Transcript Complications of Neuraxial Blockade

Soli Deo Gloria
COMPLICATIONS OF
NEURAXIAL BLOCKADE
Developing Countries Regional Anesthesia Lecture Series
Lecture 13
Daniel D. Moos CRNA, Ed.D.
U.S.A.
[email protected]
Disclaimer

Every effort was made to ensure that material and
information contained in this presentation are
correct and up-to-date. The author can not accept
liability/responsibility from errors that may occur
from the use of this information. It is up to each
clinician to ensure that they provide safe anesthetic
care to their patients.
Introduction
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Exaggerated physiological response
Associated with needle placement
Associated with catheter placement
Associated with medication toxicity
Medical Liability- In General
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Administration of regional anesthesia constitutes
18% of all claims in the US
64% are temporary and non disabling
13% involve death
10% permanent nerve injury
8% brain damage
4% are “other”
Medical Liability- Neuraxial Blockade
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76% of all claims were related to neuraxial
blockade
Epidural’s comprised 42%
Spinal’s comprised 34%
Caudal comprised 2%
The population most affected is the obstetric
population
Adverse or Exaggerated Physiological
Response Include:
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High neural blockade
Cardiac arrest
Urinary retention
Adverse or Exaggerated Physiological
Response
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This category is an extension of “normal”
physiologic manifestations.
The main point is vigilance and early treatment.
Treat hypotension early and do not let it progress
to cardiac arrest.
Knowledge, preparation, and anticipation can help
reduce adverse or exaggerated physiological
responses
High Neural Blockade
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Can occur with either spinal or epidural techniques
High Neural Blockade Causes
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Excessive doses of local anesthetic are administered
Failure to reduce dose in patients susceptible to
excessive spread (i.e. the elderly, pregnant, obese,
or short patients)
Unusual sensitivity
Unusual excessive spread
High Neural Blockade
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Constant monitoring of the patients vital signs and
block level are imperative
Use of alcohol wipes (to assess cold sensation) and/or
pinprick test will help
Incremental dosing is important with an epidural
With hyperbaric techniques you can change the
patients position to slow down the cephalad spread
(i.e. reverse Trendelenberg)
High Neural Blockade-Prevention
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Careful consideration in dosing your block
Anticipation of potential complications
Plan of action if complications occur
Continual monitoring of the patient as the block
progresses
High Neural Blockade- Initial Symptoms
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Dyspnea
Numbness and tingling of the upper extremities (i.e.
fingers)
Nausea generally precedes hypotension due to
hypoperfusion of the chemoreceptor trigger zone
Mild to moderate hypotension
High Neural Blockade- Initial Treatment
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Change position with hyperbaric technique
Stop the administration of local anesthetics with an
epidural technique
Supplemental oxygen
Open up the IV fluids
Treat hypotension with ephedrine or phenylephrine
Treat bradycardia
High Neural Blockade- Initial Treatment
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Choose your vasopressor carefully.
If patient is hypotensive and bradycardic then
ephedrine would be indicated
Ephedrine will increase heart rate as well as constrict
blood vessels
Phenylephrine can result in reflex bradycardia as it
constricts blood vessels
If patient is hypotensive and tachycardic or normal in
respect to heart rate then phenylephrine may be
indicated
High Neural Blockade- Initial Treatment
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Refractory hypotension and/or hypotension should
be treated rapidly with 5-10 mcg of epinephrine
High Neural Blockade- Spread to Cervical
Dermatomes Signs and Symptoms May Include:
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Severe hypotension
Bradycardia
Respiratory insufficiency including apnea
Unconsciousness
High Neural Blockade- Cervical
Dermatomes Treatment
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The A,B,C’s
Airway and breathing- supplemental oxygen,
maintain a patent airway, intubation, mechanical
ventilation
Circulation- aggressive intravenous fluid
administration, ephedrine, phenylephrine, epinephrine
Bradycardia should be treated with atropine
Dopamine infusions may help
High Neural Blockade- Cervical
Dermatomes Treatment
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Early and aggressive treatment may help avoid a
cardiac arrest!
Once patient has been stabilized and successfully
treated the decision to proceed is based on individual
circumstances
Considerations include time spent hypotensive,
indications of myocardial ischemia, etc.
The respiratory compromise associated with high
neural blockade are often transient
Cardiac Arrest Due to Neuraxial Blockade
Cardiac Arrest Due to Neuraxial Blockade
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Cardiac arrest can occur with either epidural or
spinal anesthesia
More common with spinal anesthesia and the
incidence may be as high as 1:1,500
Usually preceded by bradycardia
Can easily occur in the young and healthy
Cardiac Arrest Due to Neuraxial BlockadeKeys to Prevention
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Appropriate hydration (i.e. 1 liter to an average sized adult)must be administered within approximately 15 minutes since
the majority of crystalloid solution will leave the intravascular
space
Aggressively treat bradycardia, atropine, ephedrine,
epinephrine
Do not be fooled by the 26 year old marathon runnerpatients with a slow heart rate and high vagal tone are at risk
