Interpreting Cardiotocography/EFM Part I: Definitions

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Today we take a break from STIs to jump back into obstetrics, and are joined by two very special guests: Liz Kettyle and Linda Steinhardt, both of whom are certified nurse midwives (CNMs) and clinical educators at the Warren Alpert Brown School of Medicine.

ACOG PB 106 (membership required) forms the basis for this episode and in a future episode, we will discuss management of cardiotocography (CTG). Also, for a recent article surrounding the naming of CTG vs. EFM vs. all the other names for this technology, check out a recent AJOG article on its now 50-year history.

We also are using some special sound effects for these episodes! As you listen to the various sounds for different types of decelerations, keep in mind that the higher-pitched sound represents a contraction pattern, and the lower-pitched sound represents the fetal heart rate response.

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.

Menopause Part II: Hormone-Replacement Therapy

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Today we’re talking on menopause once more with Dr. Renee Eger, assistant professor and clinician educator at the Warren Alpert Medical School of Brown University. We spend the second half of our menopause series reviewing HRT and the Women’s Health Initiative (WHI).

You can read more about the WHI here. The study really is two study methodologies in one: there were up to three randomized-controlled trial arms, and an observational arm. The components concerning HRT are dealt with through one of the RCTs.

The RCT dealing with HRT enrolled women into one of three arms: a placebo, an estrogen-only arm in patients without a uterus, or and estrogen-progesterone combination in patients with a uterus. The study was halted at 5.2 years in the E-P arm due to an increase in coronary heart disease, breast cancer, VTE, and stroke, which outweighed a benefit noted in colorectal cancer and fracture risk. The E-alone arm was stopped at 6.8 years average follow up, when the risk of heart disease was found not to be different than placebo.

Subsequent studies, including the Heart and Estrogen/progestin Replacement Study (HERS) have demonstrated at least that E-P and E should not be used for primary or secondary prevention of coronary disease, and thus HRT should not be prescribed for these indications. However, many benefits are particularly pronounced in younger patients using HRT. Thus, the position of the North American Menopause Society (NAMS) reads (emphasis ours):

“For women aged younger than 60 years or who are within 10 years of menopause onset and have no contraindications, the benefit-risk ratio is most favorable for treatment of bothersome VMS and for those at elevated risk for bone loss or fracture.

”For women who initiate HT more than 10 or 20 years from menopause onset or are aged 60 years or older, the benefit-risk ratio appears less favorable because of the greater absolute risks of coronary heart disease, stroke, venous thromboembolism, and dementia.

”Longer durations of therapy should be for documented indications such as persistent VMS or bone loss, with shared decision making and periodic reevaluation. For bothersome GSM symptoms not relieved with over-the-counter therapies and without indications for use of systemic HT, low-dose vaginal estrogen therapy or other therapies are recommended.”

How should you prescribe HRT or other medications to relieve VMS? Below is a summary from ACOG PB 141. Check out CO 565 and CO 556 as well if you are really interested in the topic!

Menopause Part I: Diagnosis and Non-Hormonal Therapies

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Today’s episode features Dr. Renee Eger! Dr. Eger is an Assistant Professor at the Warren Alpert Brown University SOM, and is a North American Menopause Society (NAMS) Certified Menopause Practitioner. She is talking with us this week and next about menopause.

The ACOG PB 141 on Management of Menopausal Symptoms is an excellent resource for all therapies in use for menopausal symptoms. We’ll cover some additional resources for hormonal therapy on next week’s episode. The high yield points for today include:

-Menopause is the cessation of menses for 1 year. The average age of onset in the US is 51.
-Lifestyle modifications are first-line therapy for both vasomotor symptoms of menopause (VMS) and genitourinary syndrome of menopause (GUSM), formerly known as vulvovaginal atrophy.
-Paroxetine 7.5mg daily (Paxil) is the only FDA-approved non-hormonal pharmacologic treatment for VMS.