Although the authors cautioned against subgroup analysis, the obstetric setting was found to have a low incidence of complications, while the adult perioperative setting had the highest complications. Importantly, NAP3 did not examine minor complications or major complications without permanent harm. For example, patients may have had cardiovascular collapse requiring intensive care or have had meningitis, but as they made a full recovery were excluded from even the pessimistic calculation.
These are complications a patient would consider severe. The authors did acknowledge their figures represent a minimum possible incidence of complications; however, others have speculated that they may have overestimated risk. The NAP3 study reassured us that permanent harm as a result of spinal anesthesia is rare.
The large scope and excellent methodology of NAP3 mean a similar audit is unlikely to be repeated soon. In particular, PDPH deserves special attention. Major complications, nonetheless, do happen, and every effort must be made to prevent them. Awareness of the low risk of serious complications should not give rise to complacency. Indeed, a given complication may become so rare that a single anesthesiologist is unlikely to encounter it in a lifetime of practice. However, given the catastrophic nature of such complications, ongoing vigilance is of paramount importance.
Spinal anesthesia provides excellent operating conditions for surgery below the umbilicus. Thus, it has been used in the fields of urological, gynecological, obstetric, and lower abdominal and perineal general surgery. Likewise, it has been used in lower limb vascular and orthopedic surgery. More recently, spinal anesthesia has been used in surgery above the umbilicus see section on laparoscopic surgery. Although spinal anesthesia is a commonly used technique, with an estimated , spinal anesthetics each year in the United Kingdom alone, mortality and morbidity benefits are difficult to prove or disprove.
It was hypothesized that due to beneficial modulation of the stress response, regional anesthesia would be safer than general anesthesia. However, clinical trials have been contradictory, and debates continue over the superiority of one technique over the other.
Evaluations of the benefits of spinal blockade are troubled by the heterogeneity of studies and arguments about whether analysis should include intention to treat. In addition, much of the evidence for the benefits of neuraxial blockade pertains to epidurals, and some reviews do not differentiate between spinal and epidural anesthesia.
For example, CNB has been shown to reduce blood loss and thromboembolic events. However, the authors of these studies were wise not to analyze spinal and epidural anesthesia individually, as the subgroup sample size would have been inadequate. Further studies are required to elucidate the relative benefits of each technique. An obvious benefit of spinal anesthesia is the avoidance of the many risks of general anesthesia. However, it must be remembered that there is always the possibility of conversion to general anesthesia, and an emergent general anesthesia may be riskier than a planned general anesthesia.
Spinal anesthesia is advantageous in certain clinical settings. It is now commonplace for women having cesarean delivery to have a neuraxial nerve block. Spinal anesthesia avoids the problems associated with general anesthesia in the pregnant patient, notably risks of difficult airway, awareness, and aspiration.
Maternal blood loss has been found to be lower with spinal compared with general anesthesia. Falling maternal mortality rates have been attributed to the increase in the practice of regional anesthesia. Moreover, regional anesthesia allows a mother to be awake for childbirth and a partner to be present if desired.
However, a Cochrane review found no evidence of the superiority of regional anesthesia over general anesthesia with regard to major maternal or neonatal outcomes Likewise, a meta-analysis showed cord pH, an indicator of fetal well-being, to be lower with spinal compared with epidural and general anesthesia, although this may have been due to the use of ephedrine in the studies analyzed.
Nonetheless, spinal anesthesia remains the technique of choice for many obstetric anesthesiologists because of safety, reliability, and patient expectation. However, these recommendations, based on two reviews, illustrate the shortcomings of the available evidence. The first review had a heterogeneous population and limited power for subgroup analysis; extrapolating the findings to spinal anesthesia for hip fracture surgery is therefore questionable.
The second review found only a borderline difference in mortality at 1 month and no difference at 3 months. Moreover, all included studies had methodological flaws. The stress response to cardiac surgery is reduced by intrathecal bupivacaine in combination with general anesthesia and partially attenuated by intrathecal morphine. As modern anesthesia and perioperative care become safer, it will become increasingly more difficult to prove an advantage of one technique over another.
