The desired action of all local anesthetics is the reversible blockade of nerve conduction and, therefore, the cascade of events producing perception of pain. These drugs prevent the development of an action potential in a nerve by blocking sodium channels responsible for propagating a response in the nerve fiber (Fig. 20-3). Local anesthetics exist in both charged and uncharged form. The uncharged state of the drug crosses the lipid nerve membrane and enters the cell. Once in the cell, it reequilibrates into the charged form that is readily dissolved in water. This charged form now reaches the sodium channels and blocks them from inside (see Table 20-3).
Uncharged (1) local anesthetic passes through the nerve membrane (2) into the cell (3) where the local anesthetic gains a H+ (hydrogen ion) to become charged. (4) The Na+ channel is blocked in the nerve cell by the charged local anesthetic and does not allow the nerve to propagate a nerve impulse.
The capacity for an uncharged species to assume a charged form is the essential property of all local anesthetics. They are a combination of a weak base and a strong acid.
As a general principle, lowering the pH will increase the ionized percentage of the drug, and raising the pH will increase the uncharged form of the drug. Because the local anesthetics are usually supplied in an acidic medium, the addition of NaHCO3 will increase the relative uncharged portion, allowing the drug to cross the nerve membrane more readily resulting in a quicker onset of block.
0.1 cc NaHCO3/10 cc bupivicaine
1.0 cc NaHCO3/10 cc lidocaine
Precipitation of the local anesthetic will occur if too much NaHCO3 is added. Comparative properties of lidocaine, ropivacaine, and bupivacaine are outlined in Table 20-4.
Protein binding is another property important to understand. All local anesthetics bind to albumin and μ-1-acid glycoprotein (AAG). It is the free portion of the drug that is responsible for toxicity. In pregnancy, albumin levels are depressed, so AAG binding becomes most important. AAG is released in response to surgery, trauma, infection, and inflammation. Once AAG sites are saturated with local anesthetics, the free drug levels progressively increase. Protein binding also decreases with decreasing pH. Therefore, in an acidotic environment, a high proportion of free drug with the potential for cardiac or neurotoxicity should be anticipated.
Absorption of local anesthetics refers to the movement of the drug from the site of injection to the bloodstream. Therefore, the more vascular the area and the larger the total dose of anesthetic used, the higher the resulting serum level of the drug. The addition of a vasoconstrictor (epinephrine) to the local anesthetic can decrease the absorption and, therefore, toxicity of the drug used (see Table 20-4).
Local anesthetic toxicity may manifest with CNS or cardiac effects. As the doses increase, disinhibition and CNS excitation occurs producing seizures. Local anesthetic bind and inhibit cardiac Na+, Ca2+, and K+ channels as concentrations increase causing cardiac arrest. Treatment of adverse reactions depends on the severity of their effects from spontaneous recovery, to supportive care with oxygen and maintaining the airway, to advanced cardiac life support (ACLS).
Ropivacaine is a local anesthetic with similar characteristics to bupivicaine. This is produced solely as the S-enantiomer, whereas bupivicaine is a mixture of the S and R forms. This S-form has less ability to bind Na-channels in the myocardial conduction system. Therefore, there is less risk of cardiotoxicity with ropivacaine. As seen in Table 20-4, ropivacaine and bupivicaine have very similar physical properties except for the margin of safety, in ropivacaine, which produces less toxic side effects. There also appears to be less of a motor block compared to bupivicaine, which theorhetically should improve patient satisfaction during the laboring process. Caution has been used in administering this agent as it has several side effects that occur in a significantly high occurrence (>10% of patients). These include cardiovascular: hypotension (dose-related and age-related: 32%-69%), maternal bradycardia (6%-20%), gastrointestinal: nausea (11%-29%), vomiting (7%-14%), and neuromuscular and skeletal: back pain (7%-10%) of patients.
The pharmacologic treatment of local anesthetic systemic toxicity (LAST) is different from other cardiac arrest scenarios.
Airway management—ventilate with 100% oxygen
Seizure suppression with benzodiazepines avoiding propofol
Use ACLS avoiding vasopressin, calcium channel blockers, β-blockers, or local anesthetics reducing epinephrine dose to less than 1 μg/kg
20% Intralipid 1.5 cc/kg bolus over 1 minute; start continuous infusion 0.25 cc/kg/min
Bolus may be repeated for persistent cardiac arrest and infusion rate may be doubled to 0.5 cc/kg/min; approximate upper limit is 10 cc/kg of the lipid emulsion.
Local anesthetic concentrations and maximum doses (approximate for 70-kg patient).
Lidocaine → 5 mg/kg
Lidocaine with epinephrine → 7 mg/kg
Marcaine with or without epinephrine → 2.5mg/kg
Lumbar epidural block is the most common form of analgesia used to provide relief from the nociceptive pathways during the stages of labor. The epidural space is the interval superiorly bounded by the foramen magnum, inferiorly by the lower end of the dural sac, anteriorly by the posterior longitudinal ligament and posteriorly by the ligamentum flavum. The approach to the epidural space is posteriorly through the skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum, and into the epidural space (Fig. 20-4).
