65: Spinal Anesthesia

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CHAPTER 65 Spinal Anesthesia

James Duke, MD, MBA

1 What are the advantages of spinal anesthesia over general anesthesia?

image The metabolic stress response to surgery and anesthesia is reduced by subarachnoid block (SAB).
image Particularly in elective hip surgery, there may be up to a 20% to 30% reduction in blood loss.
image SAB decreases the incidence of venous thromboembolic complications by as much as 50%.
image Pulmonary compromise appears to be less.
image Endotracheal intubation is avoided.
image Mental status can be followed.

2 What are the usual doses of common local anesthetics used in spinal anesthesia and the duration of effect?

See Table 65-1.

TABLE 65-1 Local Anesthetic Dosing for Spinal Anesthesia

image

3 Where are the principal sites of effect of spinal local anesthetics?

The principal sites are the spinal nerve roots and spinal cord. Interestingly nerve roots may have different anatomic configurations (rootlets vs. roots); and there may be variability in fascial compartmentalization of the roots, especially between the dorsal and ventral nerve roots, accounting in part for differences between motor and sensory blockade.

4 What factors determine the termination of effect?

Resorption of the agent from the cerebrospinal fluid (CSF) into the systemic circulation limits duration. Addition of a vasoconstrictor that slows resorption prolongs duration of effect. Vasoconstrictor efficacy decreases with local anesthetics with intrinsic longer durations of effect.

5 Describe the factors involved in distribution (and extent) of conduction blockade

image Patient characteristics include height, position, intra-abdominal pressure, anatomic configuration of the spinal canal, and pregnancy. There is great interindividual variation in lumbosacral CSF volumes; magnetic resonance imaging has shown volumes ranging from 28 to 81 ml. Lumbar CSF volumes correlate well with the height and regression of the block. With the exception of an inverse relation with weight, no external physical measurement reliably estimates lumbar CSF volumes. CSF volumes are also reduced in pregnancy.
image Needle direction and site when anesthetic is injected are important.
image The total injected dose of local anesthetic is important, whereas the volume or concentration of injectant is unimportant.
image The baricity of the local anesthetic solution is important. Baricity is defined by the ratio of the density of the local anesthetic solution to the density of CSF. A solution with a ratio >1 is hyperbaric and tends to sink with gravity within the CSF. An isobaric solution has a baricity of 1 and tends to remain in the immediate area of injection. A ratio <1 is a hypobaric solution, which rises in the CSF.

6 At what lumbar levels should a spinal anesthetic be administered? What structures are crossed when performing a spinal block?

The selected level should be below L1 in an adult and L3 in a child to avoid needle trauma to the spinal cord. As an anatomic landmark, the L3-L4 interspace is located at the line intersecting the top of the iliac crests. Either a midline or paramedian approach can be used. The anatomic layers passed through include skin, subcutaneous structures, supraspinous ligament, interspinous ligament, ligamentum flavum, dura mater, and arachnoid membrane.

7 What are the most common complications of spinal anesthesia?

Common complications include hypotension, bradycardia, increased sensitivity to sedative medications, nausea and vomiting (possibly secondary to hypotension), postdural puncture headache (PDPH), and residual back pain and paresthesias (usually associated with the use of lidocaine. Less frequent but more ominous complications include nerve injury, cauda equina syndrome, meningitis, total spinal, and hematoma/abscess formation. Particular issues associated with these complications are discussed subsequently.

8 What are the physiologic changes and risk factors found with subarachnoid block–associated hypotension?

Hypotension occurs as a result of a loss of sympathetically mediated peripheral vascular resistance. Arterial and central venous pressure decrease with only mild decreases in heart rate, stroke volume, and cardiac output. Hypovolemia, age greater than 40 years, sensory level greater than T5, baseline systolic blood pressure below 120 mm Hg, and performance of the block at or above L3-L4 increase the incidence of hypotension. Hypotension (and possibly decreased cerebral blood flow) may be responsible for nausea and vomiting observed with SAB. Patients should receive a bolus of crystalloid or colloid (250 to 1000 ml) before SAB. Because of the pattern of distribution, colloid is more effective, although more expensive. Volume expansion and intravenous sympathomimetics usually reverse hypotension should it occur. Trendelenburg position may raise the level of blockade and should be used with caution and vigilance. Volume loading should also be used cautiously in patients with limited cardiac reserve. In these patients, as the block recedes, vascular tone increases, raising the central blood volume, which may precipitate heart failure. Strategies to create a unilateral block may also decrease the hypotension associated with SAB.