The ideal technique may in fact be a permutation of general anesthesia, neuraxial nerve block, peripheral nerve blockade, or local infiltration analgesia. Once armed with the evidence regarding the risks and benefits of spinal anesthesia, the anesthesiologist must decide whether the evidence applies to the individual patient and clinical situation.
Although complications can be devastating, NAP3 reassured us that major complications from spinal anesthesia are rare. Compelling benefits are harder to prove, yet there are advantages in certain clinical situations. Furthermore, the risk-benefit ratio must be compared with the risk-benefit ratio of available alternatives.
The historical rise in safety of spinal anesthesia has been paralleled by a rise in safety of alternative techniques, including epidural anesthesia, peripheral nerve blockade, local infiltration analgesia, and of course general anesthesia. This competition between alternate techniques is likely to continue.
Moreover, different modalities can be used in conjunction, complicating the final decision. The modern anesthesiologist must consider this matrix of risk-benefit ratios, which is beyond the scope of this chapter. In reviewing the functional anatomy of spinal blockade, an intimate knowledge of the spinal column, spinal cord, and spinal nerves must be present.
This chapter briefly reviews the anatomy, surface anatomy, and sonoanatomy of the spinal cord. The vertebral column consists of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal segments.
The vertebral column usually contains three curves. The cervical and lumbar curves are convex anteriorly, and the thoracic curve is convex posteriorly. The vertebral column curves, along with gravity, baricity of local anesthetic, and patient position, influence the spread of local anesthetics in the subarachnoid space. Figure 1 depicts the spinal column, vertebrae, and intervertebral disks and foramina. Five ligaments hold the spinal column together Figure 2.
The supraspinous ligaments connect the apices of the spinous processes from the seventh cervical vertebra C7 to the sacrum. The supraspinous ligament is known as the ligamentum nuchae in the area above C7. The interspinous ligaments connect the spinous processes together. The ligamentum flavum, or yellow ligament, connects the laminae above and below together. Finally, the posterior and anterior longitudinal ligaments bind the vertebral bodies together.
The three membranes that protect the spinal cord are the dura mater, arachnoid mater, and pia mater. The dura mater, or tough mother, is the outermost layer. The dural sac extends to the second sacral vertebra S2. The arachnoid mater is the middle layer, and the subdural space lies between the dural mater and arachnoid mater.
The arachnoid mater, or cobweb mother, also ends at S2, like the dural sac. The pia mater, or soft mother, clings to the surface of the spinal cord and ends in the filum terminale, which helps to hold the spinal cord to the sacrum. The space between the arachnoid and pia mater is known as the subarachnoid space, and spinal nerves run in this space, as does CSF. Figure 3 depicts the spinal cord, dorsal root ganglia and ventral rootlets, spinal nerves, sympathetic trunk, rami communicantes, and pia, arachnoid, and dura maters.
When performing a spinal anesthetic using the midline approach, the layers of anatomy that are traversed from posterior to anterior are skin, subcutaneous fat, supraspinous ligament, interspinous ligament, ligamentum flavum, dura mater, subdural space, arachnoid mater, and finally the subarachnoid space. When the paramedian technique is applied, the spinal needle should traverse the skin, subcutaneous fat, paraspinous muscle, ligamentum flavum, dura mater, subdural space, and arachnoid mater and then pass into the subarachnoid space.
When performing a spinal anesthetic using the paramedian approach, the spinal needle should traverse. The anatomy of the subdural space requires special attention. The subdural space is a meningeal plane that lies between the dura and the arachnoid mater, extending from the cranial cavity to the second sacral vertebrae.
Ultrastructural examination has shown this is an acquired space that only becomes real after tearing of neurothelial cells within the space. The subdural space extends laterally around the dorsal nerve root and ganglion. There is less potential capacity of the subdural space adjacent to the ventral nerve roots. This may explain the sparing of anterior motor and sympathetic fibers during subdural nerve block SDB Figure 4.
