Tag Archive: pregnancy


A few weeks ago Rob Orman (ER Cast) did a great interview with Dr Ingrid Lim at ACEP which looked at the diagnosis of the possible appendicitis in pregnant women.  Go and check out the 20 minute podcast at ERCast (click here) , then come back here to hear the sequel….

There are some great pearls that came out of this talk – HCG uses and interpretation (my review of some old literature), the role of US and CT as diagnostic tools in pregnancy and when to operate?  But, after this I had some acute onset confusion – as an ED doc your job is to make the diagnosis, try and sell it to a surgeon – then off to OT or not.  But what are the risks of going to do an exploratory laparoscopy / laparotomy in the common scenario where you are just not sure, don’t think a CT is worth the risk or you have no imaging available???

So after Rob O poked the fate Gods in the eye with a stick I ended up seeing 2 pregnant ?appendixes in one shift!  Thanks Rob.  So I spent the time it takes to “fast a pregnant lady” looking at the evidence, reviews and opinion that is out there in the surgical literature.  And now I am even more confused – more so than after listening to the average SMART EM podcast!  So many twists and turns – David Newman, can you help me?

All the evidence is retrospective analysis – ethics make it tough to do it any other way.  There are a couple of really big registry studies that give a big picture of the problem:

McGory et al analyzed over 3000 pregnant women undergoing appendectomy around the turn of the millenium and discovered a few points:

  • The rate of “negative appendix” was higher in pregnant vs. non-pregnant women (23% vs 18%; p <0.05) – I am gonna guess this is due to the technical difficulty with US in pregnancy and the reluctance to do a CT – so more going to OT with less ‘diagnostic’ work up.
  • The rate of perf / complex appendix was the same as in the general population ~ 30%
  • If you looked at Fetal loss and preterm delivery (bad, patient oriented outcomes) – there was an interesting pattern:
    • It was high in those with perforation / complex appendix – as you might expect – around 6% fetal loss
    • The women with simple appy, ie. not perfed, did better – around 2 % fetal loss
    • The surprise was that women with “negative appendix” – no disease had a rate of fetal loss slightly greater than the ‘simple appendicitis’ group
    • I have no idea why, maybe their pain was related to a uterine / ovarian problem – so the appy was an innocent bystander?

So the conclusion is that you need to decrease your “negative appy” rate in pregnant women – which I assume means doing more CTs and USS.  Watchful waiting may not be a good option – because they do a lot worse if they perforate and get systemically unwell etc.  I think the risk of CT (about 2x rate of childhood cancers) is small when you compare it to the risk of fetal loss (6+%)  BUT…. you are asking a woman to compare apple seeds and oranges – I think this is so dependent on the individuals world view, beliefs and maybe religion that it is just too hard to make a sweeping statement.  HMMMM…difficult…

 

So lets say – you dont have a CT (or patient refused it), the USS is inconclusive, but you are 66% sure on clinical grounds with a bit of a white-cell bump that is is an appendicitis.  You sell it to the surgeon, she says:

“well, OK it might be.  I’ll stick in a laparoscope and have a look, then proceed with appy if positive…  Oh, and then I can look and see if there is anything else going on at the same time”   Sounds like a sweet plan on first hearing it – but what does the evidence show?

Dr Walsh and colleagues in the UK did a review of the data (Int Jour Surgery) and showed more telling points in this debate:

  • Rates of fetal loss at laparoscopic appendicectomy were 6%, and significantly worse than open appendicectomy.
  • Fetal loss was greatest in the complex / perforated appendix group as with McGory
  • Fetal loss was the same for simple appendicitis as the “negative appy” groups – as in McGory
  • Showed the same higher “negative appendectomy” rate – around 27% – in non-pregnant women
  • Tocolytic agents did not make a difference in rates of preterm labour etc
  • “entry related complications” – (stabbing the uterus?) were low, but you should go with open Hasson technique – not the Veress needle.