Lumbosacral anatomy showing needle depth for epidural and subarachnoid injections.
The size of the epidural space varies along its course with the largest diameter existing at the L2 interspace with a range of 4 to 9 mm. A simple maneuver that helps open up the bony entrance to the epidural space is flexion of the lumbar spine (Fig. 20-5).
Lumbar vertebrae. When patient is fixed, the interlaminar space enlarges, increasing the ability to enter the epidural/subarachnoid space.
The contents of the epidural space include fat, vertebral venous plexus, lymphatics, arteries, and dural spinal nerve projections. In pregnancy, with the increase in intra-abdominal pressure, the venous plexus becomes distended. This phenomenon, and the accompaning increase in epidural fat that occurs during pregnancy, functions to reduce epidural volume substantially. Therefore, pregnant patients usually require less volume of local anesthetic, as compared to nonpregnant controls, to produce a similar level of blockade.
Once the epidural catheter is in place, local anesthetic is administered according to the appropriate pain pathway and corresponding stage of labor. In the first stage of labor, T10 block is sufficient. In the late first stage and second stage of labor, the nerves to be blocked include the sacral area so the parturient should be dosed in the semi-Fowler position to allow downward spread of the local anesthetic. Finally, for predelivery and the third stage of labor, the parturient may be seated upright (with a vena cava tilt) to secure sacral root spread of the drug (Fig. 20-6). This blockade may be achieved by intermittent bolus injections or by continuous infusion of the drug with changes in patient positioning altering the level of blockade.
Lumbar epidural analgesia. A-C. Epidural catheter may be placed early in the first stage of labor. D. When the patient experiences labor pain, local anesthetic may be injected to achieve a T10-L1 neuroblockade. E-F. In late first stage and mid-second stage of labor, the patient should be elevated 15 to 20 degrees to allow caudad spread of local anesthetic to achieve a T10-S5 block. G-I. To ensure sacral root dispersion of local anesthetic, once flexion and internal rotation of baby’s head occurs, more local anesthetic can be injected with the patient in the seated upright position with a left tilt to the pelvis.
With the uppermost level of analgesia at T10, the 5 lowermost vasomotor segments supplying the pelvis, lower trunk, and limbs are interrupted causing a decrease in total peripheral resistance, venous return, and CO. In normal parturients, this insult induces a reflex cardiovascular response directed toward maintaining systemic blood pressure. Coloading of an adequate intravenous crystalloid infusion, keeping the parturient on her side, and minimizing the dose of the local anesthetic all minimize the adverse decrease in blood flow to the pelvis and its structures.
High epidural anesthesia that extends to T4-S5 is associated with a significant interruption of vasomotor segments, resulting in significant hypotension. Again, fluid coload and lateral tilt of the parturient can augment the reflex corrective responses of the cardiovascular system in this situation. Extending the epidural blockade above spinal level T10 is unnecessary and counterproductive for the normal laboring patient. If epidural analgesia needs to be changed to anesthesia for a cesarian section, these risks are necessary and measures to prevent them should be instituted. In addition, Neo-Synephrine is the best vasopressor to augment blood pressure without reducing blood supply to the uterus. Studies suggest there is improved fetal acid-base status and Apgar scores with prophylactic Neosynephrine boluses and infusion as compared to ephedrine as was previously used.
Contraindications to lumbar epidural analgesia/anesthesia are reviewed in Table 20-5. The advantages and disadvantages of regional analgesia/anesthesia are outlined in Table 20-6.
TABLE 20-5.Contraindications to Lumbar Epidural Analgesia/Anesthesia ||Download (.pdf) TABLE 20-5. Contraindications to Lumbar Epidural Analgesia/Anesthesia
Parturients who refuse the block or have great fear of puncture of the spine. In our experience, many patients who are concerned initially about epidural block will consent to be managed with this technique provided they are properly informed. However, if they still refuse, it is an absolute contraindication to the technique.
Lack of skill by the administrator, not only in carrying out the procedure, but in the management of the parturient and in the prompt treatment of complications.
Infection at the puncture site or in the epidural space.
Severe hypovolemia from hemorrhage, dehydration, or malnutrition.
Lack of resuscitation equipment in the immediate area ready for prompt use.
In addition to the above, absolute contraindication to continuous caudal epidural anesthesia are infection or cyst in the area of the sacrococcygeal region and having the presenting part close to the perineum.
|Relative Contraindications Include: |
Lack of appreciation by the obstetrician as to how the procedure influences the management of labor.
A very rapid or precipitate labor, or in any case which requires immediate anesthesia. On the other hand, for the anesthesiologist who is very skilled and has had extensive experience, extension of the epidural block in patients who have had the catheter in place during labor can be done as rapidly as getting things ready for anesthesia.
