Neuraxial Flashcards
The structures from outside to inside when placing spinal are?
Supraspinous ligamnet > interspinnous > ligmintum flavum > dura > arachnoid
The reason of nausea occurs after spinal?
Unopposed parasympathetic influence, while decreased SNS.
SNS blocked due to T1-L2, where PSN comes from vagus and S2-4
The Bezold-Jarish reflex is
Intracardiac stretch receptors can reflexively decrease HR when filling pressure decreases (due to vasodilation).
The risk of death in AS patients going spinal?
Spinal -> decrease preload and afterload through (-) Symptomatic tone.
Perfusion of LV occurs in diastole, only when aortic diastolic pressure is greater than LVEDP
So decreasing afterload will decrease aortic diastolic pressure-> MI
What sign that indicates high spinal block and diaphragm block at risk?
Grip strength or small finger numbness (C8 distiurbution).
Seizure secondary to LAST?
BZDs if no cardiovascular compromise
Propofol second choice
Intralipid
Why adductor became a favorable then Femoral?
Because it block only saphenous nerve which is purely sensory (less motor block -> increases quadracips strength and early mobilaization).
However the saphenous is often difficult to discern, it runs lateral to femoral artery in proximal thigh (that’s way femoral block almost certain the nerve lateral to artery) then it crosses over to medially in distal thigh.
Because of the crossing over of the nerve distally, it’s advisable to block both sides of femoral artery when saphenous crosses distally for adductor block.
Lovenox stop/restart timing for spinal/epidural?
For 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.
For 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.
Lovenox ASRA guidelines for epidural catheter
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
PTT and INR values that are contraindications for neuraxial?
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 time to stop and restart for neuroaxial?
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.
Drug - Neuraxial block timing
Abciximab …
Argatroban/ Bivalirudin / Lepirudin ….
Alteplase …
Clopidogrel …
Dabigatran …
Dalteparin (prophy)/ (full dose) …/….
Fondaparinux (prophy)/ (full dose) …/….
Ticlopidine …
Tirofiban/ Eptifibatide ….
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
2 factors that has low association with higher spina block?
This is a question about which of these disorders DOES NOT decrease CSF volume. 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.
Warning: Feel free to stop reading here, because unfortunately although for the exam the above explanation should be correct, in reality its not so cut and dry. When applying this to an individual patient, there is a probability that certain factors will result in a high block. In other words, there is a possibility that a pregnant patient will have a high block with 15 mg of bupivicaine, but its not a certainty. The most studied of the patient factors listed above are pregnancy, obesity, and age. Both age and obesity have very low predictive power to predict a high block. Of these two factors, I would recommend choosing obesity as the least likely based on numerous studies and editorials on the subject.
Where would medication travel too if hyperbaric local given for spinal and immediate positioned supine?
Normal kyphosis of the back in the supine patient limits the movement of hyperbaric local anesthetic to about the T6 level.
What medication can be added to spinal to get a faster onset ?
Fentanyl is a lipophilic opioid which is commonly added intrathecally for many of its benefits. Due to it being highly lipid soluble, it crosses the dura “quickly” limiting its duration of action. Also being cleared from the CSF quickly, it less likely to have a significant rostral spread and produces a narrow band of analgesia near the level injected. As a single agent alone, it does not provide surgical anesthesia, but does intensify the sensory (but not motor) block (answer C). Fentanyl can lead to a faster onset of anesthesia when combined with a local anesthetic (answer B), but does not prolong the block (answer A). This is probably due to the fast onset of fentanyl and not some interaction between fentanyl and the local anesthetics making the surgical quality of the block (which essentially requires local anesthetics) faster. In the same way, one could technically say that intrathecal morphine could extend the block (as its effects will be around long after bupivicaine), but not of sufficient quality to tolerate surgery.
Fentanyl provides post-operative pain relief (a few hours) while not delaying PACU discharge (answer D)*. There are mixed reviews of whether or not fentanyl increases the motor block. Most sources say no. Because fentanyl does not produce a very dense block by itself, significant reductions in local anesthetic dose are not well tolerated. Therefore, answer E (allow a significant reduction of bupiviicaine) could be considered correct or incorrect depending on your subjective definition of “significant reduction” (very frustrating I know)! Finally, increasing the density of a block through use of opioids, epinephrine, clonidine, etc does not effect the spread of local anesthetic but can minimally change the level at which anesthesia is produced as opposed to simply loss of temperature discrimination.
