic and concentration (e.g., 2% lidocaine with epinephrine), then administer ∼5 mL boluses until we achieve the desired level (or we reach the maximum dose allowed). For a spinal, we administer a calculated dose and then use gravity to influence the level of the block.
Normal cerebrospinal fluid (CSF) has a specific gravity (density relative to water) of 1.0006 ± 0.0003. Any agent of a different density, injected into the CSF, will dis-tribute according to gravity. That is, a hyperbaric agent will “sink,” and hypobaric will “float.”
We can affect the resulting anesthetic level by tilting the patient. To achieve a T4 level for our Cesarean delivery, we inject hyperbaric local anesthetic (e.g., 12 mg of 0.75% bupivacaine with dextrose) intrathecally. When the patient assumes a supine position, the local anesthetic “sinks” to the thoracic kyphosis (Fig. 4.4). If, after a few minutes, the level of the block remains too low, we can carefully lower the patient’s head; as the drug follows gravity, the level will rise.
After several minutes (the actual time depending on the agent selected), the drug will be “fixed” and no further manipulation of its level can be achieved by altering the patient’s position.
Unfortunately, autonomic nerves (sympathetic here) are the easiest to block and cannot be independently spared. The sympathetic block extends usually at least two dermatome levels higher than the somatic sensory block. Basal sympathetic tone causes vasoconstriction peripherally, thus its elimination results in vaso-dilation (venous and arterial). Up to about a T4 level (nipple line), hypotension results primarily from decreased preload secondary to vasodilation proportionate to the sympathetic level (the higher the block, the more of the peripheral vascula-ture escapes from nervous control and is “opened”). The baroreflex response will attempt to maintain cardiac output. While its efforts to vasoconstrict the blocked area are thwarted, vasoconstriction in the unblocked area works overtime. Sym-pathetic stimulation reaches the heart via the “cardiac accelerators,” which travel in T1–4 nerves; thus a higher block may inhibit sympathetic stimulation of the heart, resulting in bradycardia and a greater decrease of cardiac output and blood pressure.
If the neuraxial anesthesia level covers the thorax, intercostal muscle function will be impaired. While not a problem for most patients, those who recruit acces-sory muscles for normal breathing may have difficulty. Fortunately, the diaphragm receives its innervation from C2–4, and therefore the neck should never be affected by neuraxial anesthesia. If it is, the block is much too high and the patient will complain (if he still can) of dyspnea. Manual ventilation with bag and mask will be required. Often, even tracheal intubation for maintenance of the airway will become necessary. Yet, many patients become dyspneic at even a mid-thoracic level of anesthesia, and usually without any decrease in their oxyhemoglobin sat-uration. We attribute this to loss of chest wall proprioception, which removes a feedback loop that reassures the patient’s brain that ventilation is maintained. If the patient complains of shortness of breath, first confirm that the level of anes-thesia is not too high. If reassured on that point, let the patient put a hand in front of his mouth so that he can feel his exhaled breath. This may restore the feed-back loop and the patient’s sense of well being. If necessary, apply supplemental oxygen.
Of the potential complications to neuraxial blockade (Table 4.3), we fear forma-tion of an epidural hematoma most. Because the spinal cord runs in the spinal canal, a closed space, anything that abnormally takes up room causes compres-sion of other structures. Should an epidural blood vessel get nicked on insertion of a needle (common), and that vessel fail to clot normally, the resulting hematoma can cause increased pressure and ischemic damage to the spinal cord.
For this reason, patients who are anticoagulated or thrombocytopenic are rarely consid-ered candidates for neuraxial blocks. This risk of epidural hematoma is present both at insertion and removal of the catheter.
Post-dural puncture headache, another complication, deserves special men-tion: the patient develops pounding headaches when sitting up and finds great relief by lying down. A hole in the dura mater does not seal immediately. The size and shape of that hole has implications for the future development of a post-dural puncture (spinal) headache. We can minimize the risk of this headache by using “pencil point” needles (Fig. 4.5) in the smallest diameter practical, e.g., 25–27 g. We do not use such small diameter needles when performing a diagnostic lum-bar puncture, as it would take too long to acquire fluid for laboratory studies. As you might imagine, post-dural puncture headaches are particularly bad when we inadvertently nick the dura with the large epidural needle1 during an attempt to place an epidural catheter. This so-called “wet tap” has a high incidence of headache, particularly in the pregnant patient. Treatment includes bedrest, anal-gesics, intravenous caffeine, and an epidural blood patch in which the patient’s own blood is sterilely injected into the epidural space, causing usually immediate relief.
Neuraxial block placement requires both skill and the patient’s cooperation. Table 4.4lists the steps for placing either a spinal or epidural anesthetic. A com-bined spinal–epidural (CSE) begins as an epidural, but after identification of the epidural space with the epidural needle (Fig. 4.6), a spinal needle is passed through that needle and into the intrathecal space for injection of drug. The spinal needle is withdrawn, and the epidural catheter threaded as above.
Many factors must be considered including location of operation and, therefore, anesthetic level required, duration of surgery, and implications for cardiovascular and respiratory function. For example, we would not use spinal anesthesia in a patient in hemorrhagic shock or with significant aortic stenosis who would not tolerate a drop in preload and afterload (Table 4.5).
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