Postpartum IUD Placement, with Dr. Sarah Prager

This week we are joined by Dr. Sarah Prager, a professor at the University of Washington in OB/GYN and Complex Family Planning. She shares with us some particular expertise in an ever-more common procedure - the postpartum IUD placement. There’s definitely a few pearls in the podcast that are worth listening for!

Definitions: 

• Immediate postplacental insertion: within 10 minutes of placental extraction

• Immediate postpartum insertion: 10 minutes to 48 hours after delivery

• Delayed postpartum insertion: 48 hours to 6-8 weeks after delivery

• Interval placement: IUD placement not related to recent delivery

• Trans-cesarean insertion: IUD placed through the hysterotomy at the time of cesarean delivery

Exclusion criteria:

• Chorioamnionitis/uterine infection

• Prolonged rupture of membranes (18-24 hours)

• Excessive postpartum bleeding that is unresolved

• Extensive genital trauma that would be negatively impacted by IUD placement

Expulsion rates: 

• 10% if placed in the first 10 minutes

• Up to 25-30% if placed after 48 hours

• Limited data on 10 minutes to 48 hours

  • Pilot study in Zambia showed 4% expulsion with “morning after delivery” IUD placement

• Provider experience matters!

  • Study from 1985 showed providers cut their expulsion rates almost in half comparing the beginning to the end of the study

• Take home message: don’t get discouraged! Your expulsion rate will decrease with experience!

Copper vs. LNG-IUD

• Most older data is with various copper IUDs (primarily the Copper T 380A – ParaGard)

• Some limited data with specifically Mirena brand LNG-IUD.

• Recent data often pooled LNG-IUD, without separating different IUDs

• Limited comparative data

  • Possibly higher expulsion rates with LNG-IUD than Copper IUD

  • Could be due to method used for insertion – inserter vs. no inserter

  • LNG-IUD inserters are long enough to reach the fundus of a PP uterus, ParaGard IUD inserters are not

  • There is a dedicated PP inserter for Copper IUD (longer, stiffer, but not available in USA at this time); unclear if it changes outcomes

• Recent study out of Kaiser showed slightly lower expulsion rates for breastfeeding vs. non-breastfeeding people.

  • Largest study to date with mostly LNG-IUD

  • Expulsion rates:

    • 10.7% expulsion by 5 years with placement 0-3 days

    • 3.9% for 3 days to 6 weeks

    • 3.2%for 6-14 weeks postpartum

    • 4.9% for interval placement

Medical Eligibility Criteria:

• CDC: category 1 or 2 at any time, regardless of type of IUD or breastfeeding status.

  • Of course, category 4 if uterus is infected

• WHO: category more nuanced depending on type of IUD and timing of placement

Method of placement:

• With the inserter

  • Need a long enough inserter

  • Often can use the LNG-IUD inserters

  • Also need the inserter to be stiff enough – sometimes doesn’t work with LNG-IUD inserters

  • Dedicated copper IUD inserter both longer and stiffer

• With an instrument

  • Can use a ring forceps

  • Can use a Kelly placenta forceps (longer)

• With your hand

  • No difference in expulsion seen compared with instrument

  • Personal bias – WAY more painful! No-one likes a hand in their uterus

    • Not reported in the early studies that compared this to using a ring

Clinical tips and tricks for successful insertion with an instrument:

• Place a ring on the anterior lip of the cervix

• Hold the IUD gently in a ring forceps (don’t click down if LNG-IUD – don’t want to disrupt the LNG delivery system!)

• Know the orientation of the IUD with respect to the orientation of the ring handles to make sure you place IUD with the proper orientation in the uterus!!!

• Once the IUD is in the lower uterine segment, gently let go of the ring on the cervix and place the non-dominant hand on the uterine fundus

• Drop your wrist! Drop your shoulder! Aim for the fundal hand

  • Angle different from interval insertions – basically aim for the umiblicus

  • Will not go wrong if you aim for the fundus! Feel it with your fundal hand!

• Let go of the IUD and gently remove the ring without pulling on the IUD or strings

• If strings are visible, cut at the os

  • Can also pre-cut the strings of LNG-IUDs so they are about 10 cm

  • Cutting strings can sometimes pull the IUD lower or out

• Can use ultrasound if you want!

If using an inserter: 

• Pre-deploy the IUD – you do not need the narrow profile with an open cervix!

• Personal bias – don’t use the inserter

If using your hand:

• Change your gloves

• Precut the strings

• Hold between the index and middle fingers with the strings laying across your palm

• Make sure you don’t pull it out when you remove your hand!

If trans-cesarean placement:

• Close 1/3 – ½ the hysterotomy then place

• Precut the strings shorter before directing down into the cervix

• Personal bias again toward instrument placement, but usually hand and inserter also work fine

Follow-up care:

• See patients at 1-2 weeks postpartum and trim strings as needed.

