UNIT 8 Regional Flashcards
What are the 5 divisions of the spinal column, and how many vertebrae are present in each?
cervical: 7
thoracic: 12
lumbar: 5
sacral: 5 fused
coccygeal: 4 fused
know the anatomy of the vertebrae
spinous process connected via lamina to transverse processes
pedicles connect to the vertebral body
all surround the vertebral foramen
what are the anatomical borders of the facet joint?
The facet joints are joints in the spine located in posterior aspect of the spine
It’s formed by the superior articular process of one vertebrae and the inferior articular process of the one directly above it.
Injury = compress the spinal nerve that exits the respective intervertebral foramina, causing pain & muscle spasm along the associated dermatome
order the 5 ligaments of the spinal column from posterior to anterior
supraspinous ligament interspinous ligament ligamentum flavum posterior longitudinal ligament anterior longitudinal ligamnet
what ligaments are penetrated during midline approach to the epidural space? How about the paramedian approach?
midline:
- supraspinous
- interspinous
- ligamentum flavum
paramedian
- ligamentum flavum
list all of the structures & spaces b/n the skin and the SC as they would be encountered during a subarachnoid block
skin subcutaneous tissue muscle supraspinous ligament interspinous ligament ligamentum flavum dura mater arachnoid mater pia mater
what are the boundaries of the epidural space?
cranial border = foramen magnum
caudal border = sacrococcygeal ligament
anterior border = posterior longitudinal ligament
lateral border = vertebral pedicles
posterior border = ligamentum flavum, vertebral lamina
What happens when you accidentally inject LA into the subdural space during a SAB? How about during an epidural?
subdural space is a potential space b/n the dura and arachnoid mater
epidural dose injected into the subdural space –> high spinal w/ delayed onset (15-20mins)
spinal dose injected into the subdural space –> failed block
What is Batson’s plexus, and what is it’s significance?
the epidural veins
they drain venous blood from the SC. valveless. pass through the anterior and lateral regions of the epidural space.
obesity & pregnancy increase intraabdominal pressure = plexus engorgement. This is associated w/ an increased risk of needle injury or cannulation
What is the plica mediana dorsalis, and what is its significance?
while its existence remains controversial, many speculate that a band of connective tissue courses b/n the ligamentum flavum & dura mater
if it does exist, it could create a barrier that would impact the spread of medications w/in the epidural space.
it has long been considered the culprit for difficult epidrual catheter insertion as well as unilateral epidural blocks
what ligament covers the sacral hiatus? What is the significance of this?
sacrococcygeal ligament
this ligament is punctured during the caudal approach to the epidural space.
What is a dermatome, and which ones are important to know as you assess a neuraxial anesthetic?
dermatome = area of skin that is innervated by a spinal nerve
C6 = thumb C7 = 2nd & 3rd digits C8 = 4th & 5th digits T4 = nipple T6 = xiphoid T10 = umbilicus T12 = pubic symphysis L4 = anterior knee
compare and contrast the site of action for spinal vs. epidural anesthesia.
spinal
- primary LA action is on the myelinated preganglionic fibers of the SPINAL NERVE ROOTS
- LA also inhibit neuronal transmission in the superficial layers of the SC
epidural
- LA must diffuse through the DURAL CUFF before than can block the nerve roots
- LA also leaks through the intervertebral foramen to enter the paraverterbral area, where they cause multiple paravertebral blocks
what factors do and do not contribute to the spread of LA in the subarachnoid space?
DO:
- baricity
- patient position
- dose
- site of injection
- volume & density of CSF
DON’T
- barbotage
- increased intraabdominal pressure
- speed of injectin
- bevel orientation
- vasoconstrictor addition
- weight
- gender
what is the primary determinant of spread for epidural anesthesia?
volume
discuss the differential blockade of spinal anesthesia
different types of nerves have different sensitivites to LA blockade
- autonomic first
- sensory second
- motor last
why is this important? autonomic blockade is 2-6 dermatomes higher than sensory block & sensory blockade is 2 dermatomes higher than motor block
How is differential blockade different w/ epidural anesthesia?
there is no autonomic differential blockade w/ epidural anesthesia
sensory blockade is 2-4 dermatomes higher than motor
compare and contrast nerve fibers in terms of subtype, myelination, function, size, conduction velocity, and block onset.
