Spinal anesthesia - Questions:
33.
What are the common positions patients are placed in for
administration of a spinal anesthetic?
34.
What are some advantages and disadvantages of having a patient in a
sitting position during performance of a spinal anesthetic?
35.
Why might an anesthetist choose to administer a spinal with a patient
in the lateral decubitus position?
36.
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 interspace is located directly
above this line? What interspace is located directly below this line?
37.
What is the reason for placing a spinal anesthetic at a level below the
L2 vertebra?
38.
On what basis are spinal needles generally classified?
39.
Which characteristics of a spinal needle will result in the lowest
incidence of postdural puncture headache?
40.
What are the two approaches used for spinal anesthesia, and what are
their relative advantages and disadvantages?
41.
When a midline approach is chosen, what are the tissue planes that
will be traversed as the needle is advanced toward the subarachnoid space?
42.
What accounts for the “pop” the anesthetist may feel when advancing
a spinal needle into the subarachnoid space?
43.
How is subarachnoid placement of the spinal needle confirmed?
44.
How can the spinal needle be handled to stabilize the needle after
proper placement in the subarachnoid space is confirmed?
45.
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?
46.
What should be done if blood-tinged cerebral spinal fluid (CSF)
appears at the hub of the needle?
47.
Describe the lumbosacral (Taylor) approach. When is this approach
advantageous?
48.
What are the three factors that most influence the distribution of the
local anesthetic solution in cerebrospinal fluid after its administration into the
subarachnoid space?
49.
How is the baricity of a local anesthetic solution to be administered
into the subarachnoid space defined? Why is this clinically important?
50.
What are the two things that most influence the duration of a spinal
anesthetic?
51.
What is the baricity of the most commonly used spinal anesthetics?
What is added to local anesthetics for spinal anesthesia to make the solution
hyperbaric? What is the principal advantage of these solutions?
52.
What role does the contour of the vertebral canal play in anesthetic
distribution, and hence, level of spinal block?
53.
What is a “saddle block”?
54.
What situations might warrant use of a hypobaric solution?
55.
What are the relative advantages and disadvantages of isobaric
solutions?
56.
What is the purpose of adding a vasoconstrictor to the local anesthetic
solution used for spinal anesthesia? What is their mechanism of action?
57.
What are the two potentially useful effects derived from adding an
opioid to the local anesthetic used for spinal anesthesia? What is their mechanism of
action?
58.
How do spinal anesthetics regress during the recovery from spinal
anesthesia?
59.
What recent events have led to concern regarding the use of lidocaine
for spinal anesthesia? What are some modifications in practice that have been
suggested should lidocaine be used for this purpose?
60.
What is TNS, and what are the factors that increase the risk of its
occurrence following spinal anesthesia with lidocaine?
61.
List the rank order for the relative incidence of TNS with the following
local anesthetics used for spinal anesthesia: bupivacaine; chloroprocaine; lidocaine;
mepivacaine; prilocaine; and procaine.
62.
What are some important restrictions with respect to the anesthetic
solution if using chloroprocaine off-label for spinal administration?
63.
What are some distinguishing characteristics between bupivacaine
and tetracaine with respect to spinal anesthesia?
64.
What is the temporal order of blockade of the motor, sensory, and
sympathetic nerves after the administration of a spinal anesthetic?
65.
What is a useful way to gain an early indication of the level of spinal
anesthesia?
66.
How do the ultimate dermatomal levels of motor, sensory, and
sympathetic block compare during spinal anesthesia?
67.
How is the extent of motor block produced by a spinal anesthetic
generally assessed?
68.
What surface landmarks are used to determine the approximate level
of spinal anesthesia?
69.
What are some advantages and disadvantages of a continuous spinal
technique?
70.
Why were microcatheters used for spinal anesthesia withdrawn from
the U.S. market?
71.
What is the likely mechanism of injury associated with
microcatheters?
72.
Has removal of microcatheters eliminated the risk of neurologic
injury?
73.
What elements of the continuous spinal technique are important to
prevent neurologic injury?
74.
What dose of anesthetic should be used when repeating a spinal
because of a failed block?
75.