  • May need to do this again at 6-week visit

• If strings not visible at follow-up, do an ultrasound to verify presence of IUD in the uterus

  • If IUD there, NO NEED FOR ROUTINE ULTRASOUND TO CHECK CONTINUED PRESENCE OF THE IUD

  • Counsel patient that efficacy unchanged, but removal may be more complicated if strings don’t emerge from the cervix

    • This should have been a counseling point during consent!

The BEAM Trial

We’re back this week to talk through another magnesium trial. This time, we explore the BEAM Trial, aka, “A Randomized, Controlled Trial of Magnesium Sulfate for the Prevention of Cerebral Palsy.”

BEAM = Beneficial Effects of Antenatal Magnesium Sulfate 

Background

• Who did the study and who published it?

  • Conducted by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Neurological Disorders and Strokes + The George Washington University Biostatistics Center 

  • Where was it published? The New England Journal of Medicine in 2008 

• Why was the study done? 

  • Cerebral palsy is a huge cause of chronic childhood disability and preterm birth is a big risk factor 

  • Previous case-control study that showed that those infants who had cerebral palsy were less likely to be exposed to mag than those that didn’t 

    • But smaller trials had shown that maybe mag did not decrease infant death or cerebral palsy.

  • Biological plausibility: mag may reduce vascular instability, prevent hypoxic damage, and mitigate cytokine or excitatory amino acid damage 

• What was the research question?

  • Will giving magnesium sulfate to women who are at high risk of preterm delivery decrease the risk of CP in their children? 

Methods 

• Who participated and when?

  • Subjects were recruited from December 1997 - May 2004

  • Study conducted at 20 participating MFMU sites across the US 

  • Eligibility: 

    • Singletons or twins between 24-31 weeks of gestation and at high risk of delivery because of PPROM (22-31 weeks) or cervical dilation of 4-8 cm and intact membranes 

      • They say 24-31, but then mean 24w0d - 31w6d 

    • Indicated preterm delivery anticipated within 2-24 hours 

  • Exclusion criteria

    • If delivery was anticipated in <2 hours 

    • If cervix >8 cm 

    • PPROM <22 weeks 

    • Unwillingness for obstetricians to intervene for benefit of fetus 

    • Major fetal anomalies or IUFD 

    • Maternal hypertension or preeclampsia 

    • Maternal contraindication to mag sulfate 

    • Receipt of IV mag in the previous 12 hours 

• How was the study done?

  • Double blind 

  • Subjects randomized to either IV mag (loading dose 6g for 20-30 min, then maintenance of 2g/hour) or placebo 

  • If delivery did not occur in 12 hours, and not imminent, infusion was stopped, and restarted if delivery became imminent again 

  • If >6 hours had passed since discontinuation of study med, then re-bolused 

  • Randomization was made with stratification for clinical center and in twin gestations, weeks of gestation (<28 or >/= 28 weeks)  

• What outcomes were they looking for?

  • Primary outcome

    • Composite of stillbirth, infant death at 1 year of age, or moderate or severe cerebral palsy as assessed at or beyond 2 years of age (ages corrected for prematurity) 

      • They followed these babies out for >2 years! 

        • Had certified pediatrician or pediatric neurologist to make diagnosis of CP with criteria that they list 

        • If CP was diagnosed, then the Gross Motor Function Classification System (GMFCS) was used to assess severity 

      • Infants that had a normal neurological exam at 1 year, could walk 10 steps independently, and had bilateral pincer grasp were declared free of CP and were considered “normal” for purposes for primary outcome 

  •  Secondary outcomes

    • Maternal outcomes and complications 

    • Adverse events potentially attributed to study intervention 

    • Neonatal complications 

    • CP at 2 years of age that is mild, mod, or severe

    • Stillbirth

    • Infant death

    • Scores on the Bayley Scale of Infant Development II administered at 2 years of age 

    • Cranial ultrasounds were done on all neonates   

  • Analyses were done stratified according to if randomization occurred at <28 weeks vs. >/= 28 weeks 

• A word on statistics

  • Power calculation

    • Assumed that primary outcome would occur in 14% of placebo group and assumed death rate of 6%, and that rate of mod to severe CP among survivors would be 8% 

      • One study in 2006 looking at survival without major morbidity was 92% at 30 weeks

      • These rates may have been much higher in 1997-2004 compared to now.

    • Deemed 2000 to be enough for detection of a 30% reduction in this outcome with Type I error of 5% and power of at least 80% 

Results

• Who did they recruit? 

  • 2241 eligible women were enrolled

    • 1096 assigned to receive mag sulfate (1188 fetuses because they included twins!) 