for cardiac arrest during spinal anesthesia
Total sympathectomy with unopposed vagal stimulation
Error on the conservative and treat the patient
Cardiac Arrest Due to Neuraxial BlockadeRisk Factors
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Baseline heart rate < 60 bpm
ASA class I
Use of Beta Blockers
Sensory level > T6
Prolonged P-R interval
Urinary Retention
Urinary Retention
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Due to blockade of S2-S4
Leads to a decrease in bladder tone and inhibition
of normal voiding reflex
Neuraxial opioids may contribute to urinary
retention
More common in elderly men and those with a
history of benign prostatic hypertrophy
Urinary Retention
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Urinary catheterizes should be provided for
patients undergoing moderate to lengthy
procedures
Postoperative assessment is important to detect
urinary retention
Prolonged urinary retention may be a sign of
serious neurological injury
Complications Associated with Needle
Placement or Catheter Insertion
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Inadequate anesthesia or analgesia
Inadvertent intravascular injection
Total spinal
Subdural injection
Backache
Postdural puncture headache
Neurological injury
Spinal or epidural hematoma
Meningitis and arachnoiditis
Epidural abscess
Sheering off the tip of the epidural catheter
Inadequate Analgesia or Anesthesia
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Rate of block failure is low but can be frustrating
Must always be prepared to convert to general
anesthesia or supplement
Rate of block failure decreases as experience
increases
Inadequate Analgesia or Anesthesia- May
be associated with:
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Outdated or improperly stored local anesthetics
(tetracaine looses potency when stored for long
periods in a warm environment)
Inadequate Analgesia or Anesthesia- May
be associated with:
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Needle movement once free flowing CSF is notedhelpful to confirm aspiration before, during, and
after injection
Even with free flowing CSF it is possible that the
spinal needle is not entirely in the subarachnoid
space resulting in a partial subdural injection and
partial spinal
Inadequate Analgesia or Anesthesia- May
be associated with:
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Epidural anesthesia is more subjective since you have
to rely on confirmation by loss of resistance or
hanging drop technique
Either technique can lead to false positives
Spread of local anesthetic is less predictable
Inadequate Analgesia or Anesthesia- May be
associated with anatomical factors with epidural
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Soft spinal ligament can occur in the very young and
in obstetrics…this results in never achieving a good
loss of resistance
If you are off the midline slightly you may be in the
paraspinous muscle and not in the spinal ligaments
Inadequate Analgesia or Anesthesia- May be
associated with anatomical factors with epidural
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Block failure may occur if the epidural catheter
migrates into the subdural space
Injection of local anesthetics into this space may
result in Horner’s syndrome, a high spinal, or an
absence of any effect
Inadequate Analgesia or Anesthesia
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Local anesthetic toxicity can occur if the epidural
catheter is placed into a vessel
A high spinal can occur if the epidural catheter is
placed in a subarachnoid space- stresses
importance of the test dose
Inadequate Analgesia or Anesthesia
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Septations within the epidural space may create a
barrier to the spread of local anesthetic and some
segments may lack anesthesia
L5, S1, S2 are all large nerve roots and the large
size may prevent penetration of local anestheticcorrect by making the area dependent and adding
local anesthetic
Inadequate Analgesia or Anesthesia
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Visceral pain can occur even if the epidural is
adequate. Visceral afferent fibers travel with the
vagus nerve.
May increase the level of epidural anesthesia to the
thoracic levels with additional local anesthetic
IV sedatives and opioids may help
Inadequate Analgesia or AnesthesiaFailed Epidural
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Not waiting long enough to let it work
Catheter is inserted too far resulting in a
“unilateral” block…pull back the catheter 1-2 cm
and add local anesthetic with the unaffected side
down
Inadvertent Intravascular Injection
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Risk with spinal anesthesia is extremely low
Risk generally lies with epidural or caudal
anesthesia
Toxicity will affect the central nervous system and
cardiovascular system
Inadvertent Intravascular Injection
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Local anesthetics vary in their potential to cause
toxicity
Least to most toxic local anesthetics are as follows:
Chloroprocaine< lidocaine < mepivacaine <
levobupivacaine< ropivacaine < bupivacaine
Inadvertent Intravascular InjectionSymptoms
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Hypotension
Arrhythmias
Cardiovascular collapse
Seizures
Unconsciousness
Inadvertent Intravascular InjectionPrevention
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Test dose
Careful aspiration prior to injection
Incremental dosing
Vigilant monitoring for early signs and symptoms of
intravascular injection
Early symptoms include increase heart rate (if epi
used), tinnitus, funny taste or metallic taste,
subjective changes in mental status
Inadvertent Intravascular InjectionPrevention
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With early symptoms stop administration and
anticipate impending complications such as seizures
and hypotension, etc.
Re-evaluate placement of catheter and reinsert as
needed
Local Anesthetic Toxicity Treatment
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Standard ACLS treatment