So where does this leave us?  The data suggests a few points to me – maybe you can read it differently:

  • Lowering the “false appendicitis” at surgery will reduce the fetal loss / complications – so you should be doing all the tests, including USS and maybe CT to reduce the risk of unnecessary operations.  Admittedly – this is far from a perfect science – there will always be some ‘lily white’ appys.
  • Cast you diagnostic net fine and wide – get a good urine off for microscopy – the commonest “final diagnosis” in the false appendix patients was pyelonephritis
  • If you are going to operate – maybe minimalism is the best bet – minimal anaesthetics drugs, shortest sleep time, maybe open is better than laparoscopic techniques for these women?
  • Of course if you go in with a gridiron incision – you might miss the other pathology – eg. torsion of ovary. So here is a downside there too.
Let me know if you have another way of thinking about all this?  KNow of any good studies that change the strategy?  I would love to know…
Casey

When I went to med school we were taught that the B-HCG level doubles every 48 hrs in early pregnancy – and if it wasn’t – you either had an ectopic or a miscarriage until proven otherwise. However, it turns out that this is not the case  - just when you thought it was safe to go back to office gynae – along comes some data that completely muddies the waters and makes it all difficult again.

Barnhart et al in 2004 showed the HCG was slower to rise in many women with normal viable intrauterine pregnancies – the 99% confidence for slowest rise (going on to normal pregnancy) was only 53% at 48 hours [eg. from 1000 iu  to 1530 2 days later] – tthis is precisely what I thought an ectopic looked like!  So I think you need to be careful when interpreting these numbers.

This study out of Oregon in 1990 [Rob Orman was at the peak of his grunge career?] followed a small group of women with high risk pregancies – and  2/3 of the women with ectopics actually had a normal “doubling”.

Kadar et al in 1994 looked at women’s uteri for an intrauterine sac based on both HCG and ‘dates’ and found that ‘dates’ are much better predictors of gestation that HCG. So if you have an idea of LMP or when the HCG first went up – you are better off than using a single HCG.

So that is the bad news – the HCG can really lead you down the garden path if you are not careful.  So do NOT rely on a single HCG, be careful of interpreting 48 hour “doubling” HCG levels and if you know the dates-  this is actually useful!

The good news – we ED types are actually pretty good when it comes to finding normal IUPs.  There was a meta-analysis in 2010 by Stein et al which showed US in ED docs hands was up in the high 90s for sensitivity and specificity for detecting IUP or its absence.

Caveat: you have to practice and get good at interpreting what you see.  For a great guide and resources check out Ultrasound Villagetheir cheat sheets are cool – I use them all the time in my practice.

19 yo. woman G1P0 now 38/40 gestation, has been well throughout pregnancy aside from mild anaemia.  She presents to ED with “red eye”, and has a red eye, but more notably has a facial nerve palsy involving the upper and lower branches of VII.  Examination confirms Bell’s palsy and the slit lamp exam reveals a line of superficial fluorescein uptake consistent with exposure keratitis – her lids are not opposing well when she sleeps – so she has a dry, dessicated cornea.

So here are the 3 learning points for me:

Well, it is roughly 3 times as common in pregnancy than the general population.  Bell’s is associated with hypertensive diease of pregnancy and a ~ 5 fold increased risk of pre-eclampsia, hypertension and he associated outcomes of preterm birth, low birth weight and C-section delivery (Shmorgun et al).  What does this mean? Well you probably need to consider inducing a woman with Bell’s.  Where is the rsk:benefit break point – I guess it depends on the presence of other features of the eclampsia syndrome?  Love to hear your thoughts.

 There has been a change in the evidence in the past 2 years with new Cochrane reviews including a few new, high qualiy trials out in 2010.  So what do they say?