      • Ultimately had 1087 women observed at delivery (1179 fetuses) 

      • 80 infants died before initial discharge home, and 18 infants died between discharge and 1 year 

      • 1133 fetuses and children included in primary analysis 

      • 1087 women included in maternal outcomes 

    • 1145 assigned to receive placebo (1256 fetuses) 

      • Ultimately had 1141 women observed at delivery (1252 fetuses) 

      • 71 infants died before initial discharge home, and 17 infants died between discharge and 1 year exam 

      • 1203 fetsues and children included in primary analysis 

      • 1141 women included in maternal outcomes analysis 

  • Baseline characteristics were similar in two groups 

  • Adherence to the protocol was very high! Only 1.4% had off-protocol use 

  • Median dose of magnesium was 31.5g (IQR 29-44.6g)

    • Just calculating that out: that’s like 12.75 hours of mag when used continuously!

• Outcomes

  • Mod or severe cerebral palsy or death (primary outcome) - not different!

    • RR 0.97, 95% CI 0.77-1.23 

      • In mag group: 118/1041 pregnancies (11.3%) 

      • In placebo group: 128/1095 pregnancies (11.7%) 

  • Mod or severe cerebral palsy on its own - significant difference

    • 1.9% vs. 3.5% in mag vs. placebo 

    • RR 0.55, 95% CI 0.32 - 0.95

  • Risk of stillbirth

    • 9.5% vs. 8.5% in mag vs. placebo (RR 1.12, 95% CI 0.85 - 1.47), not different  

• A word on the stratified outcome

  • No real difference in any outcome except for risk of mod or severe cerebral palsy 

  • In fact, when they stratified to <28 weeks and >/= 28 weeks: only difference was seen in the group that was <28 weeks

    • Mag 12/442 (2.7%) vs. Placebo 30/496 (6.0%) - RR 0.45 (0.23-0.87) 

    • If looking at >28 weeks: Mag 8/599 (1.3%) vs. Placebo 8/599 (1.3%), RR 1.0 (0.38-2.65) 

• Secondary outcomes

  • Neonatal:

    • Percentages of mild, moderate, and severe cerebral palsy (not including dx at 1 year) were much smaller in the mag sulfate group compared to placebo (p= 0.004) 

      • Mild: 2.2% vs. 3.7% 

      • Mod: 1.5% vs. 2.0% 

      • Sever: 0.5% vs. 1.6%  

  •  Obstetric

    • Overall similar such as gestational age at delivery, antenatal steroid receipt, chorio, C/S, endometritis, pulmonary edema  

  • Adverse events

    • Significantly higher in the mag group!

What was the impact of all of this? 

• We now give magnesium to people at risk of imminent delivery who are <32 weeks!

  • Committee Opinion 455: Magnesium Sulfate Before Anticipated Preterm Birth for Neuroprotection

  • As with preeclampsia, your magnesium dosing may vary by institution for a number of reasons.

• Some lingering questions:

  • How much time with mag is enough?

    • These researchers used 12 hours and then turned it off if no imminent delivery 

    • And then re-bolused if >6 hours from last mag 

    • But… how many people got 12 hours? How many people got only 3 hours? It seemed like the median number of hours was 12.75 (calculated based on dose of 31.5g, and based on 6g loading and 2g/hr) 

      • But IQR would make this about 11.5 h - 19.3 hours

  • How much time off of mag before effect wears off?

    • Study protocol redosed at 6 hours with loading dose but… what is the therapeutic range anyway? 

    • We have all these different doses from Crowther, Marret, and Rouse  

    • Did the Marret study not have any difference in effect because the numbers were small or because the mag dosing was too little?

The MAGPIE Trial

We’re going to start dedicating a few episodes to landmark trials of obstetrics and gynecology. Have a suggestion for other trials we should review? Let us know!

The MAGPIE Trial

Do Women with pre-eclampsia, and their babies, benefit from magnesium sulfate? The Magpie Trial: a randomized placebo-controlled trial 

MAGPIE = MAGnesium sulfate for Prevention of Eclampsia

Find the trial text available here from The Lancet (2002)

Some general background information 

• Magpie Trial Collaborative Group - huge group that spanned many continents and countries.

• Funded by lots of people, but ultimately coordinated by the Resource Centre for Randomised Trials at the Institute of Health Sciences in Oxford, UK

• Why was the study done? 

  • For many decades, anticonvulsant drugs were used on women with pre-eclampsia with the thought that it could prevent eclamptic seizures. Of these, magnesium sulfate was one of the medications 

  • However, in 1998, a systematic review looked at four trials compared anticonvulsants with no anticonvulsants, and of these, magnesium sulfate was thought to be the most promising choice for eclampsia prevention

  • At the time of the study, while magnesium was starting to be used more and more to prevent seizures in those that had preeclampsia, there were still those that used other medications like diazepam, other benzos, phenytoin, barbiturates, etc. 

• What was the research question? 

  • Do women with pre-eclampsia or their babies (or both) “do better” if they are given magnesium sulfate compared to placebo, regardless of whether treatment is started before or after delivery and irrespective of any previous anticonvulsant therapies

Methods 

• Who participated, and when?