What are the physiologic effects on the respiratory system of an
appropriately instituted spinal anesthetic?
76.
What are some physiologic effects on the gastrointestinal tract and
the genitourinary system that result from a spinal anesthetic?
77.
What is the effect of spinal anesthesia on blood pressure and what
accounts for this effect?
78.
How is spinal anesthetic-induced hypotension treated?
79.
What is the effect of spinal anesthesia on heart rate, and what is
believed to be the underlying mechanism?
80.
How are spinal anesthetic-induced perturbations in heart rate
treated?
81.
What is the cause and typical onset of a postdural puncture headache?
82.
What is the hallmark feature of a postdural puncture headache?
83.
What are some of the other characteristic features of a postdural
puncture headache?
84.
What serious complications may result from a postdural puncture
headache?
85.
Which patients are most at risk for development of a postdural
puncture headache?
86.
What features of a spinal needle will impact the incidence of a
postdural puncture headache?
87.
What are some of the commonly used treatment options for a
postdural puncture headache?
88.
What are the likely predominant mechanism(s) by which an epidural
blood patch may relieve a postdural puncture headache?
89.
What is a “total spinal”?
90.
How should a total spinal be managed?
91.
What are two possible causes of nausea that present soon after the
administration of a spinal anesthetic?
92.
What might contribute to backache occurring in a patient who has
received a spinal for surgical anesthesia?
Spinal anesthesia - Answers
33.
Spinal anesthesia can be performed with the patient in the lateral
decubitus, sitting, or less commonly, the prone position. To the extent possible, the
spine should be flexed by having the patient bend at the waist and bring the chin
toward the chest, which will optimize the interspinous space and the interlaminar
foramen. (263)
34.
The sitting position encourages flexion and facilitates recognition of
the midline, which may be of increased importance in an obese patient. Because
lumbar cerebral spinal fluid (CSF) is elevated in this position, the dural sac is
distended, thus providing a larger target for the spinal needle. This higher pressure
also facilitates recognition of the needle tip within the subarachnoid space, as
heralded by the free flow of CSF. When combined with a hyperbaric anesthetic, the
sitting position favors a caudal distribution; the resultant anesthesia is commonly
referred to as a “saddle block.” However, in addition to being poorly suited for a
heavily sedated patient, vasovagal syncope can occur. (263)
35.
The lateral decubitus position is more comfortable and more suitable
for the ill or frail. It also enables the anesthetist to safely provide greater levels of
sedation. (263)
36.
A line drawn across the patient's back at the level of the top of the iliac
crests is generally considered to identify the L4 vertebral level. The interspace
palpated directly above this line would be L3-4, and the interspace palpated directly
below this line would be L4-5. However, this is not invariant, and not uncommonly,
use of this conceptual line will result in estimates that are inaccurate by as much as
two interspaces. (263)
37.
The caudal limitation of the spinal cord in an adult usually lies
between the L1 and L2 vertebrae. For this reason, spinal anesthesia is not ordinarily
performed above the L2-3 interspace. Nevertheless, some risk remains because the
spinal cord extends to the third lumbar vertebra in approximately 2% of adults.
(263)
38.
A variety of needles are available for spinal anesthesia and they are
generally classified by their size (most commonly 22 to 25 gauge) and the shape of
their tip. The two basic designs of spinal needles are (1) an open-ended (beveled or
cutting) needle and (2) a closed tapered-tip pencil-point needle with a side port.
(263, Figure 17-14)
39.
The incidence of postdural puncture headache varies directly with the
size of the needle, and it is also lower when a pencil-point (Whitacre or Sprotte)
rather than a beveled-tip (Quincke) needle is used. Consequently, a 24- or 25-gauge
pencil-point needle is usually selected when spinal anesthesia is performed on
younger patients in whom postdural puncture headache is more likely to develop.
(263, Figure 17-14)
40.
Spinal anesthesia can be accomplished using a midline or a
paramedian approach. The midline approach is technically easier, and the needle
passes through less sensitive structures, thus requiring less local anesthetic
infiltration to ensure patient comfort. However, the paramedian approach is better
suited to challenging circumstances when there is narrowing of the interspace or
difficulty in flexion of the spine. (264)
41.
