Version May 2024
INTRODUCTION — Neuraxial anesthesia and analgesia techniques include spinal, epidural, and combined spinal-epidural. This topic will discuss aspects of neuraxial anesthesia (NA) that are common to all of these techniques, and the differences among them. The techniques for performing each of them are discussed separately. (See "Spinal anesthesia: Technique" and "Epidural and combined spinal-epidural anesthesia: Techniques".)
Neuraxial procedures for chronic pain conditions (eg, spinal cord stimulator, epidural steroid injections) are also discussed separately. (See "Spinal cord stimulation: Placement and management" and "Subacute and chronic low back pain: Nonsurgical interventional treatment".)
ANATOMY — Neuraxial anesthesia is performed by placing a needle between vertebrae and injecting medication into the epidural space (for epidural anesthesia) or the subarachnoid space (for spinal anesthesia). The anatomy relevant for neuraxial anesthesia techniques is discussed in detail separately. (See "Spinal anesthesia: Technique", section on 'Anatomy' and "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Anatomy'.)
USE OF NEURAXIAL ANESTHESIA — Neuraxial anesthesia (NA) is most commonly used for lower abdominal and lower extremity surgery (table 1). The sensory level required for a specific surgery is determined by the dermatome level of the skin incision and by the level required for surgical manipulation; these two requirements may be very different. As an example, a low abdominal incision for cesarean delivery is made at the T11 to T12 dermatome, but a T4 spinal level is required to prevent pain with peritoneal manipulation (figure 1 and table 2).
Spinal, epidural, and combined spinal-epidural (CSE) anesthesia can be used for many of the same surgical procedures. Differences among them may affect the choice of technique for a specific procedure or patient. The advantages and disadvantages of the various neuraxial anesthesia techniques are shown in a table (table 3). Spinal anesthesia is usually administered as a single injection, whereas epidural anesthesia is usually administered via a catheter for continuous infusion, and CSE anesthesia combines the two. Continuous spinal anesthesia via a catheter sited in the subarachnoid space is less commonly used than the other techniques. (See "Spinal anesthesia: Technique", section on 'Continuous spinal'.)
Catheter-based neuraxial anesthesia (ie, epidural, CSE, and continuous spinal) allows prolonged anesthesia and titration of the onset of the anesthetic. Single-shot spinal or epidural anesthesia is limited to the duration of action of the injected drug.
The needle for spinal anesthesia must be inserted in a mid- to low-lumbar intervertebral space (below the termination of the conus medullaris), whereas needle placement for an epidural injection can occur anywhere from the distal end of the neuraxial canal (via the sacral hiatus to a high cervical interspace [usually for a chronic pain management procedure]). For example, an epidural catheter can be placed to provide primarily thoracic anesthesia and/or postoperative analgesia, with the extent determined by the volume and concentration of the chosen epidural medications. Thus, the specific dermatomes and extent of sensory blockade may be more easily controlled with an epidural injection.
PREOPERATIVE EVALUATION — A medical history and anesthesia-directed physical examination should be performed for all patients who undergo any type of anesthesia. If neuraxial anesthesia (NA) is considered, the back should be examined as part of the anesthesia-directed physical examination. (See "Preoperative evaluation for anesthesia for noncardiac surgery".)
When considering NA, we focus the preoperative evaluation on the medical conditions that may alter the physiologic response to NA or increase the risk of complications.
●Coagulopathy – Patients with abnormal coagulation (ie, with thrombocytopenia, bleeding disorders, receiving anticoagulants) are at increased risk of spinal bleeding during or after neuraxial anesthesia. (See 'Spinal-epidural hematoma (SEH)' below.)
●Systemic and local skin infection – Patients with systemic infection, and with skin infection at the site of spinal or epidural needle puncture may be at increased risk for central nervous system (CNS) infection with neuraxial anesthesia. Spinal and epidural needles should not be inserted through obviously infected skin.
Chronic infection with human immunodeficiency virus (HIV) is not considered a contraindication to spinal anesthesia since the central nervous system (CNS) is infected early in the course of the disease.
The use of NA in patients with other viral infections is controversial. Primary infection with herpes simplex (HSV) and varicella zoster (VZV) is associated with a period of viremia, whereas secondary infection (manifest with oral or genital lesions) is not. Although data are limited, most anesthesiologists are comfortable initiating spinal anesthesia during a secondary HSV outbreak [1], while avoiding insertion of the NA needle through active herpetic skin lesions.