No benefit found in using anti-viral meds eg, valaciclovir. Not recommended.  Recent studies (Lancet Neurology) show no reduction in the time to recovery of facial function or prognosis.    So what about Steroids?  The last Cochrane review included 2 trials that showed a significant reduction in incomplete facial recovery at 6 months. Basically 75% got full recovery on steroids, whereas about 2/3 got better without steroids. There was no “cosmetic outcome” difference though between the 2 groups.  There was no additional benefit in adding anti-virals to steroids – love it when cheaper is better!

The evidence shows steroids help – but not dramatically – your patient is still at risk of eye injury due to corneal dessication over the coming weeks.

So the single most important intervention is to teach them to lubricate and tape the eye closed at night and use artificial tears by day. No evidence – just common sense I am afraid.

So what happened to our 20 yo @ 38/40.  Well, she got induced, and had a healthy baby, then started on a course of Prednisolone.

The interesting thing for me was that the Obs team seemed to employ some backward-logic here… they induced her so that they could start her on the steroids and not have to worry about exposing the fetus to the drugs!  It would seem to be a better idea to induce for the relative increased risk of eclampsia etc, as the steroids have a marginal benefit and well… we give steroids to women all the time in pregnancy for other reasons.. May be I missed something in translation?

 

Had an interesting case this week.  25 yo G3P2 presented after about 6 weeks amenorrhea with typical sxs of early pregnancy – breast tenderness, nausea and vomiting.  She had done a home urine HCG which was positive 3 days earlier.

Tonight she has come in with persistent vomiting, poor oral intake and feeling like crap.  Urinalysis showed 4+ ketones and SG = 1.030, no glucose.  But – here it the but – on questioning, she never really got any morning sickness with her 2 previous pregnancies.  So what is going on?  Is this “normal emesis gravidarum” or is there another cause?

I think we sometimes get a bit casual with this scenario – we all know how to manage the early pregnancy chucking, but we still need to consider the possible differentials before going down the well trodden treatment pathways.

Emesis / hyperemesis gravidarum – idiopathic

Urinary tract infection / pyelo

Gastroenteritis / peptic ulcer disease / Helicobacter

Surgical causes – think gallbladder, appendix

Endocrine – Thyrotoxic state, DKA,

Multiple gestation

Molar pregnancy

Medications – Fe supps are common

Transabdo Us = twin yolk sacs in the same GS

Dehydration is the big one – often requiring admsission for IV rehydration.

Rare complications include – Wernicke’s encephalopathy, other neurological lesions (myelinolytic), ketoacidosis

Mental health problem are common – depression and anxiety.

Well, a 2010 Cochrane review of the subject basically came up dry! They looked at acupressure, ginger, pyridoxine, antiemetics etc and saw no consistent benefit from any study or intervention.

So what do we do?

IV rehydration seems to help – usually when you have ketosis and objective evidence of dehydration

Antiemetics – metocloramide, promethazine

Steroids have been used

I like 5HT drugs – ondansetron – comes in a wafer, so women can use it at home and attempt to stay away from the hospital

Ginger can help, unlikely to harm.

Consider using thiamine supplemenation / multiB vitamins and watch out for low calcium – risk of later osteoporosis.

Nice review here on the topic. Surprisingly the babies of these poor women do well, there is an increased incidence of small-for-age, low birth weight and premature delivery. The miracle is that the outcomes are not worse given the sometimes severe and prolonged nutritional problems!

I have been busy learning all this week, so not much new material.  Fortunately Dr Ray Gadd out of Qld has sent me a ripper case of sepsis for you to mull and consider.    I know Ray is a keen Broome Docs reader – so let him know what your thoughts are on this case via the Comments area, we all learn from shared ideas!  I love this case because it is a true representation of the resources available to us in remote communities.  The case is definitely not “textbook” – but it is real!

Today’s case is food for thought, I will use it as a basis for some upcoming posts on Sepsis.  Over the coming weeks I hope to put together some Sepsis Resources which I reckon can make the diagnosis and management of sepsis in small / remote hospitals much easier and bring the standard of care for these super-sick patients up to a similar level they would get in any tertiary ED.

