Eixo

Question 1

1. What is the clinical significance of the curvatures of the spinal canal with respect to spinal and epidural anesthesia?

Answer 1

1. On a lateral view, the vertebral canal exhibits four curvatures, of which the thoracic convexity (kyphosis) and the lumbar concavity (lordosis) are of major importance to the distribution of local anesthetic solution in the subarachnoid space. In contrast, these curves have little effect on the spread of local anesthetic solutions in the epidural space. Scoliosis is of less importance to local anesthetic spread but can make needle insertion more awkward. (273–275)

Question 2

2. What are the rostral and caudal limitations of the spinal cord? What accounts for the disparity between the vertebral level and the spinal cord level?

Answer 2

2. The spinal cord is continuous with the medulla oblongata. In the fetus the spinal cord extends the entire length of the vertebral canal. However, because of disproportionate growth of neural tissue and the vertebral canal, the spinal cord generally terminates around the L3 vertebra at birth and at the lower border of the L1 vertebra in adults. As a further consequence of this differential growth, the spinal nerves become progressively longer and more closely aligned with the longitudinal axis of the vertebral canal. (274)

Question 3

3. What is the cauda equina, and what characteristic features are relevant to spinal anesthesia?

Answer 3

3. The cauda equina—so named because of its resemblance to a horse’s tail—is the collection of lumbar and sacral nerves that extend beyond the end of the spinal cord in the spinal canal. Each pair of spinal nerves exits via the intervertebral foramina at its respective vertebral column levels. The nerve roots of the cauda equina move relatively freely within the CSF, a fortunate arrangement that results in their being more likely to be displaced rather than pierced by an advancing needle. (274)

Question 4

4. What are the three meningeal layers surrounding the spinal cord?

Answer 4

4. The outermost meningeal layer surrounding the spinal cord, the dura mater, is a tough fibroelastic membrane that provides structural support. It originates at the foramen magnum and continues caudally to terminate between S1 and S4. Closely adherent to the inner surface of the dura lies the arachnoid membrane. Though far more delicate than the dura, the arachnoid serves as the major pharmacologic barrier preventing movement of the drug from the epidural to the subarachnoid space. The innermost layer of the spinal meninges, the pia, is a highly vascular structure closely applied to the cord that forms the inner border of the subarachnoid space. (274)

Question 5

5. Where is cerebrospinal fluid (CSF) relative to the meningeal layers? What are two interchangeable terms for this space?

Answer 5

5. CSF is contained between the pia and arachnoid meningeal layers. This space is consequently referred to as the subarachnoid space, but another term for this compartment is the intrathecal space. (274)

Question 6

6. What structures form the boundaries of the epidural space?

Answer 6

6. The epidural space is bounded cranially by the foramen magnum, caudally by the sacrococcygeal ligament, anteriorly by the posterior longitudinal ligament, laterally by the vertebral pedicles, and posteriorly by both the ligamentum flavum and vertebral lamina. (274)

Question 7

7. What structures are contained within the epidural space?

Answer 7

7. The epidural space is an irregular column containing spinal nerves, fat, lymphatics, and blood vessels. It is not a closed space but communicates with the paravertebral spaces by way of the intervertebral foramina. (274)

Question 8

8. What is the number of each type of vertebra composing the vertebral column?

Answer 8

8. The vertebral column is composed of 7 cervical vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae, as well as the 5 fused sacral and 4 fused coccygeal vertebrae. (275)

Question 9

9. What are the different characteristic features of the spinous processes and laminae of the thoracic and lumbar vertebrae? How does this impact on the clinical performance of neuraxial blocks?

Answer 9

9. The spinous processes in the thoracic area are angled more downward, which defines the angle required for placement and advancement of a needle intended to access the vertebral canal. The interlaminar space in the lumbar spine is wide, reflecting the fact that the lamina occupies only about half the space between adjacent vertebrae. In contrast, the interlaminar space is just a few millimeters wide at the level of the thoracic vertebrae. Again this offers less space to insert a needle to the epidural space, making thoracic needle placement more challenging. (275)

Question 10

10. How are the laminae of adjacent vertebrae connected?

Answer 10

10. The laminae of adjacent vertebrae are connected by the ligamentum flavum. The ligamentum flavum thickness, distance to the dura, and skin-to-dura distance vary with the area of the vertebral canal. (275)

Question 11

11. How are the tips of the spinous processes of adjacent vertebrae connected?

Answer 11

11. The tips of the spinous processes of adjacent vertebrae are connected by the supraspinous ligaments. (275)

Question 12

12. What passes through the intervertebral foramina?

Answer 12

12. The spinal nerves pass through the intervertebral foramina and supply a specific dermatome/osteotome/myotome. (275)

Question 13

13. As the nerves pass through the intervertebral foramen they become encased by the dura, arachnoid, and pia, forming what three components of a peripheral nerve?

Answer 13

13. The dura, arachnoid, and pia encasement of the peripheral nerve are the origins of the epineurium, perineurium, and endoneurium, respectively. (275)

Question 14

14. Where do the preganglionic nerves of the sympathetic nervous system originate, and what is their course of travel after leaving the spinal cord?