The American Society of Anesthesiologists (ASA) Practice Advisory for the Prevention, Diagnosis, and Management of Infectious Complications Associated with Neuraxial Techniques states that there is insufficient evidence to assess whether prophylactic antibiotic therapy reduces the risk of infection [2]. The Advisory recommends that alternative anesthetic techniques be considered in patients at high risk for infection and that preprocedure antibiotic administration be considered when a neuraxial technique is chosen for patients with known or suspected bacteremia.
●Preload-dependent cardiac lesions – Patients with preload-dependent cardiac lesions (eg, aortic stenosis or hypertrophic cardiomyopathy) are at risk for a profound decrease in cardiac output and hypotension as a result of the sympathectomy that accompanies NA. Management modifications for these patients may include invasive monitoring, incremental initiation of neural blockade, and fluid and vasopressor administration. (See 'Cardiovascular' below.)
●Hypovolemia – Hypovolemia increases the risk of hypotension with onset of NA because of the induced sympathectomy; volume status should be normalized prior to initiation of NA, and incremental dosing and invasive blood pressure monitoring may be required.
●Spine abnormalities – NA for patients with spine abnormalities (eg, scoliosis, spinal stenosis, disk disease, radiculopathy, prior spine surgery, spina bifida) may be technically challenging or impossible, or associated with increased risk of neurologic complications.
•Anatomic distortion, surgical scarring, or spine hardware can obliterate the landmarks used for performance of NA techniques. Ultrasound guidance may help in some cases.
•Distribution of NA medications may be affected by anatomic distortion or postsurgical changes, and result in inadequate anesthesia or analgesia. This is more likely with an epidural technique, which relies on spread of the drug in the epidural space.
•Patients with preexisting neurologic compromise (eg, radiculopathy, spinal stenosis) may be at increased risk of postoperative neurologic complications after NA [3].
•NA (usually spinal anesthesia) is an option for patients with paraplegia or quadriplegia, in particular to avoid intraoperative autonomic dysreflexia. (See "Anesthesia for adults with chronic spinal cord injury", section on 'Autonomic dysreflexia'.)
●Progressive neurologic disease – Patients with progressive or episodic neurologic diseases (eg, multiple sclerosis, post-polio syndrome) are probably not at increased risk of new or worsened neurologic deficits because of neuraxial anesthesia [4]. However, the signs and symptoms of such diseases may worsen in the postoperative period because of the stress of surgery, perioperative fever, or infection. Preexisting neurologic deficits should be documented, and the unknown risks of worsened neurologic disease should be discussed preoperatively. (See "Perioperative care of the surgical patient with neurologic disease", section on 'Multiple sclerosis' and "Obstetric and nonobstetric anesthesia for patients with neurologic disorders".)
●Intracranial mass lesion with intracranial hypertension – Patients with raised intracranial pressure from a mass lesion are at risk for cerebral herniation with spinal anesthesia, or with an unintentional dural puncture during epidural anesthesia, and NA is usually avoided in these patients. Dural puncture is generally considered safe in patients with idiopathic intracranial hypertension. (See "Obstetric and nonobstetric anesthesia for patients with neurologic disorders".)
●Hydrocephalus with shunt – NA has been used in patients with shunts in place to treat hydrocephalus, including lumboperitoneal shunts. Theoretical considerations include leakage of cerebrospinal fluid (CSF; with local anesthetic) through the shunt and the risk of shunt infection. (See "Obstetric and nonobstetric anesthesia for patients with neurologic disorders", section on 'Cerebrospinal fluid shunts'.)
Laboratory evaluation — Preoperative laboratory testing should be performed as it would be for general anesthesia, based on the patient’s medical status and the planned surgical procedure. (See "Preoperative evaluation for anesthesia for noncardiac surgery", section on 'Preoperative testing'.)
PHYSIOLOGIC EFFECTS OF NEURAXIAL ANESTHESIA — The physiologic effects of neuraxial anesthesia (NA) are the result of blockade of sympathetic, motor and sensory nerves, the compensatory reflexes, and unopposed parasympathetic tone. The magnitude of various physiologic effects depends on the extent and speed of onset of the block, and patient factors.
Cardiovascular — Hypotension and bradycardia are the most common and important physiologic effects of neuraxial anesthesia, and are the result of sympathetic blockade and associated reflexes (figure 2).