As the spinal needle progresses toward the subarachnoid space, it
passes through the skin, subcutaneous tissue, supraspinous ligament, interspinous
ligament, ligamentum flavum, and the epidural space to reach and pierce the
dura/arachnoid. (264, Figure 17-3)
42.
The anesthetist may feel a characteristic “pop” just before accessing
the subarachnoid space as the spinal needle is being advanced. This “pop” is
produced by the spinal needle passing through the dura mater. (265)
43.
Subarachnoid placement of the spinal needle is confirmed by the
appearance of cerebrospinal fluid in the hub of the spinal needle. (265)
44.
After proper positioning in the subarachnoid space, the spinal needle
may be stabilized by holding the hub of the spinal needle between the
anesthesiologist's thumb and forefinger and resting the dorsum of the same hand on
the patient's back. When the spinal needle is held in this manner, it should remain
stabilized even with patient movement. (265)
45.
After the syringe containing the local anesthetic solution for
administration into the subarachnoid space is attached to the spinal needle, the
anesthetist typically aspirates back on the syringe to confirm continued
subarachnoid placement of the spinal needle tip. Confirmation is made by the
characteristic swirl in the syringe as cerebrospinal fluid enters the syringe and
mixes with the local anesthetic solution. The local anesthetic solution can then be
deposited into the subarachnoid space over approximately 3 to 5 seconds. After
completion of the deposition of the local anesthetic solution into the subarachnoid
space, cerebrospinal fluid can again be aspirated to verify delivery of the anesthetic.
The spinal needle and syringe should be removed together as a single unit, and the
antiseptic wiped from the patient's back. (265)
46.
Occasionally, blood-tinged CSF initially appears at the hub of the
needle. If clear CSF is subsequently seen, the spinal anesthetic can be completed.
Conversely, if blood-tinged CSF continues to flow, the needle should be removed and
reinserted at a different interspace. Should blood-tinged CSF still persist, the
attempt to induce spinal anesthesia should be terminated. (265)
47.
The Taylor approach (first described by Dr. John A. Taylor, a
urologist) describes the paramedian technique to access the L5-S1 interspace.
Though generally the widest interspace, it is often inaccessible from the midline
because of the acute downward orientation of the L5 spinous process. The spinal
needle is passed from a point 1cm caudad and 1cm medial to the posterior superior
iliac spine and advanced cephalad at a 55-degree angle with a medial orientation
based on the width of the sacrum. The Taylor approach is technically challenging
but very useful because it is minimally dependent on patient flexion for successful
passage of the needle into the subarachnoid space. (265, Figure 17-15)
48.
The three factors that most influence the distribution of local
anesthetic solution in the subarachnoid space are the baricity of the solution, the
contour of the spinal canal, and the position of the patient during, and for the first
few minutes after, its administration. (266)
49.
Local anesthetic solutions are classified as hypobaric, isobaric, and
hyperbaric based on their density relative to the density of CSF. Baricity is an
important consideration because it predicts the direction that local anesthetic
solution will move after injection into the CSF. (266)
50.
The two things that most influence the duration of a spinal anesthetic
are the particular drug selected and whether a vasoconstrictor, such as epinephrine
or phenylephrine, is present in the local anesthetic solution. (266)
51.
The most commonly selected local anesthetic solutions for spinal
anesthesia are hyperbaric (achieved by the addition of glucose), and their principal
advantage is the ability to achieve greater cephalad spread of anesthesia.
Commercially available hyperbaric local anesthetic solutions include 0.75%
bupivacaine with 8.25% glucose and 5% lidocaine with 7.5% glucose. Tetracaine is
formulated as a 1% plain solution and is most often used as a 0.5% solution with 5%
glucose, which is achieved by dilution of the anesthetic with an equal volume of 10%
glucose. (266)
52.
The contour of the vertebral canal is critical to the subarachnoid
distribution of hyperbaric local anesthetic solutions. For example, in the supine
horizontal position, the patient's thoracic kyphosis will be dependent relative to the
peak created by the lumbar lordosis. Anesthetic delivered cephalad to this peak will
thus move toward the thoracic kyphosis, which is normally around T6-8. Placing the
patient in a head-down (Trendelenburg) position will further accentuate this
cephalad spread of local anesthetic solution. (266, Figure 17-1)
53.