The length of the spinal cord varies according to age. In the first trimester, the spinal cord extends to the end of the spinal column, but as the fetus ages, the vertebral column lengthens more than the spinal cord. At birth, the spinal cord ends at approximately L3. In the adult, the terminal end of the cord, known as the conus edullaris, lies at approximately L1.
The conus medullaris may lie anywhere between T12 and L3. Figure 5 Shows a cross section of the lumbar vertebrae and spinal cord. The typical position of the conus medullaris, cauda equina, termination of the dural sac, and filum terminale are shown. A sacral spinal cord in an adult has been reported, although this is extremely rare. The length of the spinal cord must always be kept in mind when a neuraxial anesthetic is performed, as injection into the cord can cause great damage and result in paralysis.
There are eight cervical spinal nerves and seven cervical vertebrae. Cervical spinal nerves 1 to 7 are numbered according to the vertebral body below.
The eighth cervical nerve exits from below the seventh cervical vertebral body. Below this, spinal nerves are numbered according to the vertebral body above. The spinal nerve roots and spinal cord serve as the target sites for spinal anesthesia. When preparing for spinal anesthetic blockade, it is important to accurately identify landmarks on the patient. The midline is identified by palpating the spinous processes.
The iliac crests usually are at the same vertical height as the fourth lumbar spinous process or the interspace between the fourth and fifth lumbar vertebrae.
An intercristal line can be drawn between the iliac crests to help locate this interspace. Care must be taken to feel for the soft area between the spinous processes to locate the interspace. Depending on the level of anesthesia necessary for the surgery and the ability to feel for the interspace, the L3—L4 interspace or the L4—L5 interspace can be used to introduce the spinal needle.
Because the spinal cord commonly ends at the L1-to-L2 level, it is conventional not to attempt spinal anesthesia at or above this level. More recently, segmental thoracic spinal anesthesia has been described. It would be incomplete to discuss surface anatomy without mentioning the dermatomes that are important for spinal anesthesia. A dermatome is an area of skin innervated by sensory fibers from a single spinal nerve. The tenth thoracic T10 dermatome corresponds to the umbilicus, the sixth thoracic T6 dermatome the xiphoid, and the fourth thoracic T4 dermatome the nipples.
Figure 6 illustrates the dermatomes of the human body. To achieve surgical anesthesia for a given procedure, the extent of spinal anesthesia must reach a certain dermatomal level. Dermatomal levels of spinal anesthesia for common surgical procedures are listed in Table 5. However, due to body habitus, this may not be possible. Neuraxial ultrasound allows sonoanatomical visualization of these structures and deeper structures. However, as the ultrasound beam cannot penetrate the bony vertebrae, specialized ultrasonic windows are required to visualize the neuraxis.
The technique of neuraxial ultrasound is discussed elsewhere see section on recent developments in spinal anesthesia. The choice of local anesthetic is based on potency of the agent, onset and duration of anesthesia, and side effects of the drug. Two distinct groups of local anesthetics are used in spinal anesthesia, esters and amides, which are characterized by the bond that connects the aromatic portion and the intermediate chain. Esters contain an ester link between the aromatic portion and the intermediate chain, and examples include procaine, chloroprocaine, and tetracaine.
Amides contain an amide link between the aromatic portion and the intermediate chain, and examples include bupivacaine, ropivacaine, etidocaine, lidocaine, mepivacaine, and prilocaine. Although metabolism is important for determining activity of local anesthetics, lipid solubility, protein binding, and pKa also influence activity.
Lipid solubility relates to the potency of local anesthetics. Low lipid solubility indicates that higher concentrations of local anesthesia must be given to obtain nerve blockade. Conversely, high lipid solubility produces anesthesia at low concentrations. Protein binding affects the duration of action of a local anesthetic. Higher protein binding results in longer duration of action. The pKa of a local anesthetic is the pH at which ionized and nonionized forms are present equally in solution, which is important because the nonionized form allows the local anesthetic to diffuse across the lipophilic nerve sheath and reach the sodium channels in the nerve membrane.