Answer 14

14. Preganglionic nerves of the sympathetic nervous system originate from the spinal cord at the T1 to L2 levels. From there they travel with the spinal nerves before separating to form the sympathetic chain at more distant sites such as the celiac plexus. (275)

Question 15

15. Describe the blood supply of the spinal cord. Which area of the cord is most vulnerable to ischemic insult?

Answer 15

15. The blood supply of the spinal cord arises from a single anterior and two paired posterior spinal arteries. The posterior spinal arteries emerge from the cranial vault and supply the dorsal (sensory) portion of the spinal cord. Because they are paired and have rich collateral anastomotic links from the subclavian and intercostal arteries, this area of the spinal cord is relatively protected from ischemic damage. This is not the case with the single anterior spinal artery that originates from the vertebral artery and supplies the ventral (motor) portion of the spinal cord. Ischemia affecting the anterior spinal artery may result in “anterior spinal artery syndrome,” characterized by motor paralysis and loss of pain and temperature sensation below the level affected. Ischemia can result from profound hypotension, mechanical obstruction, vasculopathy, hemorrhage, or any combination of these factors. (276)

Question 16

16. What is the artery of Adamkiewicz?

Answer 16

16. The anterior spinal artery receives branches from the intercostal and iliac arteries, but these branches are variable in number and location. The largest anastomotic link, the artery of Adamkiewicz, arises from the aorta between the T7 and L4 region. The vessel is highly variable but, most commonly, is on the left and enters the vertebral canal through the L1 intervertebral foramen. The artery of Adamkiewicz is critical to the blood supply of the lower two thirds of the spinal cord, and damage to it will produce anterior spinal artery syndrome as described earlier. (276)

Question 17

17. Describe venous drainage of the spinal cord.

Answer 17

17. There are communicating longitudinal and segmental radicular veins in the anterior and posterior spinal cord. These veins drain into the internal vertebral plexus in the medial and lateral components of the epidural space. They then drain into the azygous system. (276)

Question 18

18. What types of nerves fibers are blocked in neuraxial anesthesia, and in what temporal order does this occur?

Answer 18

18. The speed of neural blockade depends on the size, surface area, and degree of myelination of the nerve fibers exposed to the local anesthetic. The small preganglionic sympathetic fibers (B fibers, 1 to 3 µm, minimally myelinated) are most sensitive to local anesthetic blockade. The C fibers (0.3 to 1 µm, unmyelinated), which conduct cold temperature sensation, are blocked more readily than the A-delta pinprick sensation fibers (1 to 4 µm, myelinated). The A-beta fibers (5 to 12 µm, myelinated), which conduct touch sensation, are the last sensory fibers to be affected. The A-alpha motor fibers (12 to 20 µm, myelinated) are the most resistant to local anesthetic blockade. Regression of neural blockade follows the reverse order. (277)

Question 19

19. What is differential sensory block?

Answer 19

19. Differential sensory block describes how maximum block height in neuraxial anesthesia varies according to the sensory modality. The loss of sensation to cold (approximates sympathetic blockade) is 1 to 2 segments higher than the loss of sensation to pinprick, which is higher still than loss of sensation to touch. (278)

Question 20

20. What is the level of sympathetic nerve blockade compared to sensory nerve blockade in each spinal and epidural anesthesia?

Answer 20

20. The sympathectomy from neuraxial blockade is typically 2 to 6 dermatomes above the sensory block level with spinal anesthesia but is at the same level with epidural anesthesia. (278)

Question 21

21. What is the effect of neuraxial anesthesia on systemic vascular resistance, and why?

Answer 21

21. Neuraxial anesthesia commonly causes a decrease in systemic vascular resistance due to blockade of peripheral (T1-L2) sympathetic fibers as well as decreases in adrenal medullary catecholamine secretion. The degree of the vasodilatory change and corresponding hemodynamic change depends on both baseline sympathetic tone (higher sympathetic tone in elderly patients results in a greater hemodynamic change) and the extent of the sympathectomy (height of the block). (279)

Question 22

22. In healthy, normovolemic patients, what percent decrease in systemic vascular resistance is typically seen after neuraxial blockade if a normal cardiac output is maintained?

Answer 22

22. In healthy, normovolemic patients, systemic vascular resistance typically decreases by about 15% to 18% after neuraxial blockade if a normal cardiac output is maintained. (279)

Question 23

23. What is the effect of neuraxial anesthesia on cardiac output, and why?

Answer 23

23. Cardiac output is the product of heart rate and stroke volume. It is usually maintained but may decrease during neuraxial anesthesia. The heart rate does not change significantly in most patients during neuraxial anesthesia. However, in an estimated 10% to 15% of patients, significant bradycardia occurs. As with hypotension, the risk for bradycardia increases with increasing sensory levels of anesthesia. Speculated mechanisms for such bradycardia include the block of cardioaccelerator fibers originating from T1 through T4 and decreased venous return (Bezold-Jarisch reflex), especially in the presence of hypovolemia. (279)

Question 24

24. What is the effect of neuraxial anesthesia on coronary blood flow, and why?

Answer 24

24. Coronary blood flow decreases when mean arterial pressure decreases. However, patients with ischemic heart disease may benefit from a high thoracic block with improvement in global and regional myocardial function and reversal of ischemic changes. This is likely due to decreased myocardial oxygen demand and left ventricular afterload. (279)

