Today's episode features Dr. Amed Logrono from Yale's Primary Care Internal Medicine program. He talks to us about all the things that primary care doctors wished we knew as OB/GYNs!
Fortunately, ACOG also has put together some excellent resources in this regard as part of the Women’s Preventive Services Initiative (WPSI). Check out their well-woman chart for the most comprehensive resource there is on women’s health comprehensive primary screening and prevention.
In follow up to last week’s episode, this week we have a quick episode on local anesthetic systemic toxicity (LAST), a classic CREOG question.
First, a bit about how local anesthetics work:
Medications like lidocaine reversibly block sodium channels → these meds vary in lipid solubility, potency, time to onset, and duration of activity.
You can imagine that some of these medications will be absorbed systemically, especially if you inject it directly into a blood vessel, and can go to other places in the body and block sodium channels in far away places.
Organs that we generally care about in this sense are the CNS and the heart.
The CNS is more sensitive than the heart to effects of local anesthetics, so will generally manifest signs/symptoms of toxicity first.
To prevent systemic toxicity, there is a max dose for various forms of local anesthetics. If injected with epinephrine, these doses are higher due to epinephrine’s vasoconstriction activity (thus preventing systemic absorption by constricting local blood vessels):
ACOG PB 209
Effect on CNS system
Initial = Tinnitus, blurred vision, dizziness, circumoral numbness
After can have nervousness, agitation, muscle twitching due to blockage of inhibitory pathways → seizures
You can also have CNS depression like slurred speech, drowsiness, unconsciousness, and even respiratory arrest
Effect on CV system
Local anesthetics can block fast sodium channels in the Purkinje fibers of the heart → decreased rate of depolarization
Can lead to prolonged PR intervals and widened QRS complexes
Can lead to sinus bradycardia or even ventricular arrhythmias, especially with bupivacaine
Treatment
Stop injecting the local anesthetic!
Call for help - definitely call your anesthesia colleagues.
Also alert cardiopulmonary bypass team because resuscitation may be prolonged.
Some hospitals may have a LAST rescue kit.
Airway management - ventilate, and get advanced airway device if necessary
Control seizures
Benzodiazepines preferred
Avoid large doses of propofol
Treat hypotension and bradycardia - if pulseless, start CPR
Give lipid emulsion therapy - lipid emulsion 20%
If >70kg, bolus 100 mL Lipid emulsion over 2-3 min, then 200-250mL over 15-20 minutes
If <70kg, bolus 1.5 ml/kg lipid emulsion over 2-3 min, then 0.25ml/kg/min of ideal body weight
Continue monitoring - at least 4-6 hours after a cardiovascular event or at least 2 hours after a limited CNS event.
Why do we care about labor anesthesia and analgesia? We’re obstetricians!
Labor hurts!
Technically speaking, evolution of visceral pain to somatic pain in the second stage of labor when the fetus comes down to the perineum → pain through the pudendal nerve and S2-S4 distribution.
There is also a discrepancy with rating of pain and rating of satisfaction with pain relief in certain trials - possibly because there are varying expectations for pain control and labor experience
What is available?
Parenteral or systemic analgesia
IV opioids. Unfortunately, they have little effect on maternal pain scores, provide unreliable analgesia, and can have adverse effects, such as nausea or vomiting.
We usually use fentanyl, morphine or butorphanol (Stadol).
Cochrane review has not found the ideal parenteral opioid and though there is some pain relief with this, it’s poor overall.
Also, all opioids cross the placenta, and there can be some adverse effects on the fetus.
Drugs will take longer to eliminate in the newborn, and can cause respiratory depression if administered close to time of delivery.
Regional (Neuraxial) analgesia and anesthesia
More than 60% of women w/ singleton birth in the US get an epidural or a spinal
Epidural - placement of a catheter into the epidural space; can have repeat or continuous administration of medication; usually a mixture of an opioid with a local anesthetic.
Spinal - single-injection of an opioid, local anesthetic, or both into the subarachnoid space; usually used for cesarean delivery and not for labor because it usually has a limited time frame.
Combined Spinal-Epidural Analgesia
Inject into the subarachnoid space and also a placement of a catheter for ongoing analgesia
This is usually used because of rapid onset of pain relief of spinal, combined with long-acting effect of epidural.