The onset of action relates to the amount of local anesthetic available in the base form. Most local anesthetics follow the rule that the lower the pKa, the faster the onset of action and vice versa. Please refer to Clinical Pharmacology of Local Anesthetics. Pharmacokinetics of local anesthetics includes uptake and elimination of the drug. Four factors play a role in the uptake of local anesthetics from the subarachnoid space into neuronal tissue: 1 concentration of local anesthetic in CSF, 2 surface area of nerve tissue exposed to CSF, 3 lipid content of nerve tissue, and 4 blood flow to nerve tissue.
The uptake of local anesthetic is greatest at the site of highest concentration in the CSF and is decreased above and below this site. As discussed previously, uptake and spread of local anesthetics after spinal injection are determined by multiple factors, including dose, volume, and baricity of local anesthetic and patient positioning. Both the nerve roots and the spinal cord take up local anesthetics after injection into the subarachnoid space. The more surface area of the nerve root exposed, the greater the uptake of local anesthetic.
The spinal cord has two mechanisms for uptake of local anesthetics. The first mechanism is by diffusion from the CSF to the pia mater and into the spinal cord, which is a slow process. Only the most superficial portion of the spinal cord is affected by diffusion of local anesthetics. The second method of local anesthetic uptake is by extension into the spaces of Virchow-Robin, which are the areas of pia mater that surround the blood vessels that penetrate the central nervous system.
The spaces of Virchow-Robin connect with the perineuronal clefts that surround nerve cell bodies in the spinal cord and penetrate through to the deeper areas of the spinal cord. Figure 7 is a representation of the periarterial Virchow-Robin spaces around the spinal cord. Lipid content determines uptake of local anesthetics. Heavily myelinated tissues in the subarachnoid space contain higher concentrations of local anesthetics after injection.
The higher the degree of myelination, the higher the concentration of local anesthetic, as there is a high lipid content in myelin. If an area of nerve root does not contain myelin, an increased risk of nerve damage occurs in that area. Blood flow determines the rate of removal of local anesthetics from spinal cord tissue.
The faster the blood flows in the spinal cord, the more rapid the anesthetic is washed away. This may partly explain why the concentration of local anesthetics is greater in the posterior spinal cord than in the anterior spinal cord, even though the anterior cord is more readily accessed by the Virchow-Robin spaces. After a spinal anesthetic is administered, blood flow may be increased or decreased to the spinal cord, depending on the particular local anesthetic administered; for example, tetracaine increases cord flow, but lidocaine and bupivacaine decrease it, which affects elimination of the local anesthetic.
Elimination of local anesthetic from the subarachnoid space is by vascular absorption in the epidural space and the subarachnoid space. Local anesthetics travel across the dura in both directions. In the epidural space, vascular absorption can occur, just as in the subarachnoid space. Vascular supply to the spinal cord consists of vessels located on the spinal cord and in the pia mater. Because vascular perfusion to the spinal cord varies, the rate of elimination of local anesthetics varies.
The distribution and decrease in concentration of local anesthetics is based on the area of highest concentration, which can be independent of the injection site. Many factors affect the distribution of local anesthetics in the subarachnoid space. Table 6 lists some of these factors. Local anesthetics can be hyperbaric, hypobaric, or isobaric when compared to CSF, and baricity is the main determinant of how the local anesthetic is distributed when injected into the CSF.
Table 7 compares the density, specific gravity, and baricity of different substances and local anesthetics. Hypobaric solutions are less dense than CSF and tend to rise against gravity. Isobaric solutions are as dense as CSF and tend to remain at the level at which they are injected. Hyperbaric solutions are more dense than CSF and tend to follow gravity after injection.