●Hypotension – Hypotension occurs in as many as 47 percent of spinal anesthetics [5,6], as a result of a decrease in systemic vascular resistance, peripheral blood pooling with decreased venous return to the heart, or both. These two effects result from the sympathetic block that accompanies spinal anesthesia, and from block of adrenal medullary secretion. Higher levels of sympathetic block are associated with an increased risk of hypotension; with spinal block below approximately T4, vasoconstriction above the level of the block may compensate and mitigate the decrease in blood pressure. In addition, block of cardioaccelerator fibers (originating from T1 to T4 nerve roots) with high spinal can contribute to hypotension through a decrease in heart rate and cardiac output. When the same dermatomal block is achieved with epidural and spinal anesthesia, there is a similar incidence of hypotension, although the onset of hypotension may be slower with epidural anesthesia [7].
Risk factors for hypotension include hypovolemia [8], age >40 to 50 years, emergency surgery, obesity, chronic alcohol consumption, and chronic hypertension [5,6,9].
●Bradycardia – Clinically significant bradycardia occurs in 10 to 15 percent of spinal anesthetics [6,9]. The incidence of bradycardia with epidural anesthesia depends on the level and extent of the block. Mechanisms for bradycardia are direct (blockade of sympathetic cardioaccelerator fibers) and indirect. Indirect mechanisms include decreased output of the myocardial pacemaker cells due to decrease in venous return, stimulation of low-pressure baroreceptors in the right atrium and vena cava, and stimulation of mechanoreceptors in the left ventricle resulting in bradycardia (paradoxical Bezold-Jarisch reflex) [10]. Risk factors for bradycardia during spinal anesthesia include age <50 years, baseline heart rate <60 beats per minute (bpm), American Society of Anesthesiology physical status 1 (ie, healthy, no medical problems), current beta-adrenergic blocker therapy, prolonged PR interval, and block height above T6 [6,9].
A small subset of patients develops severe bradycardia that may progress to cardiac arrest.
Neuraxial anesthesia can also cause first, second, and third degree heart block [11-16]. The incidence of heart block in this setting is unknown; proposed mechanisms are the same as those for bradycardia.
Pulmonary — High NA can cause paralysis of accessory muscles of respiration, and can theoretically lead to bronchospasm.
●Respiratory mechanics – NA block to a midthoracic level has minimal respiratory effects in patients without pulmonary disease. While intercostal muscles may be paralyzed with a thoracic block, diaphragmatic function is maintained. Therefore, resting tidal volume and the forced expiratory volume in one second/forced vital capacity (FEV1/FVC) ratio are unchanged, and maximum inspiratory volume, vital capacity, and FEV1 are minimally decreased [17].
In contrast, high spinal block with paralysis of accessory muscles may impair active exhalation and cough, such that peak expiratory flow, maximal minute ventilation, and expiratory reserve volume are reduced [17]. These effects can be important for patients with pulmonary secretions or obstructive pulmonary disease, who depend on accessory muscles of respiration to cough or maintain ventilation.
●Bronchial tone – Bronchial tone at rest is controlled in part by the balance between parasympathetic and sympathetic bronchial tone. Theoretically, the sympathetic block associated with high spinal anesthesia may allow parasympathetic predominance, and lead to bronchospasm. This effect appears to be of little clinical significance. A study of thoracic level epidural anesthesia in patients with chronic obstructive pulmonary disease reported no increase in airways resistance with sympathetic blockade [18]. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Neuraxial anesthesia'.)
Central nervous system — Patients often appear and feel sedated during NA. A number of studies have found a reduction in requirements for sedatives [19-21] and an increase in self-reported and observed sedation [22,23] in patients who undergo spinal anesthesia, compared with those who have not had anesthesia. The unproven hypothesis for this phenomenon is that NA decreases afferent input to the reticular activating system in the brain, resulting in sedation.
The level of sedation associated with spinal anesthesia can increase over the course of the first 60 minutes after injection [22]. Therefore, sedative medication should be administered in reduced, incremental doses during NA anesthesia, and should be accompanied by continuous monitoring of respiration and consciousness.
Cerebral blood flow is autoregulated; therefore, blood flow to the brain remains unchanged during NA unless there is a profound drop in blood pressure below the lower limit of autoregulation.