Question 25

25. What is the effect of neuraxial anesthesia on the respiratory system, and why?

Answer 25

25. Neuraxial anesthesia has little, if any, effect on resting alveolar ventilation (arterial blood gases unchanged). Expiratory reserve volume decreases slightly, resulting in a decrease in vital capacity. High levels of motor anesthesia can produce paralysis of abdominal and intercostal muscles and lead to a decreased ability to cough and expel secretions. These changes are more marked in patients with respiratory disease or who are obese. Hypoperfusion of the respiratory centers due to severe hypotension and low cardiac output can result in respiratory arrest, but this situation is rare and reverses when hemodynamics are restored. (279)

Question 26

26. What is the effect of neuraxial anesthesia on the gastrointestinal tract, and why?

Answer 26

26. Neuraxial blockade from T6 to L1 inhibits sympathetic nervous system innervation to the gastrointestinal tract. This results in contracted intestines, hyperperistalsis, and relaxed sphincters due to unopposed parasympathetic nervous system activity. Nausea and vomiting may occur in as many as 20% of patients and can be treated with atropine if the level of blockade is high (T5). (279)

Question 27

27. What is the effect of neuraxial anesthesia on the renal system, and why?

Answer 27

27. Neuraxial anesthesia may decrease renal blood flow, but this is of little physiologic importance. (279)

Question 28

28. What are the common indications for spinal anesthesia?

Answer 28

28. Spinal anesthesia is commonly used for surgical procedures of a known duration involving the lower abdominal area, perineum, and lower extremities. It may also be indicated when the risks of general anesthesia are increased, such as in the presence of severe respiratory disease. (280)

Question 29

29. What are the common indications for epidural anesthesia?

Answer 29

29. Epidural anesthesia, like spinal anesthesia, can be used as the primary anesthetic for surgeries involving the lower abdomen or lower extremities, particularly if prolonged anesthesia is required. Epidural analgesia is more frequently used as a supplement to general anesthesia for thoracic and abdominal procedures where significant benefit derives from the ability to provide continuous postoperative analgesia. Similarly, continuous epidural anesthesia is very effective and widely used for the control of labor pain. (280)

Question 30

30. How do the hemodynamic effects of epidural anesthesia compare with those of spinal anesthesia?

Answer 30

30. Because the onset of sympathetic nervous system block is more gradual in epidural versus spinal anesthesia, the hemodynamic effects of epidural anesthesia are usually less marked. Incremental dosing of an epidural block may lessen some of the hemodynamic changes associated with neuraxial anesthesia. (280)

Question 31

31. What are the absolute contraindications to neuraxial anesthesia?

Answer 31

31. Absolute contraindications to neuraxial anesthesia include patient refusal, infection at the site of planned needle puncture, allergy to any of the drugs to be administered, and elevated intracranial pressure. (280)

Question 32

32. Does chronic back pain preclude performance of a neuraxial anesthetic?

Answer 32

32. Chronic back pain does not preclude performance of a neuraxial anesthetic. A neuraxial anesthetic may be avoided in these patients if they perceive a relationship between postoperative exacerbation of back pain and the block, even though they are not causally related. (280)

Question 33

33. Does spinal stenosis preclude performance of a neuraxial anesthetic?

Answer 33

33. Spinal stenosis does not preclude performance of a neuraxial anesthetic, although there is an association between the presence of spinal stenosis and nerve injury following neuraxial techniques. The contribution of surgical factors and natural history of the spinal disease in these cases is unknown. (280)

Question 34

34. Does previous spine surgery preclude performance of a neuraxial anesthetic?

Answer 34

34. Previous spine surgery does not preclude performance of a neuraxial anesthetic, although performance of the neuraxial block may be technically more difficult. In addition, spread of local anesthetic may be unpredictable or incomplete. (280)

Question 35

35. Does multiple sclerosis preclude performance of a neuraxial anesthetic?

Answer 35

35. Multiple sclerosis does not preclude performance of a neuraxial anesthetic, although these patients may be more sensitive to neuraxial local anesthetics and exhibit prolonged motor and sensory blockade. (280)

Question 36

36. Does spina bifida preclude performance of a neuraxial anesthetic?

Answer 36

36. Spina bifida does not preclude performance of a neuraxial anesthetic, although the potential for needle injury to the spinal cord may be increased. In addition, the spread of local anesthetic may be markedly variable. (280)

Question 37

37. Does aortic stenosis preclude performance of a neuraxial anesthetic?

Answer 37

37. Aortic stenosis does not preclude performance of a neuraxial anesthetic, although patients with a fixed cardiac output due to mitral stenosis, idiopathic hypertrophic subaortic stenosis, and aortic stenosis are intolerant of significant decreases in systemic vascular resistance commonly associated with neuraxial anesthesia. Though not an absolute contraindication, neuraxial blocks should not routinely be used in such cases, and patients should be evaluated on a case-by-case basis. (280)

Question 38

38. Do coagulation abnormalities preclude performance of a neuraxial anesthetic?

Answer 38

38. A spinal hematoma can be catastrophic, and has occurred in patients on low-molecular-weight heparin. The decision to insert a needle into the intrathecal or epidural space for a neuraxial block in patients with abnormal coagulation, either endogenous or produced by the administration of anticoagulants, must be based on a risk-benefit assessment and include discussion with the patient and the surgical team. Guidelines developed by the American Society of Regional Anesthesia (www.asra.com) are updated periodically based on evolving literature and changes in clinical practices. (281)

Question 39

39. Does infection preclude performance of a neuraxial anesthetic?

Answer 39

39. Infection does not preclude performance of a neuraxial anesthetic, although there is concern that an epidural abscess or meningitis might result from iatrogenic seeding during the procedure. Institution of appropriate antibiotic therapy and a demonstrated response before the block may decrease the risk for infection. Neuraxial techniques in patients with significant bacteremia or septic shock should be avoided. (281)

Question 40

40. What surface landmarks are used to determine the approximate level of spinal anesthesia?

Answer 40

40. The surface landmarks and their respective dermatomal levels most often used clinically are as follows: nipple, T4-T5; tip of xiphoid, T7; umbilicus, T10; and inguinal ligament, T12. (281)

Question 41

41. What are the three adjustable factors that most influence the distribution of the local anesthetic solution in CSF after its administration into the subarachnoid space?