Hypobaric solutions have a baricity of less than 1. Tetracaine, dibucaine, and bupivacaine have all been used as hypobaric solutions in spinal anesthesia. Patient positioning is important after injection of a hypobaric spinal anesthetic because it is the first few minutes that determine the spread of anesthesia. If the patient is in Trendelenburg position after injection, the anesthetic will spread in the caudal direction and if the patient is in reverse Trendelenburg position, the anesthetic will spread cephalad after injection.
The baricity of isobaric solutions is equal to 1. Tetracaine and bupivacaine have both been used with success for isobaric spinal anesthesia. Gravity does not play a role in the spread of isobaric solutions, unlike with hypo- or hyperbaric local anesthetics.
Therefore, patient positioning does not affect spread of isobaric solutions. Injection can be made in any position, and then the patient can be placed into the position necessary for surgery. Hyperbaric solutions have baricity greater than 1.
A local anesthetic solution can be made hyperbaric by adding dextrose or glucose. Bupivacaine, lidocaine, and tetracaine have all been used as hyperbaric solutions in spinal anesthesia. Patient positioning affects the spread of the anesthetic. A patient in Trendelenburg position would have the anesthetic travel in a cephalad direction and vice versa. Dose and volume both play a role in the distribution of local anesthetics after spinal injection. For further information, please refer to the section Volume, Concentration, and Dose of Local Anesthetic.
Cerebrospinal fluid is produced in the brain at 0. This clear, colorless fluid has an approximate adult volume of mL, half of which is in the cranium and half in the spinal canal.
However, CSF volume varies considerably, and decreased CSF volume can result from obesity, pregnancy, or any other cause of increased abdominal pressure. This is partly due to compression of the intervertebral foramen, which displaces the CSF. Due to the wide variability in CSF volume, the ability to predict the level of the spinal blockade after local anesthetic injection is very poor, even if BMI is calculated and used.
Multiple factors affect the distribution of local anesthesia after spinal blockade, one being CSF volume. Carpenter showed that lumbosacral CSF volume correlated with peak sensory nerve block height and duration of surgical anesthesia. The density of CSF is related to peak sensory nerve block level, and lumbosacral CSF volume correlates to peak sensory nerve block level and onset and duration of motor nerve block. However, due to the wide variability in CSF volume, the ability to predict the level of the spinal blockade after local anesthetic injection is poor, even if BMI is calculated and used.
Cocaine was the first spinal anesthetic used, and procaine and tetracaine soon followed. Lidocaine, 2-chloroprocaine, bupivacaine, mepivacaine, and ropivacaine have also been used intrathecally. In addition, there is a growing interest in medications that produce anesthesia and analgesia while limiting side effects. Lidocaine was first used as a spinal anesthetic in , and it has been one of the most widely used spinal anesthetics since. Onset of anesthesia occurs in 3 to 5 minutes with a duration of anesthesia that lasts for 1 to 1.
Lidocaine spinal anesthesia has been used for short-to-intermediate length operating room cases. The major drawback of lidocaine is the association with transient neurologic symptoms TNSs , which present as low back pain and lower extremity dysesthesias with radiation to the buttocks, thighs, and lower limbs after recovery from spinal anesthesia.
Lithotomy position is associated with a higher incidence of TNSs. Because of the risk of TNSs, lidocaine has mostly been replaced by other local anesthetics. Intrathecal use of 2-chloroprocaine was described in In the s, concerns were raised regarding neurotoxicity with the use of 2-chloroprocaine. Studies have suggested that sodium bisulfite, an antioxidant used in combination with 2-chloroprocaine, is responsible. Chronic neurologic deficits have been reported in rabbits when sodium bisulfite was injected into the lumbar subarachnoid space, but when preservative-free 2-chloroprocaine was injected, no permanent neurologic sequelae were noted.
Results from clinical trials have shown preservative-free 2-chloroprocaine to be safe, short acting, and acceptable for outpatient surgery. However, addition of epinephrine is not recommended due to an association with flu-like symptoms and back pain. Intrathecal 2-chloroprocaine is not currently approved by the Food and Drug Administration FDA , although package labeling states it may be used for epidural anesthesia.