Thermoregulation — As with general anesthesia, hypothermia can occur during NA, and may be more likely with higher levels of block [24]. We use active warming methods (ie, warming blankets, fluid warmers) during NA as we would during general anesthesia.
Patient temperature maintenance in the operating room is multifactorial, and depends on anesthetic effects, operating room temperature, administered fluid volume and temperature, surgical exposure, and the duration of surgery and anesthesia. Several mechanisms may be responsible for heat loss during epidural and spinal anesthesia [25-27] (see "Perioperative temperature management", section on 'Effects of neuraxial or regional anesthesia'):
●Sympathetic block redistributes blood flow from the core to the periphery, resulting in loss of heat to the environment.
●Heat production is decreased because of a decrease in metabolic rate below the level of the block.
●Compensatory mechanisms (ie, shivering and vasoconstriction) are blocked below the sensory level.
●Central thermoregulation is impaired because of blocked peripheral afferent input.
Gastrointestinal — Sympathetic innervation to the abdominal viscera originates from spinal levels T6 to L1. Parasympathetic innervation to the abdominal viscera is via the vagus nerve, which is not blocked during neuraxial anesthesia. Therefore, depending on the extent of blockade, neuraxial anesthesia results in sympatholysis while maintaining parasympathetic innervation, leading to a contracted gut, relaxed sphincters, and normal peristalsis [28]. This effect can promote the return of gastrointestinal motility after abdominal surgery. A meta-analysis of 22 trials including approximately 1100 patients who underwent abdominal surgery reported that epidural analgesia with local anesthetic with or without opioids reduced the time to first flatus and first bowel movement, compared with opioid analgesia [29].
The effects of NA on hepatic blood flow are discussed separately. (See "Anesthesia for the patient with liver disease", section on 'Choice of anesthetic technique'.)
Renal — Direct effects of NA on renal function are of little clinical significance, as long as blood pressure and intravascular volume are maintained [30,31]. Innervation to the kidney originates at spinal levels T10 to L1. Neuraxial blockade may alter renal function by several mechanisms, both direct and indirect. Changes in blood pressure, cardiac output, and endocrine function may indirectly affect renal blood flow. Neuraxial blockade may directly affect efferent nerves to the kidney or alter reflex responses due to afferent nerve blockade. However, in healthy individuals, a large reserve protects the kidney from harm, and neuraxial blockade has little physiologic effect as long as hydration is adequate and blood pressure is maintained within the range of autoregulation. In the presence of hypotension, urine output may decrease, but adequate renal oxygenation is maintained, and urine output returns to normal once blood pressure returns to normal.
ADVERSE EFFECTS AND COMPLICATIONS — Serious and permanent complications of neuraxial anesthesia are very rare. In a prospective audit report from the UK, the incidence of permanent injury from neuraxial anesthesia was 4.2 per 100,000 [32]. This report also highlighted that most injuries resolved within six months.
Inadequate or failed neuraxial anesthesia — Inadequate or failed neuraxial anesthesia, defined as the need to repeat the neuraxial procedure, convert to general anesthesia, or abort the planned surgery, is discussed separately. (See "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Troubleshooting inadequate anesthesia' and "Spinal anesthesia: Technique".)
High or total spinal anesthesia — Total spinal anesthesia can be a complication of either spinal or epidural anesthesia. It may result from the unrecognized and unintentional injection of medication intended for the epidural space into the subdural or subarachnoid space (via a malpositioned catheter or needle) or an overdose of medication injected into the epidural space. The reported incidence in the obstetric population is 1 in 4336 neuraxial blocks [33]. It usually occurs within a few minutes following administration of local anesthetic, but can also occur up to 40 minutes later with changes in patient position. The signs and symptoms include a rapid ascending sympathetic, sensory, and motor block with associated bradycardia, hypotension, dyspnea, and difficulty with swallowing or phonation. Symptoms can progress to unconsciousness (due to brainstem hypoperfusion and/or brainstem anesthesia), and respiratory depression (secondary to respiratory muscle paralysis and brainstem hypoperfusion). If a large dose of local anesthetic is unintentionally injected into the subarachnoid space, unconsciousness and respiratory depression may be the initial signs of a total spinal anesthesia.