  • Initial pilot trial ran from 2/23-7/14/1998 

  • Actual trial was from 7/15/1998-11/29/2001. 

  • Study was conducted in 33 countries and spanned 6 continents

  • Eligibility:

    • If they had preeclampsia and uncertainty about whether to use magnesium 

    • Had not yet given birth or <24 hr postpartum 

    • BP had to be >140/90 mmHg x2 , with proteinuria 1+ or more 

    • Note: their definition of severe preeclampsia were a little different 

      • Severe: DBP >110 mmHg x2 or SBP > 170 mmHg x2 or proteinuria >3+

        • Or DBP >100, or SBP >150, and proteinuria >2+ and at least two signs or symptoms of imminent eclampsia  

  • Exclusion criteria:

    • Hypersensitivity to magnesium, hepatic coma due to renal failure, or myasthenia gravis 

    • If urine output was <25 mL/hr, then the dose was halved  

• How was the study done? 

  • Patients were randomized and groups were balanced for severity of preeclampsia, gestation at randomization, delivered or not, if given anticonvulsant drugs before trial entry, if multiple pregnancy, and country

  • Randomized to either magnesium or placebo

    • Magnesium: 4 g magnesium loading dose over 10-15 minutes; maintenance was then followed by infusion over 24 hours of 1g/hr

      • If areas of low resource needed to do IM, then it was an initial 4 g IV combined with maintenance of 5 g magnesium IM injected into each buttock (10g total) every 4 hours for 24 hours 

    • Placebo: similar looking pack, but was saline in the same mL amounts 

  • Monitoring:

    • Monitored reflexes - if these were depressed, then mag dose was adjusted to prevent toxicity 

    • Checked reflexes and respirations q30 minutes 

    • If eclamptic seizure: trial had to be stopped; eclamptic rescue pack was given with two packs; so those that had no mag were given 4 g mag total, and those with mag previously were given another 2g  

  • Outcomes of the trial:

    • Primary: eclampsia and death of baby before discharge from hospital (for women who were randomized before delivery)  

    • Secondary: serious maternal morbidity (won’t go through all of them, but essentially resp depression, resp arrest, pneumonia, cardiac arrest, coagulopathy, renal failure, liver failure, pulmonary edema, cerebral hemorrhage), toxicity (ie. need for ca gluconate, stopping or reducing mag), and other side effects of mag sulfate (ie. n/v, flushing, drowsiness, confusion, etc)

      • If women were randomized before delivery: also looked at complications of labor and delivery, neonatal morbidity 

    • Other: LOS, admission to ICU, NICU LOS 

What were the results? 

• 10,141 women were randomized at 175 hospitals in 33 countries

  • 47% in Africa, 27% in the Americas, 15% in Asia, 10% in Europe 

  • Data was available for 10136 women, follow-up was available for 10,110 

• Baseline characteristics (ie. age, primiparity, systolic BP at entry, severe preeclampsia, other problems of preeclampsia, gestational age at entry) were not different at entry 

• Outcomes

  • Primary outcomes

    • Significantly fewer eclamptic convulsions among women with mag sulfate then those in placebo (reduction by about 58%) 

      • (0.8% vs. 1.9% - small numbers 40 vs 96), RR 0.42

      • This effect was seen in patients who had severe preeclampsia and those without severe preeclampsia (RR for both is 0.42) 

    •  No difference in baby death for those randomized before birth 

  • Maternal mortality - also lower among women allocated to mag sulfate (0.2% vs. 0.4%), Relative risk reduction of 45% 

  • Secondary outcomes

    • No clear difference in any measure of maternal morbidity or in composite measures of serious morbidity  

      • There WAS significantly increase in side effects of mag sulfate in mag group( ie. flushing, n/v, muscle weakness, headache, hypotension, dizziness, etc) 

    • No difference in neonatal morbidity 

What was the impact of all this? 

• This was a huge landmark study in Ob/Gyn because of how many people it included across many countries, in both resource rich and resource poor settings 

• Their data was very good: high compliance, high completion of the study 

• Clearly demonstrated that mag sulfate decrease the risk of eclampsia from preeclampsia

• No increased ill effects on babies 

• Also provided a regimen (4g then 1g/hr) as well as timing (24 hours) 

What about now? 

At our institution, we only treat preeclampsia with severe features with magnesium.

But in this study, they included all patients with preeclamptics. Why the change? 

