Why spinal anesthesia

After loss of consciousness, paralysis without muscle relaxant , and pupil dilation, a laryngeal mask airway LMA was inserted and positive pressure ventilation applied. Ephedrine and atropine were used for cardiovascular support if required. Mechanical ventilation was required for about an hour, after which the LMA was removed.

Cardiovascular Collapse Cardiovascular collapse can occur after spinal anesthesia, although it is a rare event. Auroy and coworkers reported 9 cardiac arrests in 35, spinal anesthetics performed.

Refer to the section on Cardiovascular Effects of Spinal Anesthesia. While minor risks are often thought of as side effects, major complications are of more concern to clinicians and patients. Perception of risk can be influenced by sensational case reports, such as given by Woolley and Roe. Early efforts to assess risk were hampered by lack of good numerator number of complications and denominator number of spinal nerve blocks data.

They concluded that objections to spinal anesthesia were undeserved. Retrospective evidence from Finland for the period — estimated the risk of major complication following spinal anesthesia at 1 in 22, A no-fault compensation scheme was thought to increase data veracity.

Swedish data Moen from the period — found a similar risk of 1 in 20,—30, Although good evidence at the time, the Scandinavian evidence was criticized because of retrospective design, which risks underreporting. Moreover, numerator data sourced from administrative databases may not indicate either causation or final outcome.

Auroy attempted to address weaknesses of an earlier study by setting up a telephone hotline, allowing contemporaneous assessment of causality. This prospective study from to investigated complications from any type of regional anesthesia.

Auroy, unlike Moen, included peripheral neuropathy and radiculopathy in the numerator data. Designing a prospective study to accurately quantify the risk of spinal anesthesia has been difficult due to the low incidence of major complications. It also investigated causality and outcome. Numerator data in NAP3 pertained to major complications over a month period — Reports came from local hospital reporters and clinicians. Litigation authorities, medical defense organizations, journals, and even Google searches of media reports were reviewed to identify missed complications.

Complications were classified as infections, hematomata, nerve injuries, cardiovascular collapses, and wrong-route errors.

Notably, PDPH was not included as a major complication. Complications were examined by a panel, and the likelihood of CNB as the cause was established. Denominator data were sourced from a 2-week census and validated by contacting a number of organizations and databases. The findings of permanent harm were presented optimistically or pessimistically see Table 4.

Optimistic figures excluded complications where recovery was likely or causality tenuous. Permanent harm after any type of CNB was pessimistically , and optimistically , The risk of death or paraplegia after any type of CNB was pessimistically , and optimistically , The incidences of complications of spinals and caudals were at least half that of epidurals and combined spinal-epidural CSE nerve blocks.

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. The subarachnoid space is the bag of fluid that surrounds your spinal cord and the nerves that come out from it.

Local anaesthetics and other painkillers are injected using a fine needle into this space. Your anaesthetist will insert the needle and when they are certain that it is in the right position they will inject anaesthetic through it. The time that the spinal lasts for varies but is usually 1 to 3 hours. Your anaesthetist will put enough anaesthetic through the needle to make sure that it lasts longer than the expected length of the operation. A spinal anaesthetic can be used for most people, usually giving a safe and effective form of pain relief both during and after an operation or procedure.

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There is a total of 5 error s on this form, details are below. The catheter is secured on the back so it can be used again if more medicine is needed. Spinal anesthesia is done in a similar way. But the anesthetic medicine is injected using a much smaller needle, directly into the cerebrospinal fluid that surrounds the spinal cord. The area where the needle will be inserted is first numbed with a local anesthetic. Then the needle is guided into the spinal canal, and the anesthetic is injected.

This is usually done without the use of a catheter. Spinal anesthesia numbs the body below and sometimes above the site of the injection. The person may not be able to move his or her legs until the anesthetic wears off.

A headache is the most common side effect of spinal anesthesia. It can usually be treated easily. Headaches are less common with epidural anesthesia. Epidural and spinal anesthesia are usually combined with other medicines that make you relaxed or sleepy sedatives or relieve pain analgesics.

These other medicines are often given through a vein intravenously, IV.