Answer 41

41. Drug, patient, and procedural factors affect block height, but not all are controllable by the anesthesiologist. The three adjustable factors that most influence the distribution of local anesthetic solution in the subarachnoid space are the dose, baricity of the solution, and position of the patient during, and for the first few minutes after, its administration. (281)

Question 42

42. How is the baricity of a local anesthetic solution to be administered into the subarachnoid space defined? Why is this clinically important?

Answer 42

42. Baricity is defined as the ratio of density of a local anesthetic solution relative to the density of CSF (measured at 37° C). Local anesthetics are classified as hypobaric, isobaric, or hyperbaric relative to CSF. This is clinically important because, together with patient positioning and vertebral curvatures, it determines the direction of anesthetic spread in the CSF. (281)

Question 43

43. What is added to local anesthetics for spinal anesthesia to make the solution hyperbaric? What is the principal advantage of hyperbaric solutions?

Answer 43

43. Local anesthetic solutions are made hyperbaric for spinal anesthesia by the addition of dextrose. The principal advantage is the more predictable spread, with the solution moving to dependent regions of the spinal canal. In the supine position, hyperbaric solutions result in a higher level of block than isobaric or hypobaric solutions. (281)

Question 44

44. What is added to local anesthetics for spinal anesthesia to make the solution hypobaric? What is the principal advantage of hypobaric solutions?

Answer 44

44. Local anesthetic solutions are made hypobaric for spinal anesthesia by the addition of sterile water. The principal advantage is that the solution spreads to nondependent regions of the spinal canal. (281)

Question 45

45. What role does the contour of the vertebral canal play in hyperbaric spinal anesthetic distribution and, hence, level of spinal block?

Answer 45

45. The contour of the vertebral canal is critical to the distribution of hyperbaric local anesthetic. For example, in the supine horizontal position, the thoracic kyphosis is dependent relative to the lumbar lordosis peak, causing anesthetic delivered cephalad to move toward the thoracic kyphosis (typically around T6-T8). A head-down (Trendelenburg) position accentuates this cephalad spread. (281)

Question 46

46. What is a “saddle block”?

Answer 46

46. A saddle block involves the intrathecal injection of a low dose of hyperbaric local anesthetic with the patient seated, and maintaining that position for up to 30 minutes to restrict spread to the sacral region, resulting in anesthesia of areas in contact with a saddle. (284)

Question 47

47. What situations might warrant use of a hypobaric solution?

Answer 47

47. Hypobaric solutions are less commonly used but may be indicated in perineal procedures performed in the prone jackknife position or in elective/emergency hip surgery, where the anesthetic can float up to the nondependent operative site. For instance, in a fractured neck of femur, the patient need not lie on the painful fracture. (284)

Question 48

48. How do the patient factors of height, weight, and age affect the spread of spinal anesthesia and thus the spinal levels that are anesthetized (block height)?

Answer 48

48. In the normal adult height range, spinal level is not significantly influenced by height. However, obese patients may have decreased CSF volume leading to increased block height, and advanced age is associated with increased block height and nerve root sensitivity. (284)

Question 49

49. How long after the administration of intrathecal local anesthetic does patient position affect block height?

Answer 49

49. The spread of intrathecal local anesthetic appears to stabilize after 20 to 25 minutes, though patient position during the first few minutes is particularly influential. (284)

Question 50

50. How do spinal needle type, needle orientation, level of injection, injection rate, and barbotage affect block height of isobaric and hyperbaric solutions?

Answer 50

50. Spinal needle type, orientation, injection rate, and barbotage do not appear to affect block height significantly. However, with isobaric solutions, a more cephalad injection generally results in a higher block, whereas hyperbaric solution block height is less affected by the level of injection. (284)

Question 51

51. What are the factors that most influence the duration of a spinal anesthetic?

Answer 51

51. The duration is most influenced by the choice of local anesthetic, the dose, and the use of additives. (284)

Question 52

52. How are local anesthetics for spinal anesthesia most commonly classified? What are the common anesthetics in each group?

Answer 52

52. Local anesthetics for spinal anesthesia are classified by duration. Short- and intermediate-acting agents include lidocaine, chloroprocaine, prilocaine, and mepivacaine; long-acting agents include bupivacaine and ropivacaine. (285)

Question 53

53. What is the concern regarding the use of lidocaine for spinal anesthesia?

Answer 53

53. Lidocaine has been associated with permanent nerve injury and transient neurologic symptoms (TNS) in up to one third of patients receiving it intrathecally, leading to its decreased use in spinal anesthesia. (285)

Question 54

54. Which local anesthetics may be suitable for day case spinal anesthesia?

Answer 54

54. [Texto conforme original – o PDF especifica quais anestésicos são adequados para procedimentos ambulatoriais]. (285)

Question 55

55. Which local anesthetics may be suitable for long duration (1-3 hours) surgical procedures?

Answer 55

55. Bupivacaine, ropivacaine, and tetracaine (with additives) are used for longer duration spinal anesthesia. (285)

Question 56

56. What are the potentially useful effects derived from adding an opioid to the local anesthetic used for spinal anesthesia? What is their mechanism of action?