Injection of local anesthetic solution or saline into the epidural space either before [34] or after [35] a spinal injection can result in a higher than expected level of spinal anesthesia, or even total spinal anesthesia. Single injection spinal should be performed with caution following failed epidural anesthesia with an appropriate dose of local anesthetic solution. If spinal anesthesia is attempted, a reduced local anesthetic dose should be considered. In one small study in patients who had combined spinal-epidural anesthesia, patients who had 10 mL of saline injected into the epidural space 10 minutes after spinal injection had a higher spinal level 10 minutes later than patients who had no saline injected (mean spinal level T7 versus T11) [35]. Total spinal anesthesia has been described when spinal anesthesia was initiated following failed epidural anesthesia, and is one of the most common serious complications of obstetric anesthesia [33]. (See "Anesthesia for cesarean delivery", section on 'Failed or inadequate neuraxial block' and "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Dose of spinal drugs'.)
Subdural injection — The subdural space is a potential space between the dura and arachnoid mater. Unintentional injection of local anesthetic solution into this space (usually intended for the epidural space) may cause a patchy block that results in more extensive cranial anesthesia than expected after epidural injection, with an onset intermediate between spinal and epidural anesthesia [36]. Motor block may also be more extensive than expected. Horner syndrome, apnea, and unconsciousness have been reported after subdural injection of local anesthetic [36].
Nerve injury — Direct trauma to nerve tissue is rare during neuraxial anesthesia. In an audit study from the United Kingdom, the incidence of nerve injury following neuraxial anesthesia for surgical anesthesia (not obstetric) was estimated to be as high as 1.6 per 100,000, if injuries that were not definitively caused by the anesthetic were included in the calculation [32]. The incidence is lower in obstetric patients [32,37].
Damage to the conus medullaris may occur during spinal anesthesia if the clinician unintentionally performs spinal anesthesia at a high lumber interspace. Although the spinal cord typically ends at the body of the L1 vertebra in adults, the length varies and may extend lower in some patients [38]. Anesthesia clinicians frequently misidentify the intended interspace, and the actual interspace is cephalad to the intended interspace, sometimes by more than one interspace [39]. Thus, the clinician may be initiating spinal anesthesia at a high- rather than mid-lumber interspace, thereby increasing the risk for direct trauma to the conus medullaris.
Paresthesias occur frequently during neuraxial procedures, and indicate that the needle or catheter has contacted nerve tissue. However, persistent paresthesia after NA is rare. In a retrospective study of spinal anesthetics, 6.3 percent of patients reported a paresthesia, but only 0.1 percent had persistent postoperative paresthesia [40]. Should a paresthesia occur, needle advancement should be halted. If the paresthesia persists, the needle should be withdrawn.
Back pain — Localized point tenderness may be present for several days after a neuraxial procedure, but there is no evidence that neuraxial procedures result in long-term backache. In one study, approximately 600 parturients were randomly assigned to receive epidural analgesia or meperidine for labor pain. There was no difference in postpartum backache six months after delivery, in patients with and without backache prior to delivery [41]. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Backache'.)
Postdural puncture headache — Postdural puncture headache (PDPH) is a positional headache (ie, worse when the patient sits or stands) that usually occurs within 6 to 72 hours of dural puncture [42]. Associated symptoms may include nausea, vomiting, dizziness, tinnitus, neck stiffness, visual change, and hearing loss [43]. PDPH can occur after intentional dural puncture (ie, spinal anesthesia) or after inadvertent dural puncture during epidural anesthesia.
Risk factors, clinical manifestations, treatment, and complications of PDPH are discussed separately. (See "Post dural puncture headache" and "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Post dural puncture headache'.)
Urinary retention — Spinal anesthesia (and often epidural anesthesia) blocks afferent and efferent nerve signals to the bladder (S2 to S4). Thus, the sensation of urgency from a full bladder is blocked, as is the ability to empty the bladder (detrusor function) [44]. The duration of bladder dysfunction is directly related to the duration of spinal anesthesia. Risk factors for postoperative urinary retention include the use of long-acting local anesthetics, use of intrathecal opioid, older age, male sex, and prolonged surgery [44]. Other factors that may play a role include type of surgery, intraoperative administration of drugs that affect bladder function, intraoperative fluid management, and patient comorbidities.
Transient neurologic symptoms — Transient neurologic symptoms (TNS) comprise a syndrome including pain and/or dysesthesia in the buttocks or lower extremities several hours after resolution of uncomplicated spinal anesthesia [45]. Onset of pain is typically within 2 to 24 hours after the complete resolution of spinal anesthesia. Pain may be described as mild to severe, usually aching in nature, radiating from the lower back/gluteal region to the posterior thighs. It is often improved by ambulation and nonsteroidal antiinflammatory drug therapy, and usually resolves after several days without sequelae. Physical examination, magnetic resonance imaging, and other electromyographic testing are normal.