Bretyllium may be more effective than other forms
of antiarrhythmics
On the Horizon- Intralipids
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Several successful resuscitations of local anesthetic
overdose as well as other lipophilic medication
overdoses
Local anesthetics are amphipathic (have an affinity
for both lipid and water)
This makes local anesthetics potentially toxic for
several tissues including the heart, brain, and
skeletal muscles
On the Horizon- Intralipids
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Intralipids expand the
lipid compartment and
allow for local anesthetic
binding (there are more
involved and technical
explanations but lets
keep it simple)
Lipid Rescue Protocol (Experimental)
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20% Intralipid
1.5 mg/kg initial bolus
0.25 mg/kg/min infusion for 30-60 minutes
Bolus may be repeated 1-2 times for persistent
asystole
May increase infusion rate if blood pressure
decreases
See lipidrescue.com for more information
Subdural Injection
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Subdural space is a potential space that is found
between the dura and arachnoid space
It contains a small amount of serous fluid
Subdural space extends from the epidural space to
the intracranial space
Local anesthetics can travel further in the subdural
space than they can in the epidural space
Subdural Injection
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Small doses of local anesthetic can travel far in the
subdural space
Small doses of local anesthetic associated with a
spinal may result in no local anesthetic blockade
Larger doses of local anesthetics associated with
epidural analgesia may result in Horner’s Syndrome
Subdural Injection
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Manifestations of Horner’s syndrome include miosis
(constriction of the pupil); ptosis (drooping of the
upper eyelid); and anhidrosis (diminished or absent
sweating).
Horner’s Syndrome
Subdural Injection
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Larger doses of local anesthetics associated with
epidural anesthesia may result in a total spinal.
Prevention is slightly more difficult as aspiration will
generally be negative
With slow incremental dosing you may note a
higher and faster progression of blockade than
would be normally expected
Backache
Backache
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Up to 30% of patients undergoing general
anesthesia will complain of back pain
Large number of patients suffer from chronic back
pain
Not a contraindication
Patient should be aware that spinal or epidural
anesthesia may result in some discomfort
Backache
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Inflammatory reaction due to tissue trauma
May result in back spasms
Short lived, analgesics, ice
May last a few weeks
Back ache may be a sign of serious complications
such as epidural/spinal hematoma, abscess
Careful evaluation to determine if a common/benign
complication or something more serious
Postdural Puncture Headache
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Caused by disrupting the integrity of the dura
Can occur due to: spinal anesthesia, “wet” tap with
epidural, epidural catheter migration, tip of the
epidural needle “indenting” the dura enough to
cause a leak.
Postdural Puncture Headache
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Headache occurs due to leakage of CSF through
the dura
Decrease in intracranial pressure occurs due to the
leak
Upright position in the patient leads to traction on
the dura, tentorium, and blood vessels resulting in
pain.
Traction on the 6th cranial nerve can result in
diplopia and tinnitus
Postdural Puncture Headache- Symptoms
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Headache associated with upright position (i.e.
sitting or standing). Relief found with a supine
position
Headache may be bilateral, frontal, retroorbital
and/or occipital with or without radiation to the
neck
Described as “throbbing” or constant
May be associated with nausea and/or
photophobia
Postdural Puncture Headache- Symptoms
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Onset is generally 12-72 hours; rarely is the onset
immediate
If untreated it may last for weeks
Postdural Puncture Headache- Associations
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Increased incidence related to needle size, needle
type and patient population
The larger the needle the higher the incidence
Cutting point needles have a higher incidence of post
dural puncture headache than pencil points
When using cutting point needles orientate the bevel
“sideways” so it will be parallel with the fibers. This
will act to “spread” the fibers as opposed to cutting
them
Postdural Puncture Headache- Associations
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Recent literature may indicate that pencil points
actually cause more trauma then cutting needles.
This actually may reduce the incidence of headache
secondary to a localized inflammatory response.
Increased post dural puncture headache in younger
patients, in female patients, and in pregnant
patients
Postdural Puncture Headache
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Some advocate the prophylactic treatment if a wet
tap occurs with an epidural needle.
Methods include epidural blood patch, epidural
dextan, or epidural saline.
A wet tap with a 17 g. epidural needle will yield a
50% incidence of pdph
A prophylactic epidural blood patch performed
within 24 hours of a “wet” tap has a 71% failure
rate.
After 24 hours there is a failure rate of 4%
Postdural Puncture Headache
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Epidural blood patches are not without risk.
Remember 50% of the patients with a “wet” tap
will not get a post dural puncture headache.
Conservative measure would be to wait and see if
symptoms occur
Prophylactic treatment will only result in unnecessary
treatment in 50% of the patients
Postdural Puncture Headache- Conservative
Treatment