Aalpha
- heavy myelination
- skeletal m motor + proprioception
- largest
- fastest
- last for block onset
Abeta
- heavy myelination
- touch, pressure
- second largest
- second fastest
- last for block onset
Agamma
- medium myelination
- skeletal m tone
- medium size
- medium velocity
- second to last for block onset
Adelta
- medium myelination
- fast pain, temp, touch
- medium size
- medium velocity
- second to last for block onset
B
- light myelination
- preganglionic ANS
- medium size
- medium velocity
- first for block onset
C
- no myelination
- postganglionic ANS, slow pain, temp, touch
- small size
- slowest velocity
- second for block onset
discuss the CV effects of neuraxial anesthesia
sympathectomy –> vasodilation in arterial & venous circulations, although predominantly affects venous capacitance vessels
- -> decreased preload, CO, and BP
- volume loading w/ approx 15mL/kg and vasopressors will minimize hypotension
bradycardia is caused by
- T1-T4 preganglionic cardiac accelerator fiber blockade
- bezold-jarisch reflex
- unloading of stretch receptors in the SA node
discuss the respiratory effects of neuraxial anesthesia
in healthy patients, there is negligible effects on MV, Tv, rr, dead space, and ABG
accessory muscle function is reduced + abdominal muscles (cough function impairment)
- particularly important w/ COPD
how does neuraxial anesthesia affect the neuroendocrine response to stress?
by inhibiting afferent traffic originating from the surgical site, it diminishes the surgical stress response.
this reduces circulating levels of catechols, RAAS, glucose, TSH, and GH
how does neuraxial affect GI function?
the gut receives PSNS innervation from CN V and SNS innervation from the sympathetic chain b/n T5-L2
- inhibition of the sympathetic chain allows PSNS function unopposed
- -> sphincter relaxation & increased peristalsis
how does neuraxial anesthesia affect renal & hepatic blood flow?
as long as systemic BP is maintained, HBF & RBF are unchanged
what is the risk of neuraxial anesthesia in the patient w/ coagulopathy? What lab values are considered contraindications to a neuraxial technique?
risk of spinal or epidural hematoma
platelet <100K
PT, aPTT, and/or bleeding time twice the normal value
What cardiac pathologies present a risk of hemodynamic collapse w/ neuraxial anesthesia?
valve lesions w/ fixed SV:
- severe AS
- severe MS
- hypertrophic cardiomyopathy
what is the risk of a neuraxial technique in the patient w/ intracranial hypertension?
there is an increased chance of brain herniation w/ sudden changes in CSF pressure
what is the relationship b/n neuraxial anesthesia & MS?
classic teaching suggests that epidural is ok, but intrathecal may exacerbate symptoms - no good supporting data however.
what is the specific gravity of CSF? What factors increase and decrease the spec gravity of CSF?
1.002-1.009
increase:
- hyperglycemia
- uremia
- high protein content
- advanced age
- colder temperature
decrease:
- liver disease
- jaundice
- warmer temperature
what is baricity, and how does it influence your selection of LA?
baricity describes the density of a LA solution relative to the CSF.
- isobaric: LA similar to CSF
- hyperbaric: LA higher density
- hypobaric: LA lower density
hyperbaric will sink, hypobaric will rise, isobaric will remain in place.
as a general rule, solutions in dextrose are hyperbaric, saline are isobaric, water are hypobaric.
how does a hyperbaric solution distribute in the sitting patient? How about the supine patient?
sitting = sacral nerve roots (i.e. saddle block)
supine = sacrum & thoracic -T4 (since these are the areas of kyphosis
How does an hypobaric solution distribute in the sitting patient? How about the supine patient?
sitting = will rise toward the brain (i.e. avoid this)
supine = lower lumbar region (area of lordosis).
- it will not float toward the cervical region bc this would first require it to sink into the thoracic kyphosis
what are the 2 classifications of spinal needles?
cutting tip & non cutting tip (pencil point & rounded bevel)
cutting point = Quincke
pencil point = Whitacre, Sprotte
rounded bevel = Greene
List 6 examples of spinal needles, and list the pros and cons of each.
cutting tip (Quincke, Pitkin)
- pros = requires less force
- cons = higher risk of PDPH, less tactile feel, needle more easily deflected, more likely to injure cauda equina
pencil point (Sprotte, Whitacre, Pencan) AND rounded bevel tip (Greene) - pros = lower risk of PDPH, more tactile feel, needle less likely to deflect, less likely to injure the cauda equina - cons = requires more force
what are the 3 different types of epidural needles & how are they different from each other
differ in the angle of the needle tip (notice that the needle angle increases in alphabetical order):
crawford = 0 degrees
hustead = 15 degrees
tuohy = 30 degrees
- this curvature + it’s blunt tip helps prevent dural puncture
How do you dose a caudal anesthetic in a child? an adult?
peds
- sacral block: 0.5mL/kg
- T10: 1mL/kg
- mid-thoracic: 1.25mL/kg
adult
- sacral: 12-15mL
- T10: 20-30mL
avoid midthoracic
what are the absolute and relative contraindications to caudal anesthesia?
absolute:
- spina bifida
- meningomyelocele of the sacrum
- meningitis
relative:
- pilonidal cyst
- abnormal superficial landmarks
- hydrocephalus
- intracranial tumor
- progressive degenerative neuropathy
discuss the mechanism of action of neuraxial opioids.
inhibit afferent pain transmission in the substantia gelatinosa (lamina II) of the dorsal horn
neurotransmission is reduced by:
- decreased cAMP
- decreased Ca++ conductance (pre-synaptic neuron)
- increased K+ conductance (post-synaptic neuron)
epidural opioids diffuse systemically as well
do neuraxial opioids cause sympathectomy, skeletal m weakness, and/or changes in proprioception?