• When looking at the MAGPIE trial, specifically at the women enrolled from high-resource settings in the Western world, the reduction rate of eclamptic seizures was not statistically significant 

  • RR 0.67, 95% CI 0.19-2.37 

• A quarter of women reported adverse effects with magnesium sulfate, primarily hot flashes, and rate of CS was increased by 5% when mag was used 

• Two small randomized trials that allocated women with preeclampsia without severe features to either placebo or mag → no cases of eclampsia among women allocated to placebo and no significant difference in proportion of women that progressed to severe preeclampsia (but small size limits this) 

• Finally, rate of seizures in preeclampsia with severe features w/ mag is 4x higher than those without severe features (4/200 vs 1/100) 

• Also, with calculations of previous data, it appears that 129 women need to be treated to prevent 1 case of eclampsia, but in those with symptoms (ie. headache, blurred vision, etc), NNT is 36 

• What does the practice bulletin say?

  • Evidence less clear about preeclampsia w/o SF and mag 

  • Can be individualized by institution or by physician  

What about dosing? 

• MAGPIE

  • Dosing is 4g loading followed by 1g/hr 

  • But at different institutions, we have seen 6g loading, 2g/hr or 4g loading, 2g/hr 

  • What’s right??  

• The case for more vs. less magnesium

  • There is sparse data about the therapeutic range, which is usually 4.8-9.6 mg/dL or 4-8 mEq/L, but accurate mg concentration clinically effective in prevention of eclampsia has not been established 

  • Higher infusion rates increase potential for toxicity, and infusion rates >2g/hr have been associated with increased perinatal mortality in systematic review of randomized trials 

  • Lower starting bolus may increase time to therapeutic dosing 

  • Then.. there’s the BEAM trial…

    • Mg for cerebral palsy prophylaxis for babies from 24-31 weeks gestation  - regimen was 6g bolus followed by 2g/hr 

    • So many institutions will try and get two birds with one stone (6g bolus, 2g/hr for both CP prophylaxis and seizure prophylaxis if <32 weeks) 

  • … As well as the ACTOMgSO4 trial 

    • Doen in Australia and New Zealand for mag for fetal neuroprotection

    • Their dose was 4g bolus and 2g/hr 

  • Institution dependent, but we have seen a lot of combinations of both! 

Take away points: 

• Magnesium sulfate can help decrease eclamptic seizures in patients with preeclampsia 

• We have very good date to suggest it can decrease this rate by about 50% 

• However, mag is not a benign drug - 25% have side effects

• You should dose the mag somewhere between 4-6g loading dose and 1-2g/hr, but this is institution dependent 

• It is also institution dependent regarding if preeclampsia without severe features needs mag (in MAGPIE, had same amount of decrease in eclamptic seizures as preeclampsia w/ SF) 

• However, the number of those that get eclamptic seizures overall is low, and even lower in those with preeclampsia w/o SF, so there can be an argument for increased toxicity/side effects with increased NNT for those with PEC w/o SF and therefore forego it 

Obstetric Lacerations: Repair and Prevention

Here’s the RoshReview Question of the Week!

After a forceps delivery of a 9 lb neonate, a perineal laceration is noted with both the external anal sphincter and internal sphincter torn. During the repair, a glistening white fibrous structure is sutured together in a continuous, nonlocking fashion. What tissue is this?

• Anal mucosa

• External anal sphincter

• Internal anal sphincter

• Transverse perineal muscle

Check out if your answer is correct and enter the Qualifying Exam QBank Giveaway at the links above!

---

Anatomic Review

• Perineal body anatomy – most common site of injury

  • This is the fibromuscular mass in the middle line of the perineum at the junction between the urogenital triangle and the anal triangle  

    • Bulbospongiosus 

    • Superficial transverse perineal muscle 

    • Deep transverse perineal muscle 

  • Below this = anal sphincter complex 

    • External anal sphincter – voluntary control; provide squeeze pressure of the anal canal 

    • Internal anal sphincter – involuntary (autonomic) control and provides up to 80% of resting pressure of the anal canal. Very important for continence 

So how often do obstetric lacerations occur? 

• Varying numbers, but about 53-79% of women will sustain some type of lac during delivery 

• Types 

  • First Degree – injury to perineal skin only 

  • Second Degree – involves perineal muscles but not involving anal sphincter 

  • Third Degree – injury involves the anal sphincter complex 

    • 3a: <50% of external anal sphincter thickness torn 

    • 3b: >50% of external anal sphincter thickness torn 

    • 3c: Both external and internal anal sphincter torn 

  • Fourth Degree – injury involves anal sphincter complex and anal epithelium 

    • Studies show (obviously) that women with 4th degree lacs are at highest risk of reporting bowel symptoms at 6 months postpartum 

    • Report bowel control 10x worse than women with third degrees 

• What about episiotomies? 