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Symptoms can be debilitating
Start with conservative measures
Supine position- will reduce symptoms, no evidence
that bed rest will reduce the duration of post dural
puncture headache. Theoretically it should
decrease the amount of CSF leak and allow
replacement of lost CSF
Postdural Puncture Headache- Conservative
Treatment
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Hydration- theoretically helps to encourage the
production of CSF. A dehydrated patient may
experience more severe symptoms and hydration is
important. The one study looking at this did not find
that hydration decreased the incidence of post
dural puncture headache.
Postdural Puncture Headache- Conservative
Treatment
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Caffeine- theoretically helps to decrease sx by
vasoconstriction of the cerebral vessels. May
decrease symptoms but does not necessarily decrease
the number of patients that will require an epidural
blood patch.
IV caffeine can be administered in a dose of 500 mg
Oral caffeine can be encouraged.
A dose of 300 mg of oral caffeine has been shown to
decrease the intensity of pdph
Caffeine Content of Common Beverages
Postdural Puncture Headache- Conservative
Treatment
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Analgesics- will decrease the severity of symptoms
and include acetaminophen and NSAIDS
Stool softners and soft diet may help decrease
Valsalva straining which may increase leakage of
CSF
Postdural Puncture Headache- Conservative
Treatment
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Conservative treatment is mainly symptomatic
Postdural Puncture Headache- Epidural
Blood Patch
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Definitive treatment
Successfully resolves 90% of all post dural puncture
headache after the first treatment
Generally offered 12-24 hours after the initiation
of conservative treatment
Not without risk
Postdural Puncture Headache- EBP
Precautions
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Check patients history for contraindications
Check coagulation status
Ensure no anticoagulants have been administered
(i.e. DVT prophylaxis)
Ensure that the patient is not bacteremic
Jehovah’s Witness patients may refuse an epidural
blood patch based on religious beliefs
Postdural Puncture Headache- Epidural
Blood Patch
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Involves injection of 15-20 ml of the patients own
blood at the level of dural puncture
May be administered one space below the dural
puncture site
Blood patch works by mass effect and stops the
leakage of CSF or alternatively by coagulating and
“plugging” the hole
Postdural Puncture Headache- Epidural
Blood Patch
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Inform the patient of risks and benefits
Same as with any neuraxial technique with the
addition of the increased risk of meningitis or
infection (the blood that is removed can be
contaminated and placed at an area that has
breached the blood brain barrier
Inform the patient that it is only 90% effective and
not 100% effective
Postdural Puncture Headache- Epidural
Blood Patch Technique
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Assemble your supplies- mask, sterile gloves,
epidural tray, additional betadine and alcohol,
sterile needle for venipuncture and tourniquet.
Prior to locating the epidural space identify a
suitable vein to draw blood. Prep the area with
betadine and consider draping the area with
sterile towels
Postdural Puncture Headache- Epidural
Blood Patch Technique
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Perform usual steps for locating the epidural space
Once epidural space is identified then have your
assistant aseptically withdraw 15-20 ml of blood.
Keep the blood sterile.
Ensure no contamination of the blood has occurred
Postdural Puncture Headache- Epidural
Blood Patch Technique
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Place 15-20 ml of blood into the epidural
space
Postdural Puncture Headache- Epidural
Blood Patch Technique
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The patient should not experience pain but may
note pressure
The patient should remain supine for 1-2 hours
The patient should avoid lifting heavy items or
straining for 48 hours (thus avoiding the
dislodgement of the epidural blood patch
Neurological Injury
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Can be transient or permanent
Prevention is done by avoiding trauma to the nerve
roots or spinal cord
Identification of appropriate landmarks is essential
Always document pre-existing neurological deficits
Ask the patient if they suffer from neuropathy, chronic
or acute low back pain, motor deficits.
Neurological Injury
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Document concurrent conditions that may contribute to
postoperative neuro deficits such as peripheral
vascular disease, diabetes, intervertebral disk injury,
spinal disorders.
Perform subarachnoid anesthesia below L1 in adults
and L3 in children
Multiple attempts will increase the risk of traumaavoid this by proper positioning, identification of
landmarks, and take your time being deliberate when
performing neuraxial techniques
Neurological Injury
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If difficulty is encountered do not be afraid to ask
another provider to help
If a paresthesia is encountered make sure it is
transient and redirect the needle
When inserting a catheter or injecting and the
patient experiences pain stop. Direct injection into
the spinal cord can lead to paraplegia
Neurological Injury
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Document the presence of paresthesia or pain
during neuraxial blockade
Alternatively if the neuraxial technique has been
performed without any problems document this (i.e.
no pain, no paresthesia, etc.)
If the patient experiences a neuro deficit
after neuraxial blockade:
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Possible causes include surgical positioning
Improper positioning in the post op period