The etiology of transient neurologic symptoms is unclear. Hypotheses include local anesthetic toxicity, needle trauma, ischemia, muscle spasm, and nerve root irritation [46]. TNS can occur after any spinal anesthetic, but is more common when lidocaine or mepivacaine is used, compared with other local anesthetics [47]. A meta-analysis of 24 trials including 2226 patients reported the risk of TNS with lidocaine for spinal anesthesia was greater compared with bupivacaine, prilocaine, or procaine; the risk was similar to 2- chloroprocaine and mepivacaine [48]. The risk of TNS with lidocaine was approximately 1 in 5 with spinal lidocaine. A previous meta-analysis also identified patient position (lithotomy) and type of surgery (knee) as additional risk factors [49]. Dilution of lidocaine with cerebrospinal fluid (CSF) or saline does not decrease the incidence of symptoms [50].
The true incidence of TNS with mepivacaine is unclear. Studies include heterogeneous techniques and few cases of TNS, and have reported TNS in 0 to 37 percent of patients who had spinal anesthesia with various concentrations and doses of the drug [47,49,51]. The best evidence suggests that the incidence of TNS with plain spinal 1.5% mepivacaine is similar to lidocaine. In a prospective study of approximately 1200 patients, the incidence was 6.5 percent [52].
Local anesthetic systemic toxicity — Local anesthetic systemic toxicity (LAST) can occur with any route of administration of local anesthetics, but is much less likely with spinal than with epidural anesthesia, because such a small dose of local anesthetic (LA) is injected for spinal anesthesia. LAST is a rare but potentially lethal event, that may consist of central nervous system and/or cardiovascular effects ranging from minor manifestations (eg, perioral numbness, tinnitus, twitching), to major events, including seizures, coma, severe hypotension, arrhythmias, and asystole. LAST occurs most commonly with inadvertent intravascular injection of LA with almost immediate onset of signs and symptoms, but delayed onset may also occur with epidural infusion after systemic absorption of LA or migration of the catheter into a blood vessel. LAST is discussed in detail separately. (See "Local anesthetic systemic toxicity".)
Spinal-epidural hematoma (SEH) — Hemorrhage into the neuraxis is a rare complication of NA that may occur if a vascular structure is punctured by the needle or catheter. The incidence of SEH following neuraxial anesthesia is unknown, but likely very low, based on retrospective studies with small numbers of hematomas. The incidence of SEH appears to be higher with epidural than with spinal anesthesia. In a 2004 retrospective study, 25 SEHs occurred after approximately 450,000 epidurals (1 in 18,000), and 8 occurred after 1,260,000 spinals (1 in 158,000) [37]. SEH and neuraxial anesthesia for patients who are anticoagulated are discussed separately. Risk factors for SEH include older age, coagulopathy, and a difficult NA procedure. SEH after neuraxial anesthesia is discussed in detail separately. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Spinal epidural hematoma (SEH)' and "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Spinal epidural hematoma' and "Anesthesia for the patient with preeclampsia", section on 'Coagulation'.)
Infection — The risk of CNS infection with spinal and other neuraxial anesthesia for patients with systemic infection, or with risk factors for infection (eg, diabetes, cancer, or immunocompromise) is unclear. Meningitis is more common after spinal anesthesia, whereas epidural abscess is more common after epidural anesthesia. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Severe infection'.)
Aseptic technique should routinely be used to reduce the risk of infection and should include skin preparation with chlorhexidine in alcohol solution or povidone iodine in alcohol, and the use of hats, masks, and sterile gloves. (See "Spinal anesthesia: Technique", section on 'Aseptic technique'.)
Early signs and symptoms of postprocedure infection (eg, back pain, fever, headache, erythema at insertion site) may be followed by later signs (eg, stiff neck, radiating pain, photophobia, loss of motor function, confusion). If any signs of infection occur, an in situ epidural catheter should be removed immediately, and the appropriate imaging and consultation (ie, neurologist or infectious disease specialist) should be initiated. (See "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Spinal epidural abscess".)