Local anesthesetics
Pudendal nerve blocks - local anesthesia that is injected transvaginally into the vicinity of the pudendal nerve below the ischial spines; usually just for second stage of labor or to help with lac repairs
Local infiltration (usually for lac repair)
Inhaled agents
Nitrous oxide - 50% of NO and 50% O2 with demand valve so only given when patients inhale using the mask.
Analgesia provided by NO is less effective than epidural when we look at pain scores; but NO is superior for mobility because patients can still move around, and also has quick termination of effect.
General Anesthesia
Exceptionally rare use for a vaginal delivery, and sometimes used for emergent cesarean sections.
The main issues is that these agents will transfer to the fetus → depression
Also harder to manage airway of pregnant patient due to anatomic changes (increased airway edema).
Risks of Regional Analgesia and Anesthesia
Maternal
Overall very low risk of maternal morbidity and mortality.
In a registry that was collected over 5 years (ended in 2009), in >300,000 recorded cases of anesthesia use, there were 157 complications.
There were 30 maternal deaths in this cohort, none of which were attributed to anesthesia.
There were 2 cardiac arrests attributable to anesthesia, 4 cases of epidural abscess or meningitis, 1 epidural hematoma, 10 failed intubations (no aspirations), 58 high neuraxial blocks
Minor complications can be things like pruritis, epidural headaches, hypotension, nausea/vomiting
Fetal
Usually related to maternal effects of hypotension or transplacental passage of analgesic or anesthetic drugs
Opioids can lead to neonatal depression (ie. respiratory depression, decreased muscle tone, decreased sucking)
Alterations to FHT can also be seen; ie. minimal variability, bradycardia, prolonged deceleration in the first 15 minutes following spinal-epidural analgesia.
Who can’t get regional anesthesia?
Thrombocytopenia - relative contraindication, but safe lower limit for platelet count hasn’t been established.
One study stated that risk of epidural hematoma among obstetric patients was 0-0.6% when platelets were 70-100k, but stated that data was insufficient to assess risk when platelets were <70k.
So in most cases, epidurals/spinals can be considered same if platelets are 70K or above, as long as platelets are stable.
Low dose aspirin - not a contraindication!
Anticoagulation
Unfractionated heparin
Prophylactic dose (i.e., 5000u BID):
Not contraindication to neuraxial techniques
Place or remove catheter 4-6 hours after last dose.
Intermediate dose (7500-10000u BID):
Likely low risk to proceed with neuraxial anesthesia if > 12 hours after last dose
High dose (>20,000u total daily):
Placement >24 hours after last dose and must have activated partial thromboplastin time within normal range or anti-factor Xa level undetected.
If taking unfractionated heparin >4 days, platelet count should be assessed for possible HIT.
Resume UF heparin >1 hour after catheter removal.
Low molecular weight heparin (ie. Lovenox)
Prophylactic dosing:
Stop medication at least 12 hours before placement or removal of epidural catheter
Therapeutic dosing:
24 hour delay in catheter placement.
Resume LMWH >4 hours after catheter removal
Space-occupying brain lesions - contraindication to neuraxial techniques because dural puncture can lead to increased intracranial pressure → hindbrain herniation.
However, not all space-occupying lesions result in increased ICP.
If imaging shows no mass effect, hydrocephalus, or other features suggestive of increased ICP, risk of herniation is minimal and epidural analgesia or anesthesia can be considered.
We’re so thrilled that a group of incoming PGY-1s at the University of Michigan, led by Liz Southworth, MD, has put together a CREOGS Over Coffee-inspired #OBGynInternChallenge for residents everywhere!
Follow along with the calendar above to get ready for your PG-1 year, and on social media using #OBGynInternChallenge to review highlights of the featured episodes. You can also use our Episode Archive page to quickly navigate to each day’s featured episode and the associated show notes.
Check out PB 196 and PB 197 for the primary reading on this topic!