  • Surgical enlargement of the posterior aspect of the vagina by incision to the perineum to facilitate the second stage of labor 

  • Rates have decreased since 2006 

    • However, 12% of vaginal births include episiotomies based on 2012 data 

  • Difficult to separate contribution of vaginal birth, operative delivery, episiotomy, and OASIS to pelvic floor function and anatomy 

  • Systematic review showed that routine episiotomy offered no immediate or long-term maternal benefit in perineal laceration severity, pelvic floor dysfunction, or pelvic organ prolapse 

    • In other reviews though, episiotomy has been associated with increased risk of postpartum anal incontinence; seen in one meta-analysis: increased risk of anal incontinence even if no extension into anal sphincter complex 

  • Routine episiotomy did not improve self-reported sexual function outcomes; more likely to have pain with intercourse in months after pregnancy and slower to resume intercourse than women whom episiotomy use was restricted 

  • So… there is a time and place for episiotomies, but don’t routinely cut them 

What are the risks for higher order lacerations, ie. OASIS? 

• Operative deliveries 

  • Forceps (OR 5.50), VAVD (OR 3.98) 

• Midline episiotomy (OR 3.82)  

• Increased fetal birth way (mean difference 192.88g) 

• Midline episiotomy + forceps substantially increases the risk of 3rd and 4th degree laceration 

• Other ones that are less modifiable: 

  • Primiparity 

  • Asian ethnicity (problematic)

  • Labor induction 

  • Labor augmentation 

  • Epidural use 

  • Persistent OP 

Ok, so now that we’ve talked about all the scariness, how do we prevent them? 

• Antepartum or intrapartum perineal massage 

  • Thought is to decrease perineal muscle resistance and reduce likelihood of lacs 

    • In studies that compared antenatal perineal massage to no-massage, digital massage from 34 weeks gestation on was associated with modest reduction in perineal trauma that required suture repair (RR 0.91), and decreased episiotomy 

    • Perineal massage during second stage of labor may reduce 3rd and 4th degree lacs when compared with “hands off” methods but was not associated with significant changes in rate of birth with intact perineum 

  • Perineal support: data is so-so 

    • Meta-analysis with >6600 women – did not demonstrate protective effect for OASIS 

    • However, three nonrandomized studies showed significant reduction 

    • But techniques of support not well described 

• Warm compress 

  • Meta-analysis with 1525 women 🡪 randomized to warm compress or no in second stage of labor 🡪 did reduce 3rd and 4th degree lacs 

  • Did not increase rate of women having intact perineums 

• Birthing position 

  • Upright or lateral birth position compared with supine or lithotomy associated with fewer episiotomies and operative deliveries, but higher rates of second-degree lacs (overall low quality data) 

  • Meta-analysis of five randomized trials showed no clear benefit 

  • Recent randomized trial: lateral birth position with delayed was compared with lithotomy positions 🡪 lateral positive with delayed pushing more likely to deliver with intact perineum 

• Delayed pushing – no difference in lacerations

How do we manage obstetric lacerations?

• Periclitoral, periurethral, labial lacerations 

  • Small tears of the anterior vaginal wall and labia are relatively common 

  • If superficial and no bleeding – can be left unrepaired 

  • However, if bleeding or distort anatomy, should repair and also consult experts if you do not feel comfortable with it 

• First and second degree 

  • Insufficient evidence exists to recommend surgical or nonsurgical repair of first or second degree lacs 

  • A lot of data does not include long-term outcomes 

  • Use clinical judgement about repair 

    • Continuous suturing is preferred over interrupted suture 

    • Associated with less pain up to 10 days postpartum, less analgesia used, and lower risk of having suture material removed postpartum 

    • Use absorbable synthetic suture like polyglactin (ie. Vicryl) 

• OASIS injuries 

  • Overt OASIS reported in 4% of women in the US

    • Occult OASIS may be later identified by endoanal ultrasonography, but have no clinical findings – occur in 27% of women after first vaginal delivery 

  • The first thing to do: really look! If you suspect, do a digital rectal exam. Examine the perineal body and also the vaginal mucosa. See if you can start to see fibers of the internal and external anal sphincter 

    • SIM has been shown to be helpful in helping providers identify and repair these 

  • How to repair for OASIS 

    • Anal mucosa – expert opinion varies on technique and suture material 

      • Subcuticular running repair that uses a transvaginal approach and interrupted sutures with knots tied in the anal lumen have been described 

      • Suggest using 4-0 or 3-0 polyglactin or chromic 

      • No comparative trials have been done 

    • Internal/external anal sphincter 

      • Identify the area of the internal and external anal sphincter 

      • Because of retraction, we will usually place an Allis on either side of the external anal sphincter muscle to bring them together. Can cross the Allis’s and do a rectal to see if you are bringing the right muscles together 

      • Suture fascial sheath as well as muscle! 