Answer 56

56. Opioids added intrathecally enhance the duration and quality of anesthesia and provide postoperative analgesia by acting primarily on the dorsal horn of the spinal cord. Lipid solubility affects their onset and duration. (286)

Question 57

57. What is the purpose of adding a vasoconstrictor to the local anesthetic solution used for spinal anesthesia? What is their mechanism of action?

Answer 57

57. Vasoconstrictors like epinephrine or phenylephrine prolong spinal anesthesia by causing α1-mediated vasoconstriction, reducing local anesthetic uptake; epinephrine may also provide direct analgesia via α2 receptor activation. (286)

Question 58

58. Which drugs other than vasoconstrictors may prolong spinal anesthesia?

Answer 58

58. Intrathecal clonidine and dexmedetomidine, acting on α2 receptors in the dorsal horn, can prolong motor and sensory block. Clonidine may prolong block by about 1 hour and dexmedetomidine is even more potent without significant hemodynamic compromise. (287)

Question 59

59. How are spinal needles classified?

Answer 59

59. Spinal needles are classified by gauge and tip design: either open-ended (beveled or cutting) or closed, pencil-point needles with a side port. (287)

Question 60

60. Which characteristics of a spinal needle will result in the lowest incidence of post–dural puncture headache?

Answer 60

60. The use of smaller gauge needles, particularly pencil-point designs (e.g., Whitacre or Sprotte) rather than beveled-tip (e.g., Quincke), reduces the incidence of post–dural puncture headache. (287)

Question 61

61. What is the advantage of performing spinal anesthesia in an awake patient?

Answer 61

61. An awake patient can provide immediate feedback if the needle is near neural tissue by reporting pain or paresthesia, aiding in preventing nerve injury. (288)

Question 62

62. What are the common positions patients are placed in for administration of a spinal anesthetic?

Answer 62

62. Spinal anesthesia can be performed with the patient in the lateral decubitus, sitting, or rarely prone position, with flexion of the spine to open the interspinous spaces. (288)

Question 63

63. What are some advantages and disadvantages of the sitting position during performance of a spinal anesthetic compared to lateral decubitus?

Answer 63

63. The sitting position helps in identifying the midline, beneficial in obese patients, but may be associated with vasovagal syncope and hypotension, whereas the lateral decubitus position may be more comfortable for frail patients and allows easier sedation. (288)

Question 64

64. What is the reason for placing a spinal anesthetic at a level below the L2 vertebra?

Answer 64

64. In adults, the spinal cord typically ends between L1 and L2; thus, to avoid cord injury, spinal anesthesia is generally performed below the L2-L3 interspace. (288)

Question 65

65. What vertebral level is crossed by a line drawn across the patient’s back at the level of the top of the iliac crests? What interspaces are located directly above and below this line?

Answer 65

65. A line at the top of the iliac crests typically corresponds to the L4 vertebral level, with the L3-L4 interspace above and the L4-L5 interspace below, although variations of up to two interspaces may occur. (288)

Question 66

66. What are the tissue planes that will be traversed as the needle is advanced toward the subarachnoid space in the midline?

Answer 66

66. The needle passes through the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, and epidural space before piercing the dura/arachnoid. (288)

Question 67

67. What accounts for the “pop” the anesthetist may feel when advancing a spinal needle into the subarachnoid space?

Answer 67

67. The characteristic “pop” is felt as the spinal needle passes through the dura mater. (288)

Question 68

68. How is subarachnoid placement of the spinal needle confirmed?

Answer 68

68. Subarachnoid placement is confirmed by the appearance of clear CSF in the needle hub. (288)

Question 69

69. After the syringe containing the local anesthetic solution for administration into the subarachnoid space is attached to the spinal needle, how can continued subarachnoid placement of the spinal needle be confirmed?

Answer 69

69. Continued subarachnoid placement is confirmed by aspirating and observing the characteristic swirl as CSF mixes with the local anesthetic solution. (288)

Question 70

70. How does the paramedian approach compare to the midline approach for spinal anesthesia? What are their relative advantages and disadvantages?

Answer 70

70. The midline approach is generally easier and involves fewer sensitive structures, while the paramedian approach is useful in patients with narrowed interspaces or calcified ligaments, as it avoids the supraspinous and interspinous ligaments. (288)

Question 71

71. What are some advantages and disadvantages of a continuous spinal technique?

Answer 71

71. Continuous spinal anesthesia allows incremental dosing and prolonged anesthesia, potentially improving hemodynamic stability; however, it carries a higher risk of post–dural puncture headache, especially with large-bore needles, and microcatheters, though smaller, have been linked to cauda equina syndrome. (288)

Question 72

72. What was the likely mechanism of cauda equina syndrome after continuous spinal techniques?

Answer 72

72. Cauda equina syndrome may result from maldistribution of local anesthetic due to pooling in the dependent sacral area when using high-resistance, low-flow microcatheters, leading to neurotoxicity. (288)

Question 73

73. After the intrathecal injection of local anesthetic, which sensation is tested for an early indication of the level of spinal anesthesia?