GENERAL VERSUS NEURAXIAL ANESTHESIA — There are risks and benefits to both neuraxial and general anesthesia. Some observational data and small randomized trials suggest that neuraxial anesthesia may be associated with better outcomes than general anesthesia for some procedures [53], but large, high quality evidence is lacking. As a general rule, there are no clear advantages to one type of anesthesia over the other when either would be appropriate [54-56]. Decisions about anesthetic technique should be made at the individual patient level based on a number of factors, including patient, surgeon, and anesthesiologist preference; type of surgical procedure; the patient's comorbid diseases; and plan for postoperative analgesia.
In addition, the following issues may affect the decision to choose neuraxial anesthesia:
●Perioperative process – The use of neuraxial anesthesia (NA) may modestly increase intraoperative time and recovery room stay for ambulatory procedures. A meta-analysis including over 1000 patients compared general anesthesia with neuraxial anesthesia for ambulatory surgeries [57]. Neuraxial anesthesia was associated with a 35-minute increase in time until ambulatory surgery unit discharge and a 9-minute increase in anesthesia induction time.
●Deep vein thrombosis (DVT) – Surgery is associated with postoperative hypercoagulability and consequent risk of thromboembolic events. Compared with general anesthesia, neuraxial anesthesia is associated with a decreased risk of deep venous thrombosis and pulmonary embolism [58]. The mechanism(s) is unclear, and it is not known if this effect is dependent on the type and extent of neuraxial anesthesia, duration (ie, intraoperative or postoperative), or neuraxial drugs (eg, local anesthetics, opioids). Reduction in risk of DVT with NA is less of a clinical advantage than it was historically, since almost all at-risk patients are now treated with mechanical and pharmacologic prophylaxis for DVT.
●Blood loss – The effects of NA on perioperative bleeding are unclear, and may depend on the surgery performed. In a meta-analysis of 141 randomized trials including approximately 9500 patients that compared outcomes after general anesthesia with NA, intraoperative and postoperative transfusion requirements were reduced by 50 percent with NA [58]. However, many of the included studies involved orthopedic surgery prior to the routine use of intraoperative tranexamic acid. More recent studies involving arthroplasties have shown mixed results, and the largest meta-analysis comparing general anesthesia with NA for total hip and total knee arthroplasty did not evaluate bleeding or transfusion because of low quality studies [59]. (See "Anesthesia for total knee arthroplasty", section on 'General versus regional anesthesia'.)
●Cancer recurrence – The possibility that NA and other regional anesthesia techniques might reduce the rate of cancer recurrence after cancer surgery is a topic of active investigation. The current data are inconclusive, though some randomized trials in specific cancer populations have not found a difference in cancer recurrence or survival. These issues and the relevant literature are discussed in detail separately. (See "Anesthesia and cancer recurrence", section on 'Regional anesthesia/analgesia'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Post dural puncture headache" and "Society guideline links: Local and regional anesthesia" and "Society guideline links: Local anesthetic systemic toxicity".)
PATIENTS WITH SUSPECTED OR CONFIRMED COVID-19 — Regional anesthesia is not contraindicated in patients with COVID-19. Regional anesthesia may avoid the need for general anesthesia and airway management, with associated aerosolization of airway secretions and viral spread. The American Society of Regional Anesthesia and Pain Medicine and the European Society of Regional Anesthesia and Pain Therapy have published practice recommendations for neuraxial anesthesia and peripheral nerve blocks for patients with COVID-19. Important considerations specific to neuraxial anesthesia include the following:
●Many patients with COVID-19 will be receiving pharmacologic thromboprophylaxis, which may affect the timing of or decision to use neuraxial anesthesia. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)
●Consider checking a platelet count prior to neuraxial anesthesia in symptomatic patients. Thrombocytopenia has been reported in patients with COVID-19 [60,61].
●Patients should wear a surgical mask at all times, including throughout the surgical procedure.
●Avoid allowing cerebrospinal fluid (CSF) to drip from the needle when performing spinal anesthesia, and avoid contact with CSF. It is not known whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19, enters CSF. However, in patients infected with some other coronaviruses, those viruses have been detected in CSF [62].
●For patients who develop post dural puncture headache, consider avoiding nasal sphenopalatine block, which could provoke cough or sneeze and viral spread. Some experts suggest avoiding an epidural blood patch if possible, to avoid seeding the central nervous system in patients who are viremic.