So – without further ado – Here is Ray’s case :  Septic Surprise (Apologies it is in PowerPoint – takes a bit to download)

This story is stolen from my big Dutch mate:

It is 6 AM, you get a call from the labour ward from the night midwife.  “Hey, I am looking after a primip and she has been progressing well, and I just did a VE – not sure if she is fully yet, it felt a bit odd - can you come and give a second opinion?”   So you wonder into the ward and don the latex…. after a quick feel you have made the following observation:

“Not sure if she is fully, but it is definitely a boy!”   AHH ! The undiagnosed breech rears its head (or bum) again.

If you are like me this is one of the scary moments in O&G.  I have only seen 3 breech births and they all were less than fun.  Breech vaginal birth was dealt a ‘final blow’by the Term Breech Trial Collaborative Group in Lancet 2000.  So I thought I would look at the evidence and ask the following questions:

Well, yes and no. The incidence of short-term poor neonatal outcomes is higher. However, this does not translate into more longer term neurological problems. So is a bad Apgar or a dodgy cord blood a good end-point to measure? The maternal stats were worse for CS as opposed to vaginal birth – basically having a big operation is bad, having a vaginal birth – not so bad for major problems – infection, bleeding, VTE etc All of this data comes from ëxperienced operators” ie. not people like me who have read a few textbooks and gone to a course about breech delivery. Mauriceau-Smellie-Veit: if you don’t know what I mean then don’t attempt a vaginal breech at home. (Hint- it isn’t a French guy with a bit of tinea) Review article here.

Hmmm… no good evidence it seems. The risk of vaginal birth is probably overblown in our minds. I think this depends on the situation and the operator a bit. Doing a CS late in the 2nd stage can be tricky, and you have already exposed the fetus to all the risk of labour, than the mother to the risk of CS. I am going to be pragmatic and say – once the breech is below the spines in 2nd stage it is probably too late to back out from a risk POV. This is really just my opinion. I decided to ask my local Expert – Dr Wendy Hughes -O&G of the Kimberley for her opinion

The bottom line is that 1 in 20 vaginal breech deliveries will have serious consequences for the baby – death or injury. The rest will be okay – completely okay. Unfortunately it’s the “rest that are okay” that sometimes leads us to be rather complacent about missing the diagnosis of breech both antenatally and in labour until it’s too late to do anything about it – until we experience a bad vaginal breech delivery. The second concern is avoiding unnecessary damage to mother from undertaking a C/S where the uterus is damaged by trying to drag the baby back up and out. Thankfully I haven’t personally been involved in a difficult C/S breech “retrieval” but I have heard horror stories from colleagues – I think one woman ended up with hysterectomy. If the baby is crowning this is definitely a case for vaginal delivery. I believe late first stage with rapid progression in labour is ditto. Early first stage (when many are diagnosed – you know SROM with niggles – oops, it’s bum first) I offer mum the choice and they almost always elect C/S. My belief is the best guide to proceeding with vaginal delivery is how quickly labour is progressing, both dilatation and descent. And the best way to avoiding the situation is to always question whether you have definitely felt the head – both abdominally and vaginally – and have a low threshold to resort to a quick scan – and ditto at antenatal clinic, particularly beyond 36 weeks – most breeches haven’t “just turned” but been that way unrecognized all along.