      • Methods: End-to-end and overlap repair 

        • Remember: overlap requires full thickness disruption and 1-1.5 cm torn muscle on either end, so don’t use it for 3a or partial thickness 3b sphincter injuries 

        • Expert opinion: use 3-0 or 2-0 polyglactin suture

        • Meta-analysis of six randomized controlled studies showed no difference between two techniques at 12 months of perineal pain, dyspareunia, or flatal incontinence, but there were lower incidence of fecal urgency and lower anal incontinence scores in women with overlap repair 

        • No significant difference in quality of life or anal incontinence symptoms 36 months after repair  

      • We tend to do end-to-end because of visualization; PISA technique

• Antibiotics for OASIS 

  • Wound complications (ie. Infection, breakdown) are decreased when intrapartum antibiotics are administered 

  • So single dose of antibiotics (studies looked at single dose of second gen cephalosporin) is reasonable. Further research is needed to determine whether severe perineal lacerations warrant routine postpartum partum antibiotics to prevent complications 

Complications from severe perineal trauma 

• First six weeks 

  • After OASIS, 25% of women experience wound breakdown, 20% experience wound infection 

  • Those with complications will have more pain than women with normal healing 

  • Possible to have fistulas (9% of rectovaginal fistulas in the US are associated with OB trauma) 

• How to care for them? 

  • Pain control, avoid constipation, and evaluate for urinary retention 

  • In one study, use of oral laxative was associated with significantly less pain and earlier bowel movement 

  • Monitored frequently for wound healing 

  • Pelvic floor exercise + biofeedback physiotherapy has been suggested 

What about next pregnancies? 

• Increased risk of OASIS in the next pregnancy, but absolute risk is low (3%) 

• Can have elective cesarean 

  • But there is no difference when there is vaginal delivery or elective cesarean in fecal urgency, anal incontinence, or bowel-related quality of life 

Thrombocytopenia in Pregnancy

Here’s the RoshReview Question of the Week!

A 23-year-old primigravid woman at 25 weeks gestation presents to the prenatal appointment to follow up on lab results. Her platelet count is noted to be 77,000/μL, decreased from 205,000/μL in the first trimester. She reports no abnormal bruising or bleeding. What is the most likely reason for her thrombocytopenia?

• Autoimmune process

• Consumptive coagulopathy

• Deficient von Willebrand factor-cleaving protease

• Hemodilution

Check your answer and enter the QE Exam Giveaway at the links above!

---

Practice Bulletin 207 is our companion reading this week!

Introduction 

• Evaluation of thrombocytopenia in pregnancy can be difficult because there are many things that could cause it - not all of them are related to pregnancy 

• Definition: when platelets are <150,000/microL 

• So what is normal? 

  • Recall in our very first few episodes that pregnancy can lead to increased plasma volume and not necessarily an equal increase in blood components 

  • This can lead to what appears to be some dilutional effects 

  • In the National Health and Nutrition Examination Survey (NHANES), the mean plt count in pregnancy is as follows: 

    • Non pregnant: 273k 

    • 1st trimester: 251k

    • Second trimester 230k

    • Third trimester 225k 

    • Delivery 217 k 

    • Postpartum (7 weeks) 264k  

• Definitely suggests that some decrease in platelet count could be expected in pregnancy

What are the causes of thrombocytopenia in pregnancy?

• Gestational thrombocytopenia - benign and self limited; may even occur in the first trimester, but usually is more common as pregnancy continues; frequency is 5-10% at the time of delivery

  • But remember this is a diagnosis of exclusion! It’s acceptable if there is mild thromboctyopenia, but again, you should look if Plt <100k  

•  Immune Thrombocytopenia (ITP) - 1-3/10,000 pregnancies, but really low plts only affect a small portion of these

  • ITP is more frequent in pregnancy than in the general adult population but may be because of recognition (checking more frequent CBCs in preg) 

  • Autoimmune condition where antiplatelet antibodies interfere with platelet production and causes destruction of circulating platelets

    • Diagnosis based on exclusion of other causes of thrombocytopenia  

• Preeclampsia/HELLP Syndrome

  • Remember that it is very rare <24 weeks, and there are usually other signs and symptoms as well like elevated BP, headache, vision changes, etc. As well as other hematologic abnormalities like anemia due to hemolysis (high LDH), and may have abnormal LFTs 

  • We won’t go too much into preeclampsia since we discuss it elsewhere, but always something to keep in mind 

• Less likely things, but still things to keep in mind 

  • DIC - Disseminated intravascular coagulation

    • There is usually an underlying cause of this such as placental abruption, sepsis, etc 

    • Patients will have bleeding and oozing at IV sites for example 

    • Usually will have low fibrinogen and elevated PT and PTT labs as well  

  • Acute fatty liver of pregnancy 

  • Thrombotic thrombocytopenic purpura (either immune or hereditary)

    • Will usually present with purpura, can have neurological changes, fever, kidney injury, can have elevated BPs and may be confused with PEC 

    • Will have reduced activity of ADMATS13, but this may be a send out lab in most places and will not come back for some time 

    • Will have schistocytes on smear 

  • Lupus 

  • Infection

  • Inherited platelet disorders

So… when should we start to worry?