Answer 73

73. Loss of cold sensation is typically tested first (using ice or alcohol), followed by pinprick and touch sensations, and then motor strength. (289)

Question 74

74. What is the Bromage scale?

Answer 74

74. The Bromage scale is used to assess the degree of motor block in the lower extremities following spinal anesthesia. (289)

Question 75

75. How do spinal anesthetics regress during the recovery from spinal anesthesia?

Answer 75

75. Regression occurs in a caudad direction from the highest dermatome, with motor recovery preceding sensory recovery. (289)

Question 76

76. What drug factors affect the spread of epidural anesthesia?

Answer 76

76. The dose and volume of the local anesthetic, which together determine the total dose, are key factors affecting epidural spread. (289)

Question 77

77. What patient factors affect the spread of epidural anesthesia?

Answer 77

77. A smaller, less compliant epidural space (eg, in elderly or patients with spinal stenosis) and increased epidural pressure (eg, in pregnancy) enhance spread; body height has minimal impact within the normal range. (290)

Question 78

78. What procedural factors affect the spread of epidural anesthesia?

Answer 78

78. The level of injection is crucial; lumbar injections tend to produce preferential cephalad spread, while mid-thoracic injections yield more symmetric blocks. Patient positioning also influences block intensity on the dependent side. (290)

Question 79

79. What is the major site of action of local anesthetics administered epidurally?

Answer 79

79. The primary site of action is the spinal nerve roots, where the dura is relatively thin. (290)

Question 80

80. Why are procaine and tetracaine rarely used for epidural anesthesia?

Answer 80

80. Procaine and tetracaine are rarely used because they tend to produce unreliable and poor quality blocks, with tetracaine also being toxic in larger doses. (290)

Question 81

81. What are the characteristics of epidural prilocaine when administered in lower concentrations and when administered in large doses?

Answer 81

81. At lower concentrations (eg, 2% solution), epidural prilocaine produces predominantly sensory block with minimal motor block; in larger doses, it may cause methemoglobinemia. (290)

Question 82

82. How do chloroprocaine, lidocaine, and mepivacaine compare in their onset time and duration of action after epidural administration?

Answer 82

82. Chloroprocaine has a short onset and duration, while mepivacaine and lidocaine have similar short onset times with intermediate durations of action. (290)

Question 83

83. Does epidural lidocaine cause transient neurologic symptoms (TNS)?

Answer 83

83. Epidural lidocaine does not cause TNS, unlike its intrathecal use. (290)

Question 84

84. How are bupivacaine and ropivacaine similar and different after epidural administration?

Answer 84

84. Both have similar onset and duration, but ropivacaine produces less motor block, allows for earlier recovery, and is less cardiotoxic than bupivacaine. (290)

Question 85

85. What are some potential advantages of adding epinephrine to the local anesthetic solution used for epidural anesthesia?

Answer 85

85. Adding epinephrine decreases vascular absorption, prolongs anesthesia and analgesia, and may help detect intravascular injection through associated heart rate changes, as well as providing direct analgesic effects via α2 receptor activation. (291)

Question 86

86. What are some potential advantages of adding opioids to the local anesthetic solution used for epidural anesthesia?

Answer 86

86. Epidural opioids enhance analgesia synergistically without prolonging motor block and reduce the required doses of both opioids and local anesthetics, thereby minimizing adverse effects. (291)

Question 87

87. How does the lipophilic nature of an opioid affect its mechanism of action when administered in the epidural space?

Answer 87

87. Lipophilic opioids, such as fentanyl, are rapidly absorbed into epidural fat and the systemic circulation, resulting in a shorter duration of action, whereas hydrophilic opioids, like morphine, remain longer in the epidural space for prolonged analgesia. (291)

Question 88

88. What are some potential advantages of adding clonidine or dexmedetomidine to the local anesthetic solution used for epidural anesthesia?

Answer 88

88. Clonidine and dexmedetomidine prolong sensory block, reduce local anesthetic and opioid requirements, and improve postoperative analgesia; clonidine may also decrease immune stress. (291)

Question 89

89. What are some potential advantages of adding bicarbonate to the local anesthetic solution used for epidural anesthesia?

Answer 89

89. Bicarbonate raises the pH, increasing the nonionized fraction of the anesthetic; however, clinical advantages in onset or block quality have not been clearly demonstrated. (292)

Question 90

90. What surface landmarks can be used to identify specific spinal process interspaces and guide placement of an epidural needle?

Answer 90

90. Landmarks include the intercristal line (typically at L4-L5), the C7 spinous process (vertebra prominens), and a line drawn between the inferior scapular margins (approximately T7). (292)

Question 91

91. What are the advantages and disadvantages of epidural catheters with multiple side orifices near the tip instead of a single end hole at the tip?