OK, it is too late to do ECV once labour is upon us! But it is worth doing. See this Cochrane review of ECV at 37/40. Another study by Dr Hannah (busy lady) looked at doing breech earlier – 34 – 36 weeks, with some success, though maybe a few more preterm labours

Go to an ALSO (Advanced Life Support in Obstetrics) course. This is a really fun and educational course, loads of evidence and a lot of practical skills to learn. Go to the ALSO website to check out courses near you

Ok here is my first Obs case.  Ultimately a poor outcome, but one where I think we can all learn some important stuff about pregnancy and the type of medical errors that can occur.  Here is the case:

26 yo, G2P1 – previous straightforward vaginal birth 2 years ago.  Unremarkable antenatal history this pregnancy. Thin, normotensive, all screening NAD. Normal USs at 12/40 and then 20 weeks – normal anatomy scan.  Rhesus +, OGC – negative  Shared antenatal care between GP and local hospital.  PMhx:

  • Recurrent SVTs, eventually treated with AV-node ablation, no ongoing symptoms.
  • Anxiety disorder with panic symptoms, responded to CBT, now well.
  • Appendectomy age 13

Now, skip forwards to labour day – presented mid-afternoon in spontaneous labour 39 + weeks.  Admitted to labour ward, commenced on partogram.  Requested an epidural at 4 cm around sunset.  Gp-Anaesthetist attended – noted high BP, 160/100 and asked for a UA – this showed 4+ protein.                  On examination:  noted to have clonus on ankle jerks.     GP sited an epidural and called the on-call O&G for further assessment

On review the BP had fallen to 140/85, pulse = 100, in active labour, afebrile, no headache / visual disturbance, abdo pain or oedema.  Decision was made to expedite labour and augmentation resulted in an SVB at 20:00 – healthy boy, Apgars 9 + 10.  The family were moved to the ward around 10 pm.

Over the next 8 hours the obs changed dramatically, in a nearly linear fashion…

  • pulse increased from 90 to 130/min
  • BPs were consistently increasing – up to 170/110
  • RR was normal, but climbed in the early hours of the morning to 28/min
  • SpO2 started falling just before sunrise – down to 90% on nasal prongs by morning

The O&G team were called several times and the obs were explained as being due to pain and then a recurrence of the panic episodes the patient had previously suffered…  the patient agreed “it felt just like my previous panic episodes!”   Treated with Panadeine forte and then temazepam 20 mg.

The following morning the team reviewed and made a diagnosis of pre-ecclampsia.  Patient was commenced on MgSO4 infusion as per protocol.

Became increasingly SOB and hypoxic despite being placed on a non-rebreather mask.  Best SpO2 in high 80′s.

Around 11AM a code blue call went out and I attended to the ward bed with the senior RNs and MWs.  The patient looked grey – combination of severe cyanosis and poor peripheral perfusion.  Marked dyspnoea, exam revealed a rapid, barely-palpable radial pulse and bilateral rales up to the shoulders.

Moved to Resus area for a trial of NIV, however became unconscious en route and was intubated on arrival to the Resus room.

Resuscitation with ventilation via ETT and CPR commenced.  Copious pink, frothy sputum coming up the tube with compressions.

Prolonged resuscitation attempts, lots of adrenaline and investigations – no return of circulation.

Fulminant ecclampsia with acute pulmonary oedema was the diagnosis that I wrote in the chart. Any other possibilities?
Large (L) adrenal pheochromocytoma. Widespread hypertensive changes – kidneys, retinae…

(1) The phaeo was not reported on the USs, though it was likely large enough to be visible if you were looking for it (2) The SVTs were investigated by a cardiologist including EPS and eventually the patient had an “empirical ablation” as nothing else was working (3) The panic symptoms were so severe that the patient’s GP had referred her to a Psychiatrist as they represented a clear change from her usual happy demeanor. (4) Never recorded a single high BP in antenatal clinic – likely due to the transient nature of the disease and the vasodilatation of pregnancy.

- Sometimes the hooves are zebras, this is a tough truth when it comes to general practice. You can spend years screening and never come up with a diagnosis like this, but you must keep it in your head, be vigilant and recognise patterns – Don’t be reassured by a specialist’s review and opinion. Go back to first principles and look at the details yourself rather than just assume the specialist has it all covered – I could spend all day on early recognition of clinical deterioration, but that is a whole other topic. Needless to say – don’t explain bad obs away and always be prepared to escalate if you are not getting good results / answers

Check out this review

Another review