Hyperbaric local anesthetic solutions can be administered with the
patient seated and this position maintained during the initial movement of
anesthetic to deliberately encourage restricted sacral anesthesia (referred to as a
“saddle block,” reflecting sensory anesthesia of the area that would be in contact
with a saddle). (266)
54.
Hypobaric local anesthetic solutions find limited use in clinical
practice and are generally reserved for patients undergoing perineal procedures in
the “prone jackknife” position or undergoing hip arthroplasty where anesthetic can
“float up” to the nondependent operative site. (267)
55.
Isobaric local anesthetic solutions undergo limited spread in the
subarachnoid space, which may be considered an advantage or disadvantage
depending on the clinical circumstances. Because the distribution of local anesthetic
solutions is not affected by gravity, spinal anesthesia can be performed without
concern that the resultant block might be influenced by patient position. Isobaric
spinal anesthesia is particularly well suited for perineal or lower extremity
procedures, as well as surgery involving the lower part of the trunk (hip
arthroplasty, inguinal hernia repair). (267)
56.
Vasoconstrictors are frequently added to spinal anesthetic solutions
to increase the duration of spinal anesthesia. This is most commonly achieved by the
addition of epinephrine (0.1 to 0.2mg, which is 0.1 to 0.2mL of a 1:1000 solution) or
phenylephrine (2 to 5mg, which is 0.2 to 0.5mL of a 1% solution). Increased
duration of spinal anesthesia is believed to result from a reduction in spinal cord
blood flow, which decreases loss of local anesthetic from the perfused areas and
thus increases the duration of exposure to local anesthetic. However, with
epinephrine, there may be a small contribution as a result of its α2-adrenergic
analgesic activity. (267)
57.
Opioids may be added to local anesthetic solutions to enhance surgical
anesthesia and provide postoperative analgesia. This effect is mediated at the dorsal
horn of the spinal cord, where opioids mimic the effect of endogenous enkephalins.
Commonly, fentanyl (25μg) is used for short surgical procedures, and its
administration does not preclude discharge home on the same day. The use of
morphine (0.1 to 0.5mg) can provide effective control of postoperative pain for
roughly 24 hours, but it necessitates in-hospital monitoring for respiratory
depression. (267)
58.
During recovery from spinal anesthesia, regression of the anesthetic is
from the highest dermatome in a caudad direction. (266)
59.
Recent reports of major and minor complications associated with
spinal lidocaine have tarnished its reputation and jeopardize its continued clinical
use. Initial reports of permanent neurologic deficits were restricted to its use for
continuous spinal anesthesia, where extremely high doses were administered.
However, subsequent reports suggest that injury may occur even with the
administration of a dose historically recommended for single-injection spinal
anesthesia. These injuries have led to suggested modifications in practice that
include a reduction in the lidocaine dose from 100mg to 60 or 75mg and dilution of
the commercial formulation of 5% lidocaine with an equal volume of saline or CSF
before subarachnoid injection. (267)
60.
Lidocaine has been linked to the development of transient neurologic
symptoms or “TNS” (pain and/or dysesthesia in the back, buttocks, and lower
extremities) in up to a third of patients receiving this anesthetic for spinal
anesthesia. Factors that increase the risk for TNS in association with lidocaine spinal
anesthesia include patient positioning (lithotomy, knee arthroscopy) and outpatient
status. (268)
61.
With respect to TNS, the approximate rank order with respect to its
incidence is lidocaine>procaine, mepivacaine>prilocaine, bupivacaine,
chloroprocaine. (268)
62.
When using chloroprocaine off-lable for spinal administration, the
solution should be preservative-free, and epinephrine should not be used. (268)
63.