Answer 91

91. Catheters with multiple side orifices offer more uniform distribution of anesthetic and improved analgesia, but may increase the risk of cannulating an epidural vein, especially in parturients. (292)

Question 92

92. Is it acceptable to place an epidural injection after the induction of general anesthesia?

Answer 92

92. While adult guidelines recommend performing epidural injections awake to detect paresthesias, in pediatric patients heavy sedation or general anesthesia may be used because the benefits outweigh the risks. (292)

Question 93

93. What is the “loss-of-resistance” technique?

Answer 93

93. The loss-of-resistance technique involves attaching a syringe (with saline, air, or both) to the needle and slowly advancing it; a sudden loss of resistance indicates that the needle has entered the epidural space. (293)

Question 94

94. What are the advantages of using air or saline during the loss-of-resistance technique?

Answer 94

94. Saline is generally preferred over air because it reduces the risk of incomplete block, pneumocephalus, and air embolism, although it may make accidental dural puncture less apparent. (293)

Question 95

95. What is the “hanging-drop” technique?

Answer 95

95. The hanging-drop technique involves placing a drop of saline at the needle hub; as the needle enters the epidural space, the negative pressure draws the drop into the needle, confirming proper placement. (293)

Question 96

96. What is the technique used for placement of a catheter following identification of the epidural space?

Answer 96

96. Once the epidural space is identified, a catheter is advanced 4 to 6 cm beyond the needle tip; then the needle is withdrawn over the catheter with care not to dislodge it. (293)

Question 97

97. How does the Tsui test help confirm epidural catheter tip location?

Answer 97

97. The Tsui test uses an electrically conductive epidural catheter to deliver a low current that stimulates spinal nerve roots, with the resulting muscle twitch indicating proper catheter placement. (293)

Question 98

98. When might the paramedian epidural approach be beneficial over the midline approach?

Answer 98

98. In the thoracic region, where the spinous processes are steeply angled and closely approximated, the paramedian approach may be beneficial either primarily or as a rescue technique. (293)

Question 99

99. What is the purpose of a “test dose” for an epidural catheter?

Answer 99

99. A test dose is administered to detect inadvertent intrathecal or intravascular placement by observing for early signs of high block or cardiovascular changes. (294)

Question 100

100. What is “combined spinal-epidural” anesthesia, and what is its clinical use? What is epidural volume extension?

Answer 100

100. Combined spinal-epidural anesthesia involves concurrent placement of a spinal anesthetic and an epidural catheter, combining rapid onset with the ability to extend or supplement the block via the epidural route. Epidural volume extension refers to using incremental epidural boluses after a low-dose spinal injection to increase block height and improve hemodynamic stability. (294)

Question 101

101. What are some indications for caudal anesthesia?

Answer 101

101. Caudal anesthesia is most popular in pediatric anesthesia due to unpredictable spread in adults; in adults it is used mainly for chronic or cancer pain management and when the lumbar approach is not feasible. (295)

Question 102

102. How does the approach to caudal anesthesia compare to that of epidural anesthesia with respect to local anesthetic dose, position, and technique?

Answer 102

102. The approach is similar to epidural anesthesia, using the same local anesthetics, though approximately twice the lumbar dose may be needed. Patient positioning (lateral or prone with knees to chest) and the loss-of-resistance technique are used to confirm entry into the caudal epidural space, with a test dose to exclude intrathecal or intravascular placement. (295)

Question 103

103. How is the sacral hiatus identified?

Answer 103

103. The sacral hiatus is identified by palpating the sacral cornua adjacent to the unfused laminae of the fourth and fifth sacral vertebrae, with the sacrococcygeal ligament spanning the hiatus. (295)

Question 104

104. Describe the technique for caudal anesthesia.

Answer 104

104. After sterile preparation and local infiltration above the sacral hiatus, the needle is inserted at a 45-degree angle through the skin and sacrococcygeal ligament (felt as a distinct pop) until contact with the sacrum is made; the needle is then slightly withdrawn, the angle reduced, and advanced 1 to 2 cm into the caudal epidural canal, with proper placement confirmed by injecting 5 mL of air or saline while palpating the caudal region. (296)

Question 105

105. Where does the dural sac end?

Answer 105

105. The dural sac normally terminates at the level of S2, although in approximately 10% of individuals it extends beyond S2. (296)

Question 106

106. What are the potential complications that should be discussed with the patient before proceeding with a spinal or epidural anesthetic?

Answer 106

106. Complications include rare but serious events such as nerve damage, bleeding, and infection, as well as more common issues like post–dural puncture headache, nausea, vomiting, and the possibility of a failed block. (296)

Question 107

107. What are factors associated with paraplegia following neuraxial anesthesia?

Answer 107

107. Paraplegia, although extremely rare, can result from direct needle trauma, neurotoxicity of the injectate, preservatives or additives causing adhesive arachnoiditis, or profound hypotension leading to anterior spinal artery syndrome; an epidural hematoma may also compress the cord. (296)

Question 108

108. What are factors associated with cauda equina syndrome following neuraxial anesthesia?

Answer 108

108. Cauda equina syndrome has been associated with exposure to large doses of local anesthetic, either as a single concentrated injection (eg, 5% lidocaine) or through prolonged exposure from a continuous infusion via a small-gauge catheter. (296)

Question 109

109. What are risk factors associated with epidural hematoma following neuraxial anesthesia?

Answer 109

109. Risk factors include difficult or traumatic needle or catheter insertion, coagulopathy, advanced age, and female gender. (296)

Question 110

110. What are some signs and symptoms of an epidural hematoma?

Answer 110

110. Signs include radicular back pain, unexpected prolonged motor blockade, and bladder or bowel dysfunction, indicating a space-occupying lesion compressing the spinal cord that requires emergent imaging and intervention. (296)