NO
discuss the commonly used intrathecal and epidural opioids
sufentanil
- intrathecal 5-10mcg
- epidural 25-50mcg
- epidural gtt 10-20mcg/hr
fentanyl
- intrathecal 10-20mcg
- epidural 50-100mcg
- epidural gtt 25-100mcg/hr
dilaudid
- epidural 0.5-1mg
- epidural gtt 0.1-0.2mg/hr
meperidine
- intrathecal 10mg
- epidural 25-50mg
- epidural gtt 10-60mg/hr
morphine
- intrathecal 0.25-0.3mg
- epidural 2-5mg
- epidural gtt 0.1-1mg/hr
rank the opioids from most lipophilic to most hydrophilic. How does lipophilicity affect rostral spread in the subarachnoid space?
most lipophilic: - sufentanil - fentanyl - meperidine - dilaudid - morphine most hydrophilic
more hydrophilic drug = less diffusion into systemic circulation, more rostral spread
more lipophilic drug = more diffusion into systemic circulation
compare and contrast PK/PD profiles of hydrophilic and lipophilic opioids used for spinal anesthesia.
hydrophilic
- stays in CSF longer
- extensive CSF spread w/ wide band of analgesia + more rostral spread
- acts only in substantia gelatinosa
- delayed onset 30-60min
- DOA longer 6-24hrs
- less systemic absorption
- early & late resp depression
- higher incidence of N/V, pruritis
lipophilic
- stays in CSF shorter
- minimal CSF spread w/ narrow band of analgesia + less rostral spread
- acts in substantia gelatinosa and systemically
- fast onset 5-10mins
- shorter DOA 2-4hrs
- more systemic absorption
- only risk of early resp depression
- lower incidence of N/V, prutritis
What are the 4 most important side effects of neuraxial opioids? Which is the most common?
- pruritis (most common)
- respiratory depression
- urinary retention
- N/V
Which LA can reduce the efficacy of epidural opioids?
chloroprocaine
Which neuraxial opioid can reactivate herpes simplex labialis?
epidural morphine
- best explained by cephalad spread of morphine to the trigeminal nucleus
- usually presents 2-5 days after epidural morphine administration
describe the patho & presentation of PDPH
puncturing the dura causes CSF to leak from the subarachnoid space. As CSF pressure is lost, the cerebral vessels dilate + the brainstem sags into the foramen magnum, stretching the meninges & pulling on the tentorium
–> PDPH
classic presentation: fronto-occipital HA +/- N/V, photophobia, diplopia, tinnitus. Supine brings relief.
Discuss the risk factors for PDPH
younger age pregnancy female cutting point needle larger diameter needle multiple dural punctures using air for LOR w/ epidural needle perpendicular to long axis of meninges
how do you treat PDPH?
bed rest hydration NSAIDs caffeine (cerebral vasoconstriction) epidural blood patchy
not opioids
how do you perform an epidural blood patch? What is the success rate?
90% success rate/patch
- if HA doesn’t resolve after 2 blood patches, other etiologies should be sought
technique:
sterile withdrawal of 10-20mL of autologous venous blood is injected into the epidural space (stop injecting when pressure is felt in legs, buttocks, or back)
what are the most common side effects of an epidural blood patch?
backache
radicular pain
what is the primary risk of neuraxial anesthesia in the anticoagulated patient? How does this complication present?
risk of epidural hematoma is similar during block placement and catheter removal.
epidural hematoma can cause paralysis. presenting symptoms = LE weakness, numbness, low back pain, bowel/bladder dysfunction.
- surgical decompression w/in 8hrs = best chance of recovery
know how long to hold off neuraxial anesthesia after various drugs:
- NSAIDs
- aspirin
- abciximab
- clopidogrel
- ticlopridine
- heparin
- enoxaparin
- warfarin
- tPA, other thrombolytics
- herbal therapies
NSAIDs & aspirin, herbals (garlic, ginkgo, ginseng)
- ok to proceed if pt has normal clotting mechanism & is not on any other blood thinners
abciximab: 1-2 days
clopidogrel: 7 days
ticlopidine: 14 days
SQ heparin: ok to proceed if all else WNL IV heparin: - hold 2-4hrs pre-blcok - hold 1hr post-block - hold 2-4hrs after removal
enoxaparin: 12-24hrs depending on dosing
warfarin: 5 days (ok to remove cath if INR<1.5)
thrombolytics: absolute contraindication