9 What are the etiology and risk factors for subarachnoid block–associated bradycardia?

Bradycardia may occur secondary to unopposed vagal tone from a high sympathectomy, blockade of the cardioaccelerator fibers (T1-T4), and the Bezold-Jarisch reflex (slowing of the heart rate secondary to a decrease in venous return). Patients with underlying increased vagal tone (children and adults with resting heart rates <60) are at increased risk. Bradycardia may be treated with anticholinergic agents (atropine) or β-adrenergic agonists such as ephedrine.

10 Why are patients who have received spinal anesthetics especially sensitive to sedative medications? What is deafferentation?

Caplan and associates (1988) published a landmark review of healthy patients who, while undergoing elective surgery using spinal anesthesia, experienced a sleeplike state without spontaneous verbalization followed by respiratory and cardiac arrest. Despite the fact that these were witnessed arrests, the patients were difficult to resuscitate and either died or had severe neurologic deficits. Subsequently it has been determined that patients receiving spinal anesthetics are especially sensitive to sedative medications. The cause of this may be loss of peripheral input into the reticular activating system (RAS), that part of the brainstem responsible for maintaining arousal. It appears that motor spinal fibers and afferent sensory input into the RAS contribute to wakefulness and this input is diminished by spinal anesthesia, rendering the patient prone to oversedation. Spinal (and epidural) anesthesia increases the hypnotic potential of midazolam, isoflurane, sevoflurane, and thiopental.

11 Review the clinical features of total spinal anesthesia

Total spinal anesthesia results from local anesthetic depression of the cervical spinal cord and brainstem. Signs and symptoms include dysphonia, dyspnea, upper extremity weakness, loss of consciousness, pupillary dilation, hypotension, bradycardia, and cardiopulmonary arrest. Early recognition is the key to management. Treatment includes securing the airway, mechanical ventilation, volume infusion, and pressor support. The patient should receive sedation once ventilation is instituted and the hemodynamics stabilize. The effects of total spinal anesthesia usually resolve by the conclusion of the surgical procedure, and, unless otherwise contraindicated, the patient can be extubated.

12 If a patient has a cardiac arrest while having a subarachnoid block, how should resuscitative measures differ from standard advanced cardiac life support protocols?

Since these patients have loss of sympathetic tone and decreased peripheral vascular resistance, rapidly escalating doses of epinephrine will be necessary to increase peripheral resistance and coronary artery perfusion. Until effective, consider doubling each subsequent dose of epinephrine (e.g., 1 mg, then 2 mg, then 4 mg, and so on).

13 What are the clinical features of a postdural puncture headache and the treatment?

A potentially severe headache may develop after dural puncture, presumably secondary to the rent in the dura and resultant CSF leak, which may cause traction on the meninges and cranial nerves. The headache typically occurs soon after the puncture. It is characteristically intense, often localized to the occipital region and neck, and worse in the upright position. Diplopia or blurred vision may occur. Newer pencil-point needles have reduced the incidence of PDPH to about 1%. Women, younger patients, parturients, and obese patients tend to have a higher incidence of PDPH. Hydration, analgesics, and caffeine mostly temporize the headache; epidural blood patching (administration of about 20 ml) has >75% success rate. It is important to rule out severe hypertension or central nervous system maladies as a cause of the symptoms before assuming that the patient has a PDPH.

14 What is the risk of neurologic injury after spinal anesthesia?

Direct trauma to nerve fibers may occur from the spinal needle and may be heralded by a paresthesia, for which the spinal needle should be redirected. Hematoma formation from epidural venous bleeding (from direct trauma or coagulopathy) or abscess formation is suggested by persistent neurologic deficits or severe back pain. Early recognition and management are imperative to avoid permanent neurologic sequelae. In patients who have received any medication with anticoagulant potential, it is important not to attribute persistent neurologic deficits to residual effects of local anesthesia. Adhesive arachnoiditis has been reported and is presumably caused by injection of an irritant into the subarachnoid space.

15 What is the effect of spinal anesthesia on temperature regulation?

Because patients become vasodilated and cannot shiver in response to decreases in body temperature, hypothermia is a risk. Curiously, patients may not perceive cold because the vasodilated extremities are warm. In addition, hypothermia may not be detected by the clinician because temperature monitoring is not widely practiced in patients receiving regional anesthesia and it would be necessary to monitor a site that reflects core body temperature such as the tympanic membrane. Patients receiving regional anesthetics should also be warmed using heated forced air devices.