Onset time is fast, and the duration is around to minutes. The dose ranges from 20 to 60 mg, with 40 mg as a usual dose. Procaine is a short-acting ester local anesthetic. Procaine has an onset time of 3 to 5 minutes and a duration of 50 to 60 minutes. A dose of 50 to mg has been suggested for perineal and lower extremity surgery. Concerns about the neurotoxicity of procaine have limited its use. For all these reasons, procaine is currently rarely used for spinal anesthesia.
Bupivacaine is one of the most widely used local anesthetics for spinal anesthesia and provides adequate anesthesia and analgesia for intermediate-to-long-duration operating room cases.
Bupivacaine has a low incidence of TNSs. Onset of anesthesia occurs in 5 to 8 minutes, with a duration of anesthesia that lasts from 90 to minutes. For outpatient spinal anesthesia, small doses of bupivacaine are recommended to avoid prolonged discharge time due to duration of nerve block.
Bupivacaine is often packaged as 0. Other forms of spinal bupivacaine include 0. Tetracaine has an onset of anesthesia within 3 to 5 minutes and a duration of 70 to minutes and, like bupivacaine, is used for cases that are intermediate to longer duration. With tetracaine, TNSs occur at a lower rate than with lidocaine spinal anesthesia.
The addition of phenylephrine may play a role in the development of TNSs. Mepivacaine is similar to lidocaine and has been used since the s for spinal anesthesia. Ropivacaine was introduced in the s. For applications in spinal anesthesia, ropivacaine has been found to be less potent than bupivacaine. Dose range-finding studies have demonstrated the ED95 of spinal ropivacaine in lower limb surgery Intrathecal use of ropivacaine is not widespread, and large-scale safety data are awaited.
An early study identified back pain in 5 of 18 volunteers injected with intrathecal hyperbaric ropivacaine. TNSs have been reported with spinal ropivacaine although the incidence is not as common as seen with lidocaine.
Other small studies have not demonstrated any major side effects. Table 8 shows some of the local anesthetics used for spinal anesthesia and dosage duration and concentration for different levels of spinal blockade.
Vasoconstrictors have been added to local anesthetics, and both epinephrine and phenylephrine have been studied. Anesthesia is intensified and prolonged with smaller doses of local anesthetics when epinephrine or phenylephrine is added. Tissue vasoconstriction is produced, thus limiting the systemic reabsorption of the local anesthetic and prolonging the duration of action by keeping the local anesthetic in contact with the nerve fibers.
However, ischemic complications can occur after the use of vasoconstrictors in spinal anesthesia. In some studies, epinephrine was implicated as the cause of CES because of anterior spinal artery ischemia.
Regardless, many studies do not demonstrate an association between the use of vasoconstrictors for spinal anesthesia and the incidence of CES. Phenylephrine has been shown to increase the risk of TNSs and may decrease nerve block height.
Epinephrine is thought to work by decreasing local anesthetic uptake and thus prolonging the spinal blockade of some local anesthetics. However, vasoconstrictors can cause ischemia, and there is a theoretical concern of spinal cord ischemia when epinephrine is added to spinal anesthetics. Animal models have not shown any decrease in spinal cord blood flow or increase in spinal cord ischemia when epinephrine is given for spinal blockade, even though some neurologic complications associated with the addition of epinephrine exist.
Dilution of epinephrine with local anesthetic is a potential source of drug error, with mistakes potentially incorrect by a factor of 10 or If using epinephrine packaged as 1 mg in 1 mL, which is a solution, a simple rule can be followed. Adding 0. Epinephrine prolongs the duration of spinal anesthesia. In the past, it was thought that epinephrine had no effect on hyperbaric spinal bupivacaine using two-segment regression to test neural blockade.
