Espresso: Treatment of Acute Hypertension in Pregnancy and Postpartum

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Our second espresso episode focuses on the acute treatment of severe-range BPs in the pregnant and postpartum patient. More or less, we let the freshly released ACOG CO 767 speak for itself.

Below you’ll find the algorithms we describe in the podcast, which are present in ACOG CO 767. In addition to the below, always remember:

-Obtain IV access and labs (CBC, Creatinine, AST, ALT, urine protein:creatinine ratio) for any newly diagnosed patient with severe-range pressures.
-Avoid labetalol in patients with known asthma, as the beta-blockade effect can trigger respiratory issues, as well as those with CHF or pre-existing cardiac disease. Labetalol may also cause neonatal bradycardia due to beta-blockade.
-Immediate-release nifedipine should not be administered sublingually due to possibility of developing precipitous hypotension. Similarly, parenteral hydralazine may also cause precipitous maternal hypotension.
-IV magnesium sulfate should be given at a 4g or 6g bolus initially, followed by 2g/hr drip for the prevention of eclamptic seizures, if not previously given. Adjusted dosing may be required if renal insufficiency is noted on laboratories. Magnesium sulfate is not an antihypertensive agent.

Breastfeeding Part I

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Today we start a two part series on breastfeeding with Dr. Erin Cleary, Assistant Professor of Obstetrics and Gynecology and Clinician Educator at the Warren Alpert Brown School of Medicine. She’s also the incoming MFM fellow at the Ohio State University — so look out for her in July, Buckeye listeners!

Also, thank you Dr. Daniel Ginn, our first Patreon sponsor — and apologies for the dad joke with your name!

We start today with a discussion of the anatomy of the breast, and in particular with lactation. At the bottom of this post is a corresponding Netter image to guide your listening.

The physiology of lactation is somewhat confusing, but in bulleted summary:
Lactogenesis I Early in pregnancy, human placental lactogen, prolactin, and chorionic gonadotropin contribute to maturation of the breast tissue to prepare for lactogenesis.

  • In the second trimester, secretory material which resembles colostrum appears in the glands.  A woman who delivers after 16 weeks gestation can be expected to produce colostrum.

  • Differentiated secretory alveolar cells develop at the ends of the mammary ducts under the influence of prolactin.  Progesterone acts to inhibit milk production during pregnancy. This makes sense from a viewpoint of energy expenditure- grow your baby first in utero, then switch to focus on growing it with milk.

Lactogenesis II is the onset of copious milk production at delivery.  In all mammals, it is associated with a drop in progesterone levels; in humans, this occurs during the 1st 4 days postpartum, with “milk coming in” by day 5

  • During the next 10 days, the milk composition changes to mature milk.  Establishing this supply is Lactogenesis III, and is NOT a hormonally-driven process like Lactogenesis I or II. Rather, this is supply/demand-driven with expression of milk

  • When the milk is not removed, the increased pressure lessens capillary blood flow and inhibits the lactation process.  Lack of sucking stimulation means lack of prolactin release from the pituitary.

Next week, we’ll be back again with Dr. Cleary discussing breastfeeding myths and contraindications, so stay tuned!

Netter’s Anatomy. Copyright Elsevier texts.

Gestational Diabetes Trio, Featuring A Special Interview with Dr. Donald Coustan

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Happy Holidays to all, and to celebrate the season we have a very sweet triple episode release today! The first two episodes are focused on the pathophysiology, diagnosis, and treatment of GDM, while the third is a special interview with Dr. Donald Coustan, Professor and Chair Emeritus of the Department of Obstetrics and Gynecology at Brown University. Dr. Coustan was recently profiled by AJOG as a “Giant in Obstetrics and Gynecology.” We hope you enjoy the interview and his perspective on GDM and OB-GYN more generally.

The ACOG PB (PB 190) on GDM was recently updated in February 2018. There is also a new bulletin on Pregestational Diabetes (PB 201), though we don’t spend much time on pregestational diabetes today.

We discuss multiple ways to diagnose GDM, based on different organization’s recommendations. The classic Carpenter-Coustan criteria endorsed by ACOG and the National Diabetes Data Group (NDDG) are based on two-step testing. An initial 50 gram glucose tolerance test is performed, and patients move on to the second screen if their 1hr glucose is measured at 130-140 mg/dL, pending on the institution. It is generally accepted that a value >200 mg/dL is diagnostic without moving on to the second step.

The three hour test is based on a 100g glucose load. The cutoffs vary by time point. Two elevated values are needed to diagnose GDM; however, there is increased risk for the patient even with just one elevated value on three hour testing. The classic Carpenter-Coustan criteria as well as the NDDG criteria are shown here from PB 190:

ACOG PB 190: The Carpenter-Coustan criteria are the most commonly used in the USA.

There is also single-step testing proposed by the International Association for the Study of Diabetes in Pregnancy, that uses a 75g, two-hour glucose tolerance test. Any one elevated value (fasting > 92, 1 hour > 180, or 2 hour > 153) is diagnostic of GDM, and no second screen is needed. The ADA has endorsed these criteria recently but also admits that there is not clear-cut evidence to support one screening strategy over another. ACOG endorses the two-step screening at this time.

Much of the research regarding treatment of GDM that we review in the podcast is well-reviewed in PB 190, so we won’t rehash it here. If non-pharmacologic treatments fail (monitored fasting and postprandial blood glucose levels are consistently elevated), an oral agent or insulin is required, with insulin being the gold-standard. How do you initiate insulin? See our guide below!

And remember — postpartum patients with GDM need a 2 hour, 75 gram glucose tolerance test between 4 and 12 weeks postpartum to rule out type 2 diabetes. A fasting > 125 or a 2 hour > 200 is diagnostic. A fasting between 100-125 or a 2 hour between 140-199 demonstrates impaired glucose tolerance. And even with normal values, anyone with GDM has a 15-70% chance of developing T2DM later in life, so it’s an important part of the pregnancy history to correspond back to the patient’s PCP.

Espresso: Medical Management of Postpartum Hemorrhage

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Welcome to our first Espresso Episode! Just like an espresso, this should be a short, sweet, but highly caffeinated review of more familiar topics. These are intended for rapid-fire review — perfect for while you’re running up to that postpartum hemorrhage!

In today’s episode, we really just stick to the medication management for postpartum hemorrhage, though as anyone with experience with these might remember, there are a lot more components than just these medicines to make hemorrhage management successful. That said, an exam, bimanual massage, and uterotonic agents will resolve many of the cases you’ll see on the floor. More important for CREOGs are likely the dosing and side effects of these medicines, which we also review today. The ACOG PB 183 table on these medicines is also below for visual learners.

For when you have a bit more time to sit and breathe after the run up the stairs, check out ACOG PB 183 to review postpartum hemorrhage in full (ACOG membership required).

ACOG PB 183


Nausea and Vomiting of Early Pregnancy

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On today’s episode, we discuss one of the most common ailments of early pregnancy, and recommendations for diagnosis and therapy. ACOG PB 189 (ACOG membership required) goes into all the details and makes for excellent further reading, and to learn all about that PUQE scale!

Probably the highest yield piece of information from PB 189 is the recommended therapy algorithm, which you’ll find below. For your practice, don’t forget about helpful adjunct therapies for acid reflux symptoms, like ranitidine or famotidine.

ACOG PB 189