The recommended doses (5 to 20mg) and reported durations of
action (90 to 120 minutes) of bupivacaine and tetracaine are similar. However,
bupivacaine produces slightly more intense sensory anesthesia (as evidenced by a
lower incidence of tourniquet pain), whereas motor block with tetracaine appears
to be slightly more pronounced. The more important distinction between these local
anesthetics is that the duration of tetracaine spinal anesthesia is more variable and
more profoundly affected by the addition of a vasoconstrictor. Consequently,
tetracaine remains the most useful spinal anesthetic in circumstances in which a
prolonged block is sought. Unfortunately, the inclusion of a vasoconstrictor with
tetracaine results in a significant incidence of transient neurologic symptoms, as
opposed to the rarity of these symptoms when tetracaine is used alone. (268)
64.
Sympathetic nerves are blocked before both motor nerves and
sensory nerves after the administration of a spinal anesthetic. (268)
65.
A useful way to gain an early indication of the level of spinal
anesthesia is by testing the patient's ability to discriminate temperature in the
relevant dermatomes. For example, in an unblocked area, an alcohol sponge will
produce a cold sensation, whereas in the blocked areas the same alcohol sponge will
feel warm or neutral. (268)
66.
The dermatomal order of blockade produced by a spinal anesthetic,
from highest to lowest, is sympathetic, sensory, then motor. (268)
67.
Skeletal muscle strength can be tested by asking the patient to
dorsiflex the foot (S1-2), raise the knees (L2-3), or tense the abdominal rectus
muscles (T6-12). (269)
68.
The surface landmarks and their respective dermatomal level most
often used clinically are: nipple, T4-5; tip of xiphoid, T7; umbilicus, T10; inguinal
ligament, T12. (269)
69.
Inserting a catheter into the subarachnoid space increases the utility
of spinal anesthesia by permitting repeated drug administration as necessary to
maintain the level and duration of sensory and motor block. Anesthesia can thus be
provided for prolonged operations without delaying recovery. An added benefit is
the possibility of using lower doses of anesthetic. (With a catheter in place, smaller
doses can be titrated to the patient's response. In contrast, with the single-injection
technique, relatively high doses must be administered to all patients to ensure
successful anesthesia in a large percentage of cases.) However, use of large-bore
epidural needles and catheters for continuous spinal anesthesia poses significant
risk of postdural puncture headache. (269, Figure 17-4)
70.
Microcatheters (27 gauge and smaller) used for continuous spinal
anesthesia were withdrawn from clinical practice in the United States after reports
of cauda equina syndrome associated with their use. (269)
71.
It is likely that the injury associated with the use of microcatheters
resulted from the combination of maldistribution and repetitive injection of local
anesthetic solution. It is speculated that pooling of local anesthetic solution in the
dependent sacral sac produced a restricted block that was inadequate for surgery.
In response to inadequate anesthesia, injections were repeated and ultimately
achieved adequate sensory anesthesia, but not before neurotoxic concentrations
were reached in the caudal region of the subarachnoid space. It is possible that the
microcatheter contributed to this problem because the long narrow-bore tubing
creates resistance to injection and thereby results in a low flow rate that can
encourage a restricted distribution. (269)
72.
Removal of microcatheters from clinical practice has not eliminated
risk. The problem of maldistribution is not restricted to microcatheters or lidocaine,
and the same injuries have occurred with larger “epidural” catheters used for
continuous spinal anesthesia and other local anesthetics. (269)
73.
Guidelines for continuous spinal anesthesia include the following
elements:
▪
Insert the catheter just far enough to confirm and maintain placement
▪
Use the lowest effective local anesthetic concentration
▪
Place a limit on the dose of local anesthetic to be used
▪
Administer a test dose and assess the extent of any sensory and motor
block
▪
If maldistribution is suspected, use maneuvers to increase the spread
of local anesthetic (change the patient's position, alter the lumbosacral curvature,
switch to a solution with a different baricity)
▪
If well-distributed sensory anesthesia is not achieved before the dose
limit is reached, abandon the technique (269, Figure 17-4)
74.
Similar to continuous spinal anesthesia, single-injection spinal
anesthesia may fail due to local anesthetic maldistribution. This issue becomes
important when considering whether to repeat a “failed” spinal and, if so, the dose
of anesthetic that should be used for the second injection. In the past, it was
considered acceptable to readminister a “full dose.” However, if failure derives from
maldistribution of the local anesthetic solution, this strategy may introduce a risk of
injury. Accordingly, if a spinal anesthetic is to be repeated, it should be assumed that
the first injection was delivered in the subarachnoid space as intended, and the
combination of the two doses should not exceed that considered reasonable as a
single injection for spinal anesthesia. (270)
75.