However, another study showed that epinephrine prolongs the duration of hyperbaric spinal bupivacaine when pinprick, transcutaneous electrical nerve stimulation TENS equivalent to surgical stimulation, and tolerance of a pneumatic thigh tourniquet were used to determine neural blockade.
There is controversy regarding prolongation of spinal bupivacaine neural blockade when epinephrine is added. The same controversy exists about the prolongation of spinal lidocaine with epinephrine. All four types of opioid receptors are found in the dorsal horn of the spinal cord and serve as the target for intrathecal opioid injection. Receptors are located on spinal cord neurons and terminals of afferents originating in the dorsal root ganglion.
Fentanyl, sufentanil, meperidine, and morphine have all been used intrathecally. Side effects that may be seen include pruritus, nausea and vomiting, and respiratory depression. Enhanced postoperative analgesia has been demonstrated in cesarean deliveries, fixation of femoral fractures, and knee arthroscopies when clonidine was added to the local anesthetic solution.
Clonidine prolongs the sensory and motor blockade of a local anesthetic after spinal injection. Sensory blockade is thought to be mediated by both presynaptic and postsynaptic mechanisms. Clonidine induces hyperpolarization at the ventral horn of the spinal cord and facilitates the action of the local anesthetic, thus prolonging motor blockade when used as an additive.
However, when used alone in intrathecal injections, clonidine does not cause motor nerve block or weakness. Side effects can occur with the use of spinal clonidine and include hypotension, bradycardia, and sedation. Neuraxial clonidine has been used for the treatment for intractable pain.
Acetylcholinesterase inhibitors prevent the breakdown of acetylcholine and produce analgesia when injected intrathecally. The antinociceptive effects are due to increased acetylcholine and generation of nitric oxide. It has been shown in a rat model that diabetic neuropathy can be alleviated after intrathecal neostigmine injection. Although spinal neostigmine provides extended pain control, the side effects that occur do not allow its widespread use. The pharmacodynamics of spinal injection of local anesthesia are wide ranging.
The cardiovascular, respiratory, gastrointestinal, hepatic, and renal effect consequences of spinal anesthesia are discussed next. It is well recognized that spinal anesthesia results in hypotension.
In fact, a degree of hypotension often reassures the anesthesiologist that the nerve block is indeed spinal. However, hypotension may cause nausea and vomiting, ischemia of critical organs, cardiovascular collapse, and in the case of the pregnant mother may endanger the fetus. Historically, there have been shifts in the definitions, suggested mechanisms, and management of hypotension.
Defining hypotension is troublesome. One study found 15 different definitions of hypotension in 63 publications. The incidence of hypotension in a single cohort of patients varied from 7. There have been many suggested mechanisms for spinal anesthesia—induced hypotension, including direct circulatory effects of local anesthetics, relative adrenal insufficiency, skeletal muscle paralysis, ascending medullary vasomotor nerve block, and concurrent respiratory insufficiency.
The primary insult, however, is the preganglionic sympathetic nerve block produced by spinal anesthesia. It therefore follows that because the nerve block height determines the extent of sympathetic blockade, this in turn determines the amount of change in cardiovascular parameters. However, this relationship cannot be predicted. Sympathetic nerve block may be variably between two and six dermatomes above the sensory level and incomplete below this level.
The sudden sympathetic nerve block with spinal anesthesia gives little time for cardiovascular compensation, which may account for a similar sympathetic nerve block with epidural anesthesia, but less hypotension. Sympathetic nerve block causes hypotension via its effects on preload, afterload, contractility, and HR—in other words, the determinants of cardiac output CO —and by decreasing systemic vascular resistance SVR.
Preload is decreased by sympathetic nerve block-mediated venodilation, resulting in pooling of blood in the peripheries and decreased venous return. During sympathetic nerve block, the venous system is maximally vasodilated and therefore reliant on gravity to return blood to the heart. Thus, patient positioning, and aortocaval compression in the case of a gravid uterus, markedly influences venous return during spinal anesthesia. Arterial vasomotor tone can also be decreased by sympathetic nerve block, decreasing SVR, and afterload.