16 What are contraindications to spinal anesthesia?

Absolute contraindications include local infection at the puncture site, bacteremia, severe hypovolemia, coagulopathy, severe stenotic valvular disease, infection at the site of the procedure, and intracranial hypertension. Relative contraindications include progressive degenerative (demyelinating) neurologic disease (e.g., multiple sclerosis), low back pain, and sepsis.

17 Review the current recommendations for administering regional anesthesia to patients with altered coagulation caused by medications

The American Society of Regional Anesthesia and Pain Medicine has defined the risks of regional anesthesia in the anticoagulated patient. This and Questions 18 and 19 summarize key points:

image Patients on thrombolytic/fibrinolytic therapy should not receive regional anesthesia except in the most extreme circumstances. Patients who have had regional anesthesia before such therapy has been instituted should receive serial neurologic checks.
image Oral anticoagulants should be stopped 4 to 5 days before the planned procedure, and prothrombin time/International Normalized Ratio normalized.
image Concurrent administration of medications that affect bleeding by different mechanisms (e.g., antiplatelet drugs, aspirin, heparin) complicates the decision to perform regional anesthesia; therefore decisions must be individualized. Patients taking only nonsteroidal antiinflammatory drugs can safely have either single-shot or catheter regional anesthetics.
image Thrombocytopenia and an altered coagulation cascade are likely contraindications to regional anesthesia.

18 Should spinal (or epidural) anesthesia be performed when unfractionated heparin is administered?

image If heparin is to be administered, coexisting thrombocytopenia, antiplatelet medications, oral anticoagulants, and other bleeding dyscrasias suggest that regional techniques should be avoided.
image The subcutaneous administration of minidose unfractionated heparin is not contraindicated. but it is best to time performance of the block when the heparin effect is minimal. Similarly, a heparin dose should be held if it is scheduled soon after performance of the block.
image In vascular patients who will receive large doses of heparin, avoid regional techniques if other coagulopathies are present, delay heparin administration for at least 1 hour after the procedure, and time removal of the catheter for when heparin effect has diminished (1 hour before subsequent doses or 2 to 4 hours after the last dose). There are no data to guide in decision making should a bloody tap occur.
image Prolonged therapeutic anticoagulation may increase the risk of spinal hematoma, especially if other coagulation abnormalities coexist.

19 Should spinal (or epidural) anesthesia be performed when low-molecular-weight heparin is administered?

image Patients who have received low-molecular-weight heparin (LMWH) should be believed to have altered coagulation, and a single-shot spinal injection is the safest procedure for these patients. As in the case with unfractionated heparin, other factors that increase the likelihood of bleeding will increase the risk of spinal hematoma when LMWH is administered.
image Timing of the neuraxial procedure and dosing LMWH is extremely important, as is the dose of LMWH. Needle placement should occur at least 10 to 12 hours after an LMWH dose. Neuraxial procedures should be delayed for 24 hours when the patient is receiving larger LMWH doses: enoxaparin 1 mg/kg q12h, enoxaparin 1.5 mg/kg daily, dalteparin 120 units/kg q12h, dalteparin 200 units/kg daily, or tinzaparin 175 units/kg.
image A bloody spinal tap should not cause cancellation of the surgery but should delay administration of LMWH by 24 hours.
image If a patient is to have an epidural catheter for postoperative pain management and is also to receive LMWH after surgery, twice daily dosing has a greater risk of spinal hematoma formation than single daily dosing, and the benefits of an epidural catheter in a patient receiving twice-daily dosing should be weighed against the risks. Although some authorities are more aggressive, a safe practice is to delay the first dose for at least 24 hours after surgery, and a catheter should be removed a minimum of 10 to 12 hours after the last dose of LMWH.

20 What are the sites of action, benefits, and side effects of intrathecal opioids?

Opioids produce intense visceral analgesia and may prolong sensory blockade without affecting motor or sympathetic function. The major sites of action are the opiate receptors within the second and third laminae of the substantia gelatinosa in the dorsal horn of the spinal cord. Lipophilic agents such as fentanyl and sufentanil have a much more localized effect than the hydrophilic agents such as the hydrophilic opioid morphine. Fentanyl and sufentanil have a rapid onset of action and an effective duration greater than 6 hours. Morphine lasts 6 to 24 hours. Side effects include respiratory depression (which may occur late with hydrophilic agents), nausea, vomiting, pruritus, and urinary retention. Opioid antagonists or agonist/antagonists reverse the complications but if given in large doses may also reverse analgesia.