Direct trauma related to surgery
Rule out hematoma or abscess
OB patients at risk for neuro deficits related to csec and vaginal delivery
Obstetric Causes
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Incidence of neurological complications in OB range
from 1:2,600-6,400 and often related to difficult
deliveries.
Prolapse of intervertebral disk and subsequent
nerve root compression can occur.
Obstetric Causes
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Injury related to descending head or mid to high
forcep use include lumbrosacral injury (L4, L5).
Results in foot drop, weakness of hip adduction and
quadriceps.
Acute hip flexion and retractors during a cesarean
section can result in injury to the femoral nerve (L2,
L3, L4). Results in quadricep paralysis, abscent
patellar reflex, and altered sensation of anterior
thigh and medial calf.
Obstetric Causes
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Incorrect lithotomy positioning and retractors during
a cesarean section can injury the lateral femoral
cutaneous nerve (L2, L3). This will alter sensation on
the anterolateral thigh.
Incorrect lithotomy position with knee extension and
external hip rotation may injure the sciatic nerve
(L4,L5,S1,S2,S3). This will result in sciatic type pain
(from gluteal area to foot) and the inability to flex
the leg.
Obstetric Causes
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Lithotomy position with acute flexion of thigh may
lead to injury to the obturator nerve (L2,L3,L4). This
may lead to weak or paralyzed thigh adduction.
Compression of lateral knee may lead to common
peroneal nerve injury (L4, L5, S1, S2). This will
result in foot drop and the inability to stand erect.
Obstetric Causes
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Lithotomy positioning may result in injury to the
saphenous nerve (L2, L3, L4). Loss of sensation in
the medial foot and anteromedial lower leg.
Document New Neurological Deficits
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Is the neuropathy in the distribution of neuraxial
blockade? (usually transient)
Is there sharp back pain? Leg pain? (severe
symptoms may indicate epidural hematoma or
Transient Neurological Symptoms)
Is there progressive numbness, motor blockade, or
sphincter dysfunction? (may be spinal or epidural
hematoma)
Document New Neurological Deficits
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Trauma to conus medullaris generally results in
sacral dysfunction and you will see:
Paralysis of biceps femoral muscle
Sensory loss of the posterior thigh, perineal area, or
great toes
Bowel and bladder dysfunction
Document New Neurological Deficits
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After evaluation of sx it is reasonable to have a
neurological consult
Spinal/Epidural Hematoma
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1:150,000 for epidurals
1:220,000 for spinals
Factors associated with Spinal/Epidural
Hematoma
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Abnormal coagulation due to disease/meds
Multiple attempts at neuraxial blockade
Formation after the removal of the epidural
catheter
Spinal/Epidural Hematoma
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Presence of blood in the subarachnoid or epidural
space will result in the compression of neural tissue
There is no way to apply pressure and stop the
bleeding due to the anatomy.
Compression results in ischemia and subsequent
injury
Spinal/Epidural Hematoma Symptoms
(generally rapid)
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Sharp back and leg pain
Progression of numbness and motor weakness
Sphincter dysfunction
Spinal/Epidural Hematoma
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Rapid diagnosis is essential
MRI/CT scan can diagnose this complication
Surgical decompression must occur in 8-12 from the
onset of symptoms to avoid permanent injury
Meningitis
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Meningitis is very rare
Must always use strict sterile technique
Always wear a mask and change it frequently even
in OB
Meningitis
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Most common cause of bacterial meningitis is from
contamination of the puncture site by aerosolized
mouth particles
Viridans streptococcus is the dominant organism and
is found in the mouth
Stresses the importance of masks!
Meningitis
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To a lesser extent skin bacteria can result in
meningitis
Care should be taken in securing the device with
sterile materials
Skin bacteria could track there way into the
epidural space
Meningitis
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Presentation is very similar to a post dural puncture
headache
Exception is there is no postural component to the
headache, there is generally a fever, and alteration
in level of consciousness
Arachnoiditis
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Very rare
More common in the past when supplies where
reused
Chemical arachnoiditis can occur with intrathecal
injection of steroids
Lumbar arachnoiditis is more commonly associated
with surgical procedures or trauma
Epidural Abscess
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Rare
Incidence 1:6,5001:500:000
May develop
independent of
neuraxial techniques
Epidural Abscess-risk factors
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Back trauma
IV drug abuse
Neurological surgical procedures
Those associated with neuraxial techniques are
commonly due to indwelling epidural catheters
Symptoms develop between 5 days and several
weeks
Epidural Abscess-Stages of Development
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
Stage 1: back and vertebral pain intensified by
percussion. Any patient with back pain and a fever
should alert the anesthesia provider to the
possibility of an abscess
Stage 2: progresses to nerve root and radicular
pain
Epidural Abscess-Stages of Development
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
Stage 3: motor, sensory and/or sphincter
dysfunction
Stage 4: paralysis and or paraplegia
Epidural Abscess-Prognosis