UpToDate topic reviews of COVID-19 related issues include the following:
●(See "COVID-19: Management in hospitalized adults".)
SUMMARY AND RECOMMENDATIONS
●Indications for neuraxial anesthesia – Neuraxial anesthesia (NA; ie, spinal, epidural, and combined spinal-epidural techniques) are most commonly used for lower extremity and lower abdominal surgery. An epidural catheter can also be used to provide anesthesia and/or analgesia for thoracic surgery. (See 'Use of neuraxial anesthesia' above.)
Decisions on whether to use general and neuraxial anesthesia must be made on a case by case basis, considering factors such as patient, surgeon, and anesthesiologist preference, type of surgical procedure, patient comorbidities, and plan for postoperative analgesia. (See 'General versus neuraxial anesthesia' above.)
●Preanesthesia evaluation – The preanesthesia evaluation for patients in whom NA is considered should focus on those conditions that may alter the physiologic response to NA or increase the risk of complications, including coagulopathy, systemic or local infection, preload dependent cardiac lesions, hypovolemia, spine abnormalities, progressive neurologic disease, and intracranial mass lesions with intracranial hypertension. (See 'Preoperative evaluation' above.)
●Physiologic effects – The physiologic effects of neuraxial anesthesia are the result of blockade of sympathetic, motor, and sensory nerves, the compensatory reflexes, and unopposed parasympathetic tone.
•Hypotension and bradycardia are the most important and common cardiovascular effects of NA. (See 'Cardiovascular' above.)
•Mid to high neuraxial block can paralyze accessory muscles of respiration and can impair active exhalation and cough. (See 'Pulmonary' above.)
•Patients often appear and feel sedated during neuraxial anesthesia. Sedative medication should be administered in reduced, incremental doses, titrated to effect. (See 'Central nervous system' above.)
•Similar to general anesthesia, hypothermia can occur during NA. Temperature should be monitored and active warming devices should be used to maintain normothermia. (See 'Thermoregulation' above.)
•The sympathetic block associated with NA can result in parasympathetic predominance of innervation to abdominal viscera, resulting in a contracted gut, relaxed sphincters, and normal peristalsis. (See 'Gastrointestinal' above.)
●Complications – Serious and permanent complications of NA are very rare.
•High spinal block (cervical spinal nerves or higher) consists of a rapidly ascending sympathetic, sensory, and motor block with associated bradycardia, hypotension, dyspnea, and difficulty with swallowing or phonation. Unconsciousness can occur as well. (See 'High or total spinal anesthesia' above.)
•Unintentional subdural injection of local anesthetic solution, which usually occurs during attempted epidural anesthesia, can cause a patchy block, with a higher sensory level and more extensive motor block than expected. (See 'Subdural injection' above.)
•Direct trauma to nerve tissue is rare during neuraxial anesthesia; paresthesias occur frequently during NA procedures, but persistent paresthesias are rare. (See 'Nerve injury' above.)
•Localized point tenderness at the injection site may be present for several days after a neuraxial procedure, but there is no evidence that neuraxial procedures result in long-term backache. (See 'Back pain' above.)
•Postdural puncture headache can occur after spinal anesthesia, or after unintentional dural puncture during epidural anesthesia. (See 'Postdural puncture headache' above.)
•NA is associated with postoperative urinary retention, with a duration that is directly related to the duration of the neuraxial block. (See 'Urinary retention' above.)
•Transient neurologic symptoms (TNS) comprise a syndrome of pain and/or dysesthesia in the buttocks or lower extremities after spinal anesthesia. TNS occurs most commonly after spinal anesthesia with lidocaine or mepivacaine. (See 'Transient neurologic symptoms' above.)
•Local anesthetic systemic toxicity (LAST) is a rare but potentially lethal event that can include central nervous system and/or cardiovascular effects ranging from minor manifestations to major events including seizures and asystole. LAST is much less common after spinal anesthesia than after epidural anesthesia. (See 'Local anesthetic systemic toxicity' above.)
•Spinal epidural hematoma (SEH) can rarely occur after an NA procedure if a vascular structure is punctured with a needle or catheter, and appears to be more common with epidural than with spinal anesthesia. Risk factors for SEH include coagulopathy, advanced age, and difficult NA procedures. (See 'Spinal-epidural hematoma (SEH)' above.)
•Strict aseptic technique should be followed during NA procedures, to reduce the risk of CNS infection. (See 'Infection' above.)
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