• When platelets are: 

  • If platelets are between 100k-150k if there are risk factors present (but usually, do not need work up and can be attributed to gestational thrombocytopenia) 

  • At any point <100k (usually this is beyond the lower end of gestational thrombocytopenia)

    • Plts of <100k only occur in 1% of uncomplicated pregnancies 

    • Remember that there is increased risk of spontaneous bleeding if Plt <20k 

    • Some institutions have cut offs for platelets for ability to give neuraxial analgesia - some places are 70-80k, some places are 100k. Please check with your institution and your patients, because this may require treatment or your patient won’t get an epidural! 

Ok, so that’s a lot of causes… how do I go about figuring out what to do? 

• Evaluation of the patient

  • Get a good history and physical - this can sometimes help you determine what it is not

    • If patient is well appearing, with no pain, vaginal bleeding, elevated blood pressure or other complaints, it’s usually not going to be something like AFLP, DIC, TTP, or preeclampsia  

    • Look through the patient’s chart: what were their platelets before? What other medical problems? What about new medications? 

    • Any history of lupus, TTP, liver disease, anemia

    • You have the CBC - did the lab do a smear? Are there abnormalities on the smear, like schistocytes? 

    • Most of the time, if you have someone who is sitting in the clinic and appears well, you may have some time  

• The asymptomatic patient with Plt >100k

  • Usually, plts between 100-150k without other cytopenis or other major clinical findings can be attributed to gestational thrombocytopenia 

  • The other major cause could be ITP, but minor ITP with plt >100k also does not need treatment 

  • Our practice is to check plts monthly to make sure they do not drop below 100k, or below threshold for neuraxial analgesia 

• The asymptomatic patient with Plt <100k 

  • Review the CBC - make sure there are no other cytopenias; ask for a smear 

  • Evaluate for HIV (usually already done in pregnant patients), as this could also lead to thrombocytopenias 

  • Obtain other coagulation panel like PT, PTT, fibrinogen level 

  • Also obtain CMP - evaluate kidney and liver function 

  • If no obvious signs, it is ok to get hematology involved early

  • More likely to be ITP if <100k, and patients can be treated with steroids or even IVIG in refractory cases if needed 

  • This is to make sure that the platelets do not drop further so that they cannot get neuraxial analgesia or so that they don’t drop too low as to cause issues with bleeding 

• What if they are symptomatic and <100k?

  • A lot of this is going to depend on their history and physical again - we are usually pretty good at evaluating for preeclampsia - get their vital signs and do your exam

    • Do they have fever? Purpura? 

  • Labs: CBC, CMP, coag panel, HIV, LDH, urinalysis, bilirubin 

  • If you are suspicious of TTP (ie. fevers, kidney injury, neurological changes) 

    • Make sure to get CT head to rule out bleed 

    • ADAMTS13 

    • Hematology consult 

  • Ok to get MFM and hematology involved early 

Management 

• Treatment for bleeding or severe thrombocytopenia 

  • If Plt are <10k or <20k, there is increased risk of spontaneous bleed 

  • If Plt <20k and severe bleed (ie. intracranial), you should give platelets regardless of the underlying cause of thrombocytopenia (yes, even in ITP if it will get consume)

• Some platelet thresholds to consider in delivery 

  • Vaginal delivery: 20-30k 

  • C/S: 50k 

  • Neuraxial anesthesia: institution based; ours is 80k; most institutions will have a count between 50-80k 

• Other considerations 

  • Operative vaginal deliveries are relatively contraindicated if there is severe maternal thrombocytopenia 

  • This is because there is concern that there could also be fetal thrombocytopenia (ie. immune mediated or hereditary) 

  • However, if you must perform an operative delivery, forceps is favored over vacuum 

  • Remember: Just because someone has ITP does not mean they can’t have an operative delivery 

• Treatment of specific disorders 

  • ITP - steroids or IVIG 

    • Dosing of steroids: prednisone 1mg/kg/day for two weeks followed by gradual taper; may need 2 weeks to see peak effect (usually 1-4 weeks for peak) 

    • IVIG should be given at least 1 week in advance to allow for maximal efficacy and platelet count retesting if trying to raise platelet counts for epidural 

    • If refractory, other methods in pregnancy are not well studied, and you should have a conversation with your MFM and hematology colleagues 

  • TTP - plasma exchange

  • Preeclampsia or DIC due to abruption: delivery! 

• What about fetal testing of platelets?

  • There isn’t really evidence to suggest we should test fetal platelets (ie. either via PUBS or from fetal scalp during labor

  •  We won’t discuss fetal/neonatal thrombocytopenia here, but just some brief reasons to test neonatal platelets: 

    • Maternal ITP 

    • Neonatal thrombocytopenia in previous pregnancy (concern for NAIT, though this is usually not associated with maternal platelet issues) 

    • Congenital anomalies associated with thrombocytopenia 

    • Bleeding or petechia on the infant 

    • Neonatal infections (ie. CMV, rubella)