Regional And Neuraxial Flashcards
Benefits of neuraxial Anesthesia?
That altogether translates into fewer DVTs, less bleeding and transfusions (in some specific surgical cohorts), less splinting and respiratory complications, less pain, and for reasons less clear (likely related to the immune response), lower rate (slightly) of cancer recurrence (for specific tumors undergoing specific management). Older data regarding decreased coronary events with neuraxial anesthesia probably cannot be generalized to more modern techniques (anesthetics).
Order of structures when placing neuraxial
Supraspinous ligament, then interspinous ligament, then ligamentum flavum, then dura, then arachnoid
Tell me what comes from the posterior vs anterior part of nerves
The posterior nerve root carries somatic and visceral sensation (pain) (answers B, C & D) and the anterior nerve root carries motor and sympathetic outflow (answers A & E). Review hand dermatomes!
What is a differential blockade, and how can it happen?
In the case of hyperbaric local anesthetic (for example), the more caudad areas near the site of injection will have higher concentrations of local anesthetic and cephalad areas have lower concentrations. As concentrations lower, motor nerves are not inhibited, but sensory nerves are (accounting for loss of motor block but dense sensory block). At even more cephalad levels the concentration is low enough to the point where temperature (and pinprick) discrimination is lost, but the sensory block is inadequate to block pain. This is called a differential blockade.
The sympathetic chain runs from what?
T1 to L2
Why no spinals in AS?
Decreased afterload will therefore decrease aortic diastolic pressures, leading to myocardial ischaemia. Because cardiac output against a stenotic aortic valve requires high LVEDP (now decreased due to the spinal) and adequate contractility (now decreased due to the myocardial ischaemia), cardiac output falls, leading to a vicious cycle.
Neuraxial in a COPDer extreme
Altogether, in most cases (and probably every case below the umbilicus), neuraxial anesthesia is a safer choice for a severe COPD’er. Neuraxial anesthesia will affect intercostal (inspiration and expiration) and abdominal (expiration/cough) muscles and decrease pulmonary reserve. However, tracheal intubation and general anesthesia in a severe COPD’er also has many (many, many, many) deleterious effects on post-operative pulmonary function.
Having seizures after getting a block-give ____ and then give ___ if that’s not around.
Benzos and then give Propofol of benzos aren’t available
What is TNS? Most common offender? How to reduce the incidence?
Transient neurologic symptoms (TNS) is a well described “benign” phenomenon likely caused by radicular irritation following spinal anesthesia. Lidocaine is the most common offender (answer C) and its incidence is increased with obesity and lithotomy position. Symptoms typically resolve within a couple days to a week. Aspirating equal volume of CSF prior to injection can reduce the incidence.
Why has chloroprocaine had a bad rep?
Chloroprocaine has had an especially bad rap through the years (answer D). Prolonged neurologic deficits have been associated with its intrathecal use, possibly due to preservatives used in the solution. Severe back-pain has also been reported after epidural chloroprocaine has been used, again with the possibility of preservatives being the cause.
Why does intralipid work for LAST? Why not Propofol in ACLS setting?
Intralipid supplies a lipid sink in which bupivicaine can be bound to and should be administered immediately. Propofol’s lipid emulsion may theoretically bind bupivicaine in this circumstance too, but its afterload and contractility depressing effects make it contraindicated in this setting.
Tell me about Neuraxial and once daily dosing of enoxaparin
To keep things straight in your mind, you should think of enoxaparin at the once daily prophylactic dose and the twice daily treatment dose as two distinct drugs. Also, realize that the guidelines are not different for spinals and epidurals, its just that the epidurals have the catheter to worry about. So to start off with, and keep things simple, lets review a single shot spinal/ epidural. With low dose, once daily enoxaparin, you can place the block 12 hours after the last dose of enoxaparin and then restart low dose enoxaparin 12 hours later. The same is true for prophylactic twice daily therapy as well.
Tell me about twice daily enoxaparin dosing
r high dose, twice daily treatment dose enoxaparin, you can place the block 24 hours after the last dose of enoxaparin and the recommendation has been changed from restarting high dose enoxaparin 24 hours after the block (or catheter removal) to no recommendation. Some believe that if there is clear evidence that a vein was violated (positive haeme), then delay subsequent enoxaparin 24 hours regardless of the dose.