Spinal anesthesia has little, if any, effect on resting alveolar ventilation
(arterial blood gases unchanged), but high levels of motor anesthesia that produce
paralysis of abdominal and intercostal muscles can lead to a decreased ability to
cough and expel secretions. Additionally, patients may complain of difficulty
breathing (dyspnea)—despite adequate ventilation—because of inadequate
sensation of breathing from the loss of proprioception from abdominal and thoracic
muscles. (270)
76.
Spinal anesthesia above T5 inhibits sympathetic nervous system
innervation to the gastrointestinal tract, and the resulting unopposed
parasympathetic nervous system activity results in contracted intestines and
relaxed sphincters. Similarly, the ureters are contracted, and the ureterovesical
orifice is relaxed.
77.
Hypotension (systolic blood pressure <90mm Hg) is estimated to
occur in about a third of patients receiving spinal anesthesia. This hypotension
results from a sympathetic nervous system block that (1) decreases venous return
to the heart and decreases cardiac output and/or (2) decreases systemic vascular
resistance. Modest decreases in systemic blood pressure are most likely due to
decreases in systemic vascular resistance, whereas large decreases in systemic
blood pressure are believed to be the result of decreases in venous return and
cardiac output. (270)
78.
Spinal anesthesia–induced hypotension is treated physiologically by
restoration of venous return to increase cardiac output. In this regard, the internal
autotransfusion produced by a modest head-down position (5 to 10 degrees) will
facilitate venous return without greatly exaggerating cephalad spread of the spinal
anesthetic. Adequate hydration before the institution of spinal anesthesia is
important for minimizing the effects of venodilation from sympathetic nervous
system block. Sympathomimetics with positive inotropic and venoconstrictor
effects, such as ephedrine (5 to 10mg IV), are often chosen as first-line drugs to
maintain perfusion pressure during the first few minutes after the institution of
spinal anesthesia. Phenylephrine (50 to 100μg IV) and other sympathomimetics that
increase systemic vascular resistance may decrease cardiac output and do not
specifically correct the decreased venous return contributing to the spinal
anesthesia–induced hypotension. Nevertheless, anesthesiologists have long used
phenylephrine successfully to treat decreases in systemic blood pressure associated
with spinal anesthesia. Furthermore, this drug is of particular value when
administration of ephedrine is associated with significant increases in heart rate.
(270)
79.
The heart rate does not change significantly in most patients during
spinal 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 this bradycardia
include the block of cardioaccelerator fibers originating from T1 through T4 and
decreased venous return (Bezold-Jarisch reflex). (271)
80.
Although bradycardia is usually of moderate severity and promptly
responsive to atropine or ephedrine, there are reports of precipitous bradycardia
and asystole in the absence of any preceding event. This catastrophic event can
probably be prevented through maintenance of preload and reversal of bradycardia
by aggressive stepwise escalation of treatment (ephedrine, 5 to 50mg IV; atropine,
0.4 to 1.0mg IV; epinephrine, 0.05 to 0.25mg IV), whereas the development of
profound bradycardia or asystole mandates immediate treatment with full
resuscitative doses of epinephrine. (271, Figure 17-16)
81.
Postdural puncture headache is a direct consequence of the hole in
the dura, which results in the loss of CSF at a rate exceeding its production. Loss of
CSF causes downward displacement of the brain and a resultant stretch on sensitive
supporting structures. Pain also results from distention of the blood vessels, which
must compensate for the loss of CSF because of the fixed volume of the skull. The
pain associated with postdural puncture headache generally begins 12 to 48 hours
after transgression of the dura, but it can occur immediately and has been reported
to occur up to several months after the event. (271, Figure 17-17)
82.
The hallmark of a postdural puncture headache is its postural
component: it appears or intensifies with sitting or standing and is partially or
completely relieved by recumbency. This feature is so distinctive that it is difficult to
consider the diagnosis in its absence. (271)
83.