Cephalopelvic disproportion unless the block is used for a trial of labor prior to cesarean section.
TABLE 20-6.Advantages and Disadvantages of Regional Analgesia/Anesthesia ||Download (.pdf) TABLE 20-6. Advantages and Disadvantages of Regional Analgesia/Anesthesia
In contrast to opoids, regional analgesia produces complete relief from pain in most parturients.
The hazards of pulmonary aspiration of gastric contents that is inherent in general anesthesia is diminished and can be even eliminated.
Provided it is properly administered and no complications occur, regional analgesia/anesthesia causes no serious maternal or neonatal complications.
Administered at the proper time, it does not impede the progress of labor at the first stage.
Continuous techniques can be extended for delivery and may even be modified for cesarean section if this becomes necessary.
Regional analgesia permits the mother to remain awake during labor and delivery so that she can experience the pleasure of actively participating in the birth of her child.
Regional anesthesia for cesarean section also permits the mother to be awake and immediately develop bonding with the newborn.
Provided the mother is doing well, the anesthesiologist can leave her and resuscitate the newborn if this is necessary.
Regional techniques require greater skill to administer than do administration of systemic drugs or inhalation agents.
Technical failures occur even in experienced hands.
Certain techniques produce side effects (eg, maternal hypotension) that, if not promptly and properly treated, can progress to complications in the mother and fetus.
Techniques that produce perineal muscle paralysis interfere with the mechanism of internal rotation and increase the incidence of posterior positions and, thus, require instrumental deliveries.
These procedures can only be carried out in the hospital.
A combined spinal/epidural analgesia technique provides rapid onset of spinal opioid analgesia, plus the flexibility of the epidural blockade. Sufentanil 10 μg or fentanyl 25 μg injected spinally, when the epidural catheter is inserted, can reliably give several hours of analgesia to patients in the early first stage of labor (<5 cm dilation). The continuous infusion of a weak local anesthetic (0.125%/0.0625% bupivicaine or 0.2%/0.1% ropivacaine) with a low-dose narcotic (sufentanil 1-2 μg/cc or fentanyl 5-10 μg/cc) can provide good perineal analgesia for later stages of labor. If needed, higher concentrations of bupivacaine or lidocaine can be bolused for more complete nerve blockade. Less motor blockade, less hypotension, less local anesthetic administered with inherent toxicity risk, and faster onset of analgesia are all benefits of this combined technique.
The side effects of intrathecal opioids and corresponding treatment are listed in Table 20-7.
TABLE 20-7.Intrathecal Opioids Side Effects and Recommended Treatment ||Download (.pdf) TABLE 20-7. Intrathecal Opioids Side Effects and Recommended Treatment
|Side effect ||Treatment |
|Itching ||Benadryl, 25 mg IV |
| ||Propofol, 10 mg IV |
| ||Naloxone, 40 μg IV |
|Nausea and vomiting ||Reglan, 10 mg IV |
| ||Propofol, 10 mg IV |
| ||Naloxone, 40 μg IV |
| ||Zofran, 4 mg IV |
|Hypotension ||IV fluids |
| ||Ephedrine |
|Urinary retention ||Catheterization |
| ||Naloxone, 400 μg IV |
Fetal Bradycardia in Epidural Analgesia and Combined Spinal/Epidural Techniques
Fetal bradycardia is a nonreassuring fetal heart rate after induction of neuraxial anesthesia that may be due to maternal hypotension or uterine hyperactivity. It is mostly associated with the combined spinal/epidural technique but can be seen with any technique that produces profound analgesia.
The placental circulation is dependent on the maternal SBP, and with a sudden onset sympathetic block from the local anesthetic, this can decrease placental perfusion and therefore cause fetal bradycardia. Local decreases in perfusion can occur without ever ascertaining a drop in the maternal SBP.
Another proposed explanation is that the fetal bradycardia is due to intrathecal opioid-induced uterine hypertonus. The uterine tetany is thought to be due to rapid onset of analgesia, which causes a sudden decrease in maternal plasma epinephrine and subsequent withdrawal of epinephrine’s β-sympathomimetic relaxant effects on the myometrium. This is followed with decreased placental blood flow, fetal asphyxia, and fetal bradycardia.
Preanalgesic adequate hydration of the patient must be achieved with coloading using crystalloids, as well as, the prevention of overdosing with high blocks beyond that necessary to achieve analgesia for the nerve roots involved with the labor pains. With this physiological understanding of the dynamics occurring, treatment is based on relaxing the uterus. Uterine hypertonus may be reversed with 1 or 2 doses of intravenous nitroglycerin (60-90 μg). The hypotension that results is treated with phenylephrine (40-80 μg). Persistent hypertonus can be treated with another dose of nitroglycerin or a β-agonist, such as terbutaline 0.25 mg intravenously; however, terbutaline results in an extended period of uterine relaxation and maternal tachycardia.