Remember way back when, when we talked about physiologic changes of pregnancy (Part I and Part II)? Recall that pregnant women are 4-5x more likely than non-pregnant women to experience VTE, owing in part to factors we can trace back to Virchow’s Triad: hypercoagulability, venous stasis, and endothelial injury. In pregnancy we have hypercoagulability: increased clotting potential, decreased anticoagulant activity, and decreased fibrinolysis And we certainly have venous stasis, particularly in the lower extremities due to compression of the IVC by the uterus. Persons with inherited thrombophilias are at even higher risk of VTE owing to these factors.
Inherited Thrombophilas
There are lots of different types of inherited thrombophilias:
Factor V Leiden:
The most common mutation is factor V leiden heterozygosity, and is responsible for about 40% of all VTEs during pregnancy.
By itself, it doesn’t really put you at that much of an increased risk for VTE (only about 5-12/1000 deliveries), but if you have a personal history of VTE as well, then risk goes up to about 10%.
Prothrombin Gene
Heterozygote is next most common mutation; like factor V Leiden, if you are a homozygote, you’re at higher risk of VTE than heterozygote.
Antithrombin gene deficiency
Unommon (only 0.02% prevalence), but it is highly thrombotic
In non pregnant people, the risk of VTE is 25x normal.
More severe deficiencies is associated with increased VTE risk; so, if you have a personal history of VTE, and you have a severe antithrombin deficiency (<60% activity), your risk of VTE in pregnancy could be as high as 40%.
Testing for Inherited Thrombophilias
Testing is generally considered in two scenarios: either a patient who has a history of VTE herself, or the patient has a family member with a known high risk inherited thrombophilia. Screening is generally not recommended for women who have experienced fetal loss or various adverse pregnancy outcomes, outside of those meant for antiphospholipid syndrome testing.
ACOG PB 196
Basis for Anticoagulation in Inherited Thrombophilias
We can divide these mutations in to high and low risk thrombophilias:
High risk = Factor V Leiden homozygosity, prothrombin gene homozygosity, antithrombin deficiency, or factor V leiden + prothrombin gene heterozygosity (meaning one mutation of each gene)
Low risk = Factor V Leiden heterozygosity, prothrombin gene heterozygosity, protein C or protein S deficiency, and antiphospholipid antibody
It is important to realize that according to ACOG, there is insufficient evidence that anticoagulation use will prevent adverse pregnancy outcomes in patients with inherited thrombophilias, such as preeclampsia, FGR, or placental abruption. The indication for anticoagulation is for the purpose of preventing VTE.
Choice of Anticoagulant Agent
Unfractionated heparin (UFH) and low molecular weight heparin (LMWH) - neither cross the placenta and are safe, and are first line choices.
Warfarin - we KNOW that there are harmful fetal effects, especially in first trimester, so don’t use it as first line. The only case that this is used in pregnancy is for women with mechanical heart valves because there is a higher risk of VTE even with LMWH or UFH.
Usually will use LMWH or UFH from weeks 6- 13 in pregnancy and switch back to warfarin later.
Oral direct thrombin inhibitors should be avoided in pregnancy and postpartum because insufficient data on safety.
When and How Much Anticoagulation?
In the Practice Bulletins, there is a large table of conditions with recommendation for anticoagulation. We’ve broken it down a bit for you, as the progression actually is logical once it’s written out.
For inherited thrombophilias, you’ll need to remember the high risk and low risk groupings:
(c) CREOGS Over Coffee, 2020
The other group that should be considered for anticoagulation are patients who may have had a VTE in the past, but do not have evidence of inherited thrombophilia:
(c) CREOGS Over Coffee, 2020
Delivery Considerations on Anticoagulation
Peri-delivery, the use of anticoagulation can be challenging if patients desire or require neuraxial analgesia. PB 196 reviews recommendations for holding anticoagulation before delivery. In general:
Prophylactic doses of UFH or LMWH should be held 12 hours prior to anticipated delivery/admission.
Therapeutic doses of UFH or LMWH should be held for 24 hours prior to anticipated delivery/admission.
UFH may be resumed 1 hour after catheter removal or neuraxial blockade, whether at prophylactic or therapeutic doses.
LMWH may be resumed:
12 hours after neuraxial blockade and 4 hours after catheter removal, whichever is longer, at prophylactic doses.
24 hours after neuraxial blockade and 4 hours after catheter removal, whichever is longer, at therapeutic doses.
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The views expressed herein represent those of the podcast authors personally, not of their institutions.
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