21 What is transient neurologic syndrome and its cause?

Transient neurologic syndrome (TNS) was first described in 1993. Common findings include pain or dysesthesias in the buttocks radiating to the dorsolateral aspect of the thighs and calves. The pain has been alternatively described as sharp and lancinating or dull, aching, cramping, or burning. Usually symptoms improve with moving about, are worse at night, and respond to nonsteroidal antiinflammatory drugs. The pain is moderate to severe in at least 70% of the patients with TNS and diminishes over time, resolving spontaneously within approximately a week in about 90% of those affected. It is extremely rare for pain to continue beyond 2 weeks. It is significant to note that no objective neurologic findings are encountered.

TNS is associated with the use of spinal lidocaine in the majority of cases, and its incidence, although variable in studies, probably averages about 15%. Much more rarely TNS has been associated with the use of bupivacaine, prilocaine, procaine, and mepivacaine. The concentration of lidocaine does not appear to be a factor (TNS has been observed with 5% hyperbaric and 2% isobaric lidocaine). There is no association with the presence of dextrose, opioids, epinephrine, or the baricity or osmolarity of the solution. Further, neither gender, weight, age, needle type, difficulty with, nor paresthesias during block placement are factors, although lithotomy positioning may have been a factor. Bupivacaine is not associated with TNS. Interestingly, pregnancy may protect against lidocaine-associated TNS.

KEY POINTS: Spinal Anesthesia image

1. Loss of afferent sensory and motor stimulation renders a patient sensitive to sedative medications secondary to deafferentation. For the same reason neuraxial anesthesia decreases the minimum alveolar concentration of volatile anesthetics.
2. Vagal predominance suggests that a patient may be at risk for cardiovascular collapse during neuraxial anesthesia.
3. Patients with sympathectomies from regional anesthesia require aggressive resuscitation, perhaps with unfamiliarly large doses of pressors, to reestablish myocardial perfusion after cardiac arrest.
4. Suspect TNS in a patient who has received a lidocaine spinal anesthetic and has postanesthetic complaints of pain in buttocks and dorsal lower extremities. Note that there are no objective neurologic findings with this syndrome.

22 Since lidocaine is associated with TNS, what would be an appropriate local anesthetic selection for an ambulatory procedure?

Bupivacaine administered in 5- to 7.5-mg doses will achieve peak sensory blocks in the midthoracic region with durations of sensory blockade of about 2 hours, and duration of motor blockade of about an hour and time to discharge may not be appreciably different than if lidocaine had been used. Doses of bupivacaine greater than 10 mg will result in delays in voiding. This may not necessarily delay discharge to home if there is not a history of difficulty voiding and the procedure was in a nonpelvic area. Bladder ultrasound has been used to identify patients requiring catheterization.

23 Can continuous spinal anesthesia be performed?

Continuous spinal anesthesia is a technique regaining popularity. In the early 1990s many cases of cauda equina syndrome were noted after inappropriate dosing of spinal microcatheters. It appeared that the lack of turbulence associated with injecting through microcatheters led to a pooling of local anesthetic caudad to the lumbar lordotic curve, leading to repeated and inappropriate dosing of local anesthetics.

Continuous spinal anesthesia is safe and effective using 18- to 22-G epidural needles and catheters (and improved, specially designed kits). The incidence of hypotension is less, as is the need to rescue with vasopressors. This technique allows for titration of local anesthetics to effect and has been successfully used in elderly patients, patients with aortic stenosis, and trauma patients. This is an attractive technique for the elderly because they tend not to develop PDPH despite dural punctures with large-gauge epidural needles.

Website image

American Society of Regional Anesthesia and Pain Management

http://www.asra.com

SUGGESTED READINGS

1. Caplan R.A., Ward R.J., Posner K., et al. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology. 1988;68:5-11.

2. Zaric D., et al. Transient neurologic symptoms after spinal anesthesia with lidocaine versus other local anesthetics: a systematic review of randomized, controlled trials. Anesth Analg. 2005;100:1811-1816.

3. Hocking G., Wildsmilth J.A.W. Intrathecal drug spread. Br J Anaesth. 2004;93:568-578.

4. Moen V., Dahlgren N., Irestedt L. Severe neurological complications after central neuraxial blockades in Sweden 1990–1999. Anesthesiology. 2004;101:950-959.

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