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
Dependent upon when diagnosed, the earlier the
better
Epidural catheter should be removed immediately
Tip sent for cultures (not always accurate)
Epidural site should be examined for signs and
symptoms of infection
Blood cultures should be sent for evaluation
Any drainage from the site should be sent for
evaluation
Epidural Abscess-Prognosis/Treatment





Neuro consult
Most common agents include staph auerus and
staphylococcus epidermis
Antibiotic coverage
MRI/CT
Possible decompression lami
Epidural Abscess-Prevention



Sterile technique (hat, mask, sterile gloves, hand
washing, sterile field, proper prep of the skin etc.)
If there is any doubt to contamination, stop and
start over
If epidural cath becomes disconnected you must
decide whether to aseptically reattach it or remove
the catherter
Epidural Abscess-Prevention




Reduce epidural catheter manipulation
Maintain a closed system always
Use bacterial filter that comes with the kit
Remove the catheter after 96 hours and if needed
then replace it with a new one at a new site
Shearing Off the Tip of the Epidural
Catheter




Never attempt to withdraw the epidural catheter
through the epidural needle
If you need to remove the catheter remove both the
needle and catheter as one unit
When dc an epidural catheter use steady pressure
never jerk the catheter
If difficulty is encountered change the patients
positions (i.e. fetal position) to maximize the
intervertebral space
Shearing Off the Tip of the Epidural
Catheter



If tip breaks off deep in the epidural space leave it
and observe for complications
If tip breaks off in the superficial tissue it should be
surgically removed
A remnant of epidural catheter superficially can
lead to infection
Complications Associated With Medication
Toxicity