Postdural puncture headache is typically occipital or frontal (or both)
and is usually described as dull or throbbing. Associated symptoms such as nausea,
vomiting, anorexia, and malaise are common. Ocular disturbances, manifested as
diplopia, blurred vision, photophobia, or “spots,” may occur and are believed to
result from the stretch of the cranial nerves, most commonly cranial nerve VI, as the
brain descends because of the loss of CSF. Although symptomatic hearing loss is
unusual, formal auditory testing will routinely reveal abnormalities. (271)
84.
Though generally a transient problem, loss of CSF may rarely result in
significant morbidity because caudal displacement of the brain can result in tearing
of bridging veins with the development of a subdural hematoma. (271)
85.
Age is one of the most important factors affecting the incidence of
postdural puncture headache. Children are at low risk, but after puberty, risk
increases substantially and then slowly declines with advancing age. Females have
long been suspected to be at increased risk, and a recent meta-analysis confirms this
impression, even in the absence of pregnancy. A previous history of postdural
puncture headache places one at increased risk for the development of this
complication after a subsequent spinal anesthetic. (272)
86.
The incidence of postdural puncture headache varies directly with the
diameter of the needle that has pierced the dura. The shape of the hole created by
the needle also has an impact on loss of CSF; this has led to the development of
“pencil-point” needle tips, which appear to spread the dural and arachnoid fibers,
and to produce less tear and a smaller hole for a given diameter needle. (272)
87.
Initial treatment of postdural puncture headache is usually
conservative and consists of bed rest, fluids, analgesics, and possibly caffeine. More
definitively, a blood patch can be performed in which 15 to 20mL of the patient's
blood, aseptically obtained, is injected into the epidural space. (272)
88.
The immediate effect is related to the volume effect of the injected
blood, whereas long-term relief is thought to occur from sealing or “patching” of the
dural tear. (272)
89.
Total spinal anesthesia is the term applied to excessive sensory and
motor anesthesia associated with a loss of consciousness. Apnea and loss of
consciousness are often attributed to ischemic paralysis of the medullary
ventilatory centers because of profound hypotension and associated decreases in
cerebral blood flow. However, loss of consciousness may also be the direct
consequence of local anesthetic effect above the foramen magnum inasmuch as
patients may lose or fail to regain consciousness despite restoration of systemic
blood pressure. Total spinal anesthesia is typically manifested soon after injection of
the local anesthetic solution into the subarachnoid space. (272)
90.
Treatment of high or total spinal anesthesia consists of maintenance
of the airway and ventilation, as well as support of the circulation with
sympathomimetics and intravenous fluid administration. Patients are placed in a
head-down position to facilitate venous return. An attempt to limit the cephalad
spread of local anesthetic solution in CSF by placing patients in a head-up position is
not recommended, because this position will encourage venous pooling and
potentially jeopardize cerebral blood flow, which may contribute to medullary
ischemia. Tracheal intubation is usually warranted and is mandated for patients at
risk of aspiration (e.g., pregnant women). It may be appropriate to administer an
intravenous induction drug before tracheal intubation if consciousness is retained
and cardiovascular status is acceptable. (273)
91.
Nausea occurring after the initiation of spinal anesthesia must alert
the anesthetist to the possibility of systemic hypotension sufficient to produce
cerebral ischemia. In such cases, treatment of hypotension with a sympathomimetic
should eliminate the nausea. Alternatively, nausea may occur because of a
predominance of parasympathetic activity as a result of selective block of
sympathetic nervous system innervation to the gastrointestinal tract. Similar to
bradycardia, the incidence of nausea and vomiting parallels the sensory level of
spinal anesthesia. (273)
92.
Backache presenting after spinal anesthesia is frequently due to the
position that was maintained during surgery. Patients with decreased sensory
perception induced by a spinal anesthetic may remain in positions for long periods
of time that may otherwise have been too uncomfortable, thus resulting in ligament
strain that might not have otherwise occurred. In support of this is the fact that
roughly 25% of patients complain of backache after surgery regardless of the
anesthetic technique. (273)
revision as physicians gain experience with the use of medications such as
clopidogrel in the perioperative period. (511)