2015 enoxaparin and catheter guidelines
As of 2015 here are the guidelines regarding lovenox:
Enoxaparin Daily prophylactic:
Place it 10-12 hours after last dose/ Ok to restart 6-8 hours after catheter placed / Remove catheter 10-12 hours after last dose/ Restart 4 hours after catheter removed
Enoxaparin BID prophylactic:
Place it 10-12 hours after last dose/ Do not use while catheter in place/ Restart 4 hours after catheter removed
Enoxaparin Daily therapeutic:
Place it 24 hours after last dose/ Do not use while catheter in place / No recommendation when to restart after catheter removed
INR, PTT, and clopidigrel as it relates to Neuraxial Anesthesia
A bit of a trick question (as warfarin would not expected to raise PTT significantly), but an elevated PTT (some say above 40) is a contraindication. As far as INR, anything below 1.5 is within guidelines. Regarding aspirin and NSAIDS, there is no contraindication, even with mildly elevated INR. Clopidogrel should be discontinued for 7 days prior to epidural placement.
Heparin and NA:
A couple important points that you must know is this: For heparin, neuraxial placement can occur at anytime on prophylactic dosing, otherwise a PTT should be drawn and be less than 40. After the block is placed, heparin at any dose can be started 1 hour after.
List of AC and timing for block placement
Drug - Neuraxial block timing
Abciximab 2 days
Argatroban/ Bivalirudin / Lepirudin PTT < 40
Alteplase 10 days
Clopidogrel 7 days
Dabigatran 3 days
Dalteparin (prophy)/ (full dose) 12 hours/ 24 hours
Fondaparinux (prophy)/ (full dose) 48 hours/ 72 hours
Ticlopidine 14 days
Tirofiban/ Eptifibatide 8 hours
Soooo…if you place a spinal using hyperbaric bupi, it’ll go to which level?
T5/T6/T7. Normal kyphosis of the back in the supine patient limits the movement of hyperbaric local anesthetic to about the T6 level.
What CSF volume makes blocks go more cephalosporins? What conditions?
With decreased CSF volume, intathecal anesthetics tend to result in a higher block. Pregnancy and ascites can both result in engorgement of the epidural veins, leading to a reduction in volume of the dural sac and CSF. Advanced age have predictable decreases in CSF volume. Severe kyphoscoliosis is really a case by case basis, but it is a known and recognized risk factor. Surprisingly, obesity is not associated with higher spinal blocks.
Adding epi to bupi vs to terracaine
The addition of epinephrine has minimal effect on bupivacaine and ropivicaine, but can extend tetracaine up to an additional half hour.
What happens when you add Fentanyl to a spinal anesthetic?
Faster onset of block, but NO increased duration, no increased intensity of motor block, and no significant dose reduction of LA-because it doesn’t cause a dense enough block alone.
Yep me about the lipophikic opioids and not lipophobic ones: , and why does the lipophopic one have more rosy rap spread and hang around for longer? Tell me more about intrathecal morphine and it’s onset, if it causes respiratory depression, etc. would you give IT morphing for outpatient t procedures?
By learning intrathecal fentanyl (question 25) and morphine, you can essentially get a gauge of other opioids as they represent the two extremes: lipophilic (fentanyl, sufentanyl) and hydrophilic (morphine). Because morphine is hydrophilic (lipophobic), it crosses the dura slower and has a much longer lifespan within the CSF than fentanyl.
Because morphine is hydrophilic (lipophobic), it crosses the dura slower and has a much longer lifespan within the CSF than fentanyl. Because of the slow clearance of the drug (and its hydrophilic properties) it has the greatest rostral spread among opioids. This means two important (board-worthy) things: First, a lumbar intrathecal injection will produce analgesia well into high thoracic levels. More lipophilic drugs like fentanyl will create a more narrow band around the site of injection. Drugs less lipophilic than fentanyl and less hydrophilic than morphine like hydromorphone or meperidine will have an intermediate level of rostral spread
Second, because of its long duration of action and high rostral spread, respiratory depression has two peaks, an early peak and a late peak. Like all opioids, soon after intrathecal injection, opioids can be detected in the CSF surrounding the brainstem, which can lead to respiratory depression. Unlike other opioids, morphine’s slow rostral spread leads to another peak of respiratory depression at about 6 hours after injection (answer A), but can occur later. A 600 mcg dose (less than 300 mcg is typical) leads to late respiratory depression in most people. Also, because of the late peak in respiratory depression, intrathecal morphine should not be used for outpatient procedures. Analgesia from intrathecal morphine has a slow onset (answer B) due to its hydrophilic nature and duration of action (in most cases) longer than 24 hours. Peak analgesic effects are typically at 6-12 hours after injection.