Systemic toxicity (covered earlier)
Transient neurological symptoms
Cauda equina syndrome
Transient Neurological Symptoms

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



Described in 1993
Most common after spinal anesthesia/rare for it to
occur with epidural anesthesia
Symptoms include LBP with radiation to the legs
Sx occur after anesthetic has regressed and normal
sensation has occurred
Sx occur from 1-24 hours after normal sensation
Almost any local anesthetic can cause TNS
Transient Neurological SymptomsAssociated Local Anesthetics



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


Lidocaine
Tetracaine
Bupivacaine
Mepivacaine
Prilocaine
Procaine
Ropivacaine
Transient Neurological SymptomsAssociated Local Anesthetics






Most common local anesthetic to cause TNS is
lidocaine
Most in the anesthesia community have abandoned
lidocaine as a spinal anesthetic
Leaves us with few good choices
Procaine often too short lived
Prilocaine has a high incidence of nausea and
vomiting
Mepivacaine has similar profile to lidocaine for both
duration and incidence of TNS
Transient Neurological Symptoms


Unknown mechanism of action
Theorized that lidocaine is more neurotoxic to the
unsheathed nerve
Transient Neurological SymptomsContributing Factors



Lithotomy position – may be due to stretching of the
lumbrosacral nerve roots and decreased perfusion
Early ambulation after the spinal reason not
elucidated
Treatment is symptomatic and generally is short
lived
Cauda Equina Syndrome


Associated with spinal catheters and 5% lidocaine
Differs from TNS in that it is permanent and
associated with sphincter dysfunction, sensory and
motor deficits, and paresis
Cauda Equina Syndrome

Generally appears in a peripheral nerve pattern
and may be due to misdistribution of the hyperbaric
lidocaine
Cauda Equina Syndrome




Neurotoxicity of local anesthetics is as follows:
Lidocaine=tetracaine > bupivacaine > ropivacaine
Pain is similar to nerve root compression
Has been reported after single shot spinals as well
as rarely after epidural anesthesia
Analyzing Complications of Spinal and
Epidural Anesthesia




Sweden
1990-1999
Reviewed 1,260,000 spinals and 400,000
epidurals (half of which were for OB)
Overall incidence of complications were 127 out of
1,660,000.
Moen V, Dahlgren N, Irestedt L. Severe neurological complications after
central neuraxial blockade in Sweden 1990-1999. Anesthesiology. 2004; 101:
950-959.
Analyzing Complications of Spinal and
Epidural Anesthesia
Incidence for spinal anesthetics 1:20,000-30,000
 Incidence for epidural in OB was 1:25,000
 Incidence for non OB epidural was 1:3,600
(this differs from US experience)

Moen V, Dahlgren N, Irestedt L. Severe neurological complications after
central neuraxial blockade in Sweden 1990-1999. Anesthesiology. 2004;
101: 950-959.
Analyzing Complications of Spinal and
Epidural Anesthesia- Risk Factors



LMWH administered within 10 hours before a spinal
or epidural or removing a catheter 2 hours before
treatment
Disease that cause coagulation problems such as
renal/liver, OB syndrome with hemolysis, elevated
liver enzymes, low platelets
Ankylosing Syndrome
Moen V, Dahlgren N, Irestedt L. Severe neurological complications after central
neuraxial blockade in Sweden 1990-1999. Anesthesiology. 2004; 101: 950-959.
Analyzing Complications of Spinal and
Epidural Anesthesia- Risk Factors



Spinal deformity
Trauma while during the block
Osteoporosis
Moen V, Dahlgren N, Irestedt L. Severe neurological complications after
central neuraxial blockade in Sweden 1990-1999. Anesthesiology. 2004;
101: 950-959.
Analyzing Complications of Spinal and
Epidural Anesthesia



Most complications seen with orthopedic surgery
followed by general surgery and then urology
Complications higher after epidural anesthesia
when compared to spinal anesthesia
Patients with cauda equina syndrome, traumatic
cord injury, and paraplegia had a 100% of
permanent injury.
Moen V, Dahlgren N, Irestedt L. Severe neurological complications after
central neuraxial blockade in Sweden 1990-1999. Anesthesiology.
Analyzing Complications of Spinal and
Epidural Anesthesia- The take home