Question 111

111. What are factors associated with nerve injury following neuraxial anesthesia?

Answer 111

111. Factors include radicular pain or paresthesia during the procedure and the use of epidural or combined spinal-epidural techniques. (296)

Question 112

112. What are factors associated with post–dural puncture headache following neuraxial anesthesia?

Answer 112

112. Factors include patient age, sex, pregnancy, needle diameter, bevel direction, multiple punctures, and the needle tip design; noncutting, pencil-point needles reduce the risk. (296)

Question 113

113. What is the cause and typical onset of a post–dural puncture headache?

Answer 113

113. It is caused by CSF leakage through the dural puncture, leading to brain sag and traction on pain-sensitive structures; symptoms typically begin within 3 days, with about 66% occurring within 48 hours. (296)

Question 114

114. What are the signs and symptoms of a post–dural puncture headache?

Answer 114

114. The headache is usually frontal or occipital, worsens with upright posture, and improves when supine; associated symptoms may include nausea, vomiting, neck pain, dizziness, tinnitus, diplopia, hearing loss, and in severe cases, cranial nerve palsies or seizures. (297)

Question 115

115. What are the treatment options for a post–dural puncture headache?

Answer 115

115. Initial treatment is conservative (bed rest, hydration, caffeine, oral analgesics) with most cases resolving within 7 days; if unsuccessful, an epidural blood patch (up to 20 mL) may be performed, with a second patch possible after 24–48 hours if needed. (297)

Question 116

116. What are transient neurologic symptoms (TNS)? What are factors associated with TNS following neuraxial anesthesia?

Answer 116

116. TNS are characterized by pain or dysesthesia in the buttocks and lower extremities without neurologic deficits, typically occurring within 24 hours of spinal anesthesia; factors include use of concentrated lidocaine or mepivacaine, addition of dextrose or phenylephrine, higher osmolarity, and the lithotomy position. (297)

Question 117

117. What are factors associated with hypotension following neuraxial anesthesia?

Answer 117

117. Factors include a high block (T5 or higher), age 40 or older, baseline systolic BP under 120 mm Hg, combined spinal and general anesthesia, spinal puncture at or above L2-L3, and the addition of phenylephrine; other factors include alcoholism, hypertension history, increased BMI, and urgency of surgery. (298)

Question 118

118. What are factors associated with bradycardia following neuraxial anesthesia?

Answer 118

118. Factors include a baseline heart rate under 60 bpm, age younger than 37, male gender, nonemergency status, use of β-blockers, and prolonged surgery duration. (298)

Question 119

119. What are factors associated with cardiac arrest following neuraxial anesthesia?

Answer 119

119. Cardiac arrest is rare and is primarily associated with hypoxemia and oversedation, occurring more frequently with spinal than epidural anesthesia. (298)

Question 120

120. What are factors associated with respiratory depression following neuraxial anesthesia?

Answer 120

120. Respiratory depression is mainly related to the dose-dependent use of neuraxial opioids, with rostral spread affecting brainstem respiratory centers; risk increases with age and concurrent sedative use. (298)

Question 121

121. What are some infections that can occur following neuraxial anesthesia, and what are some associated factors?

Answer 121

121. Infections such as bacterial meningitis and epidural abscess can occur; risk factors include systemic infection, diabetes, immunocompromise, and prolonged catheter duration, with epidural-related infections being about twice as common as spinal ones. (298)

Question 122

122. What is the association between backache and epidural anesthesia in parturients?

Answer 122

122. There is no association between new-onset backache and epidural anesthesia in parturients up to 6 months postpartum. (298)

Question 123

123. What are factors associated with nausea and vomiting following neuraxial anesthesia?

Answer 123

123. Factors include opioid exposure (activating the chemoreceptor trigger zone), hypotension, unopposed parasympathetic activity causing hyperperistalsis, high block level (T5 or higher), a baseline heart rate over 60 bpm, and a history of motion sickness. (298)

Question 124

124. What is the cause of urinary retention following neuraxial anesthesia?

Answer 124

124. Urinary retention results from blockade of the S2, S3, and S4 nerve roots, leading to diminished detrusor muscle function and reduced urgency sensation. (298)

Question 125

125. How can pruritus following neuraxial anesthesia be treated?

Answer 125

125. Pruritus from intrathecal opioids may be managed with naloxone, naltrexone, or nalbuphine; ondansetron and propofol have also been used. (299)

Question 126

126. How can the risk of shivering following neuraxial anesthesia be reduced?

Answer 126

126. The risk of shivering can be minimized by adding neuraxial opioids (especially fentanyl or meperidine), prewarming the patient with a forced air warmer, and avoiding cold epidural or IV fluids. (299)

Question 127

127. How can the risk of unintentional intravascular injection of local anesthetic during epidural anesthesia be reduced?

Answer 127

127. Strategies include positioning the patient laterally (especially in obstetric cases), preinjecting fluid, using a single-orifice catheter, limiting catheter advancement to less than 6 cm, aspirating before dosing, and administering the anesthetic incrementally. (299)

Question 128

128. What are the clinical characteristics of unintentional subdural injection during epidural anesthesia?

Answer 128

128. Unintentional subdural injection is characterized by a higher-than-expected sensory block with disproportionately less motor block, and it is relatively uncommon (occurring in less than 1% of epidural injections). (299)