Arterial vasodilation, unlike venodilation, is not maximal after spinal blockade, and vascular smooth muscle continues to retain some autonomic tone after sympathetic denervation. However, we try to tailor the spinal to minimize delays in discharge from the recovery room.
If you are having an outpatient procedure your numbness must resolve before you can be discharged to home. Although infrequent, one complication of spinal anesthesia deserves mention. Spinal headache or post dural puncture headache, PDPH is the most common complication of spinal anesthesia.
The headache usually presents within the first two days after a spinal anesthetic. Its hallmark is a moderate to severe headache that improves when you lie flat and becomes worse when you sit or stand.
Spinal headaches are not dangerous and do not cause any long term effects. Most of the time, they will resolve on their own within five to seven days. If the headache is severe or not improving after conservative treatment, an epidural blood patch can be performed. Search form Search. A spinal anaesthetic is an alternative to a general anaesthetic for some operations. It allows the patient to stay awake during the operation without feeling any pain.
For many operations a general anaesthetic GA will be required. This is where the anaesthetist gives the patient medication, usually through a drip cannula into a vein, and sends them off to sleep. This keeps the patient unconscious, still and pain-free for the duration of the operation.
A breathing tube is inserted after the patient is asleep so the breathing can be controlled throughout the operation. When the operation is finished the anaesthetist allows the patient to wake up. An alternative to a general anaesthetic is a spinal anaesthetic. A spinal anaesthetic can be used for most operations below the waist.
A spinal anaesthetic is performed by an anaesthetist. A very fine needle is inserted into the middle of the lower back and local anaesthetic is injected through the needle into the fluid that surrounds the spinal cord. The local anaesthetic numbs the nerves that supply the tummy, hips, bottom and legs. Once the nerves are completely numb you will not feel any pain from an operation and you will also not be able to move your legs. Other medications can also be injected which provide excellent pain relief for several hours after the operation.
You may, however, have a sensation of movement or pressure - this is entirely normal. A screen will put up so that you will not be able to see the operation. If you are choosing this option it might be useful to bring some music and headphones with you so that you can listen to it during the operation. In this instance, once the spinal anaesthetic has been performed and the anaesthetist is happy with the block see later for details the anaesthetist will give some medication into your drip to make you feel relaxed and sleepy.
In some situations the anaesthetist might feel that a combination of a spinal anaesthetic and a general anaesthetic is the best option for you. Also in some situations for example, if the operation takes an unexpectedly long time or you start to feel discomfort during the operation it might be necessary to add in a general anaesthetic to overcome these issues. Your anaesthetist will see you before the operation to discuss all the options with you. They will help you come to a decision as to what the best option is for you.
There will be an operating department practitioner to assist the anaesthetist and another member of the theatre team to support and help you during the procedure. Before the spinal anaesthetic is given, the anaesthetist will put a drip cannula in your hand and you will be attached to a monitor ECG, blood pressure and oxygen saturations.
Most often the spinal anaesthetic will be done whilst you are awake. Your anaesthetist will instruct you as to what position you need to get into for the procedure to be done. This will be in one of two positions:. These positions help to open up the spaces between the bones in your back, which is where the anaesthetist needs to put the spinal anaesthetic. Once you are in the correct position your back will be cleaned with antiseptic, the anaesthetist will scrub their hands and put on a surgical gown, gloves, hat and mask.
These steps help to minimise the risk of infection. The anaesthetist will feel your back quite firmly to identify certain landmarks and identify where exactly the spinal anaesthetic needs to be inserted. Local anaesthetic will firstly be injected to numb the skin; then the fine spinal needle will be inserted. At this point it is particularly important to keep very still.
You should not feel significant pain; however, if the needle goes close to one of the nerves that supply your legs you may feel a shooting pain down one of your legs. If this occurs it is important that you keep still and let your anaesthetist know, telling them which leg you felt the pain in.
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