Complications occur 4-5 times more frequently after
spinal anesthesia when compared to epidural
OB population had a lower incidence of
complications compared to non ob female
population
Osteoporosis is now a risk factor
Severe complications have a high rate of being
permanent
Moen V, Dahlgren N, Irestedt L. Severe neurological complications
after central neuraxial blockade in Sweden 1990-1999.
Anesthesiology. 2004; 101: 950-959.
Allergic Reactions



Very low incidence with local anesthetics.
Esters are more likely to cause reactions. They are
metabolized into PABA (a known allergen).
Methylparaben is a preservative used in some multi
dose vials and is structurally similar to PABA.
Should use preservative free local anesthetics.
Allergic Reactions


Most reactions are related to vagal reactions,
toxicity of local anesthetics, effects of epinephrine
such as tachycardia, flushing, and tachypnea.
Allergic reactions to anesthetics are rare.
Propensity to cause allergic reactions are as follows
muscle relaxants> thiopental > propofol >
etomidate = ketamine = benzodiazepines > local
anesthetics
Allergic Reactions




Anaphylactic reactions involve in a number of mediators that result in an exaggerated response.
Airway- angioedema of upper airway, bronchospasm, and edema of the lower airway. Signs and
symptoms include bronchospasm, cough, dyspnea, pulmonary edema, laryngeal edema, and hypoxia.
Vascular- increased permeability allows edema to occur resulting in hypovolemia and shock. Primary
symptom will be hypotension and shock.
Heart- hypoperfusion and hypoxemia results in arrhythmias and myocardial ischemia. Coronary
vasoconstriction may occur. Tachycardia and arrhythmias are common.

Other vital organs- resulting shock and lactic acidosis leads to additional ischemic trauma.

The effect of mediators will manifest dermatologically as urticaria, facial edema, and pruritus.
Allergic Reactions

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Treatment includes the following:
Stop the administration of the suspected medication
Administer 100% O2 and consider intubation if the patient
is not already intubated.
Epinephrine administered in doses of 0.01-0.5 mg IV or IM
Administer fluids rapidly to combat the hypovolemia and
shock (1-2 L of crystalloid)
Diphenhydramine in a dose of 50-75 mg IV
Rantidine or cimetidine IV
Hydrocortisone up to 200 mg IV or alternatively
methylprednisolone in a dose of 1-2 mg/kg IV.
References

Ankcorn C. & Casey WF. Spinal Anaesthesia- A Practical Guide. Update in Anaesthesia. Issue 3; Article 2. 1993.

Baer ET. Post-dural puncture bacterial meningitis. Anesthesiology, 105:2, 2006.

Brown DL. Spinal, Epidural, and Caudal Anesthesia. In Miller’s Anesthesia 6th edtion. Miller, RD ed. Pages 1653-1675. Elsevier, Philadelphia, Penn. 2005.

Burkard J, Lee Olson R., Vacchiano CA. Regional Anesthesia. In Nurse Anesthesia 3rd edition. Nagelhout, JJ & Zaglaniczny KL ed. Pages 977-1030.

Casey WF. Spinal Anaesthesia- A Practical Guide. Update in Anaesthesia. Issue 12; Article 8. 2000.

Dijkema LM, Haisma HJ. Case Report- Total Spinal Anaesthesia. Issue 14; Article 14. 2002.

Dobson MB. Conduction Anaesthsia. In Anaesthesia at the District Hospital. Pages 86-102. World Health Organization. 2000.

Kleinman, W. & Mikhail, M. (2006). Spinal, epidural, & caudal blocks. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books.

Nitti, J.T. & Nitti, G.J. (2006). Anesthetic complications. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books.

Pollard, JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesthesia & Analgesia, 92:252-6, 2001.

Sime, AC. Transient neurologic symptoms and spinal anesthesia. AANA Journal, April 2000.

Tsui, B.C.H & Finucane, B.T. (2008). Managing adverse outcomes during regional anesthesia. In D.E. Longnecker et al (eds) Anesthesiology. New York: McGraw-Hill Medical.

Visser L. Epidural Anaesthesia. Update in Anaesthesia. Issue 13; Article 11. 2001.
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Warren, D.T. & Liu, S.S. (2008). Neuraxial Anesthesia. In D.E. Longnecker et al (eds) Anesthesiology. New York: McGraw-Hill Medical.