Archive for June, 2011


Clinical case 016: Toddler vs. TV

Filed Under: Clinical Cases, Emergency, Paediatrics, Pearls and Pitfalls, Surgery by Casey Parker — 5 Comments
June 29, 2011

This is an older case that sticks in my mind.  A great example of the subtle signs and compensation kids can show despite being very sick!

3 yo boy carried into the ED of a small, peripheral metro hospital by mother – screaming.  She is crying, and between sobs says:  ”I was in the kitchen when I heard a crash.  I rushed into the living room to find him lying on the floor, on a bean bag, with the new TV face down on the floor beside him.  He must have tried to climb the TV cabinet and pulled the TV down!”  [CP: this was a while back when TVs were boxy and v. heavy in the front.  Pre-plasma / baby bonus era!]

The boy is screaming unconsolably, undressed and there is not a mark on him, no graze, no haematoma, nothing.  Scalp all looks normal, no haematoma etc.

Obs: pulse 180, RR – 30 (screaming), Spo2 98% RA, BP – hard to record, not perfusing his hands or feet well, cap refill slow @ 4 -5 secs.  Belly is scaphoid, soft.  Chest looks and feels normal – no obvious fractures, HS normal, air entry equal, trachea midline.

IV access pronto x 2 and 20 ml/kg of N/saline bolus given by hand.

10 minutes later the kid is settling, sobbing quietly.  Obs have improved = pulse 160, RR = 16, cap refill now 2 – 3 secs, hands a bit pinker.

So what is going on?  We start thinking:  ?occult belly bleed eg. spleen, concealed haemothorax, maybe an intracranial bleed…

Normal CXR, no fractures, pneumothorax or effusion seen…

This was the bad old days, before bedside US in the ED was widely available.  So we were scratching our heads for a minute or two when Mum noted he had become very quiet – too quiet for a 3 yo. in an ED.  Recheck of his Obs:  responds to name and gentle prodding, seems sleepy.  Pulse now 190/min, BP done = 50/20, cap refill once again – sluggish, pale hands.  Hmmmm…. not good.   Another bolus of 20 ml/kg of N/saline given over the next 10 minutes and urgent transfer to the tertiary hospital arranged – “we need to get him to a Paeds surgeon / CT” is the thinking.

Ambulance with lights/sirens up the freeway 30 minutes.  A third 20ml/kg saline bolus en route.  Obs remain bad, peripheral pulse is weak @ 190 – 200.  On arrival the plan is to go to CT if he is stable or OT if not – ?laparotomy.

This boy had a ruptured right atrium with cardiac tamponade. Fortunately a cardiothoracic team had just completed a case and he went into their theatre. Urgent ECHO showed the tamponade, so he had a sternotomy and decompression which revealed the ruptured atrium! The surgeon suspected hat his heart was crushed between the sternum and the thoracic spine – like in zealous CPR – and pop went the atrium!

This was one tricky case.  What would you have done differently?     I think the bedside US / RUSH protocol would have made the diagnosis in quick time.

Check out these ECHO images and discussion from Ultrasound Village

OK, there has been a bit of debate about emergency thoracotomy after this post.  So I will direct you to Scott Weingart’s podcast on the topic.

Thoracotomy for trauma thanks to EmCrit

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Lessons Learned from TC George

Filed Under: Anaesthetics, Emergency, Pearls and Pitfalls, Specialist Tips by Casey Parker — 8 Comments
June 27, 2011

On Thursday 8th March 2007, Tropical Cyclone George crossed the coast just north of Port Hedland, it was a large, catgory 5 cyclone and it was unusual as it maintained its intensity for 100s of km inland where it struck Indee station and the Fortescue Metals Group Rail Village  (FMG RV1).  The destructive winds wreaked havoc in the work camp at RV1 and destroyed a number of the transportable “donga” units used to house the workers. The image below was taken from the helicopter as we approached the camp, the building in the foreground that has been flatttened was the Medical / First Aid post – so this created a unique logistical challenge!  See the story below. For more pics / maps see the BOM Site report into Cyclone George

I was actually the Night Shift Doc in Karratha the night TC George hit Hedland – we were on Yellow alert for the impending cyclone, and as is usual – it was quiet – cyclone protocol means a curfew for the locals – so it was a good night, plenty of sleep for all.   I arrived at the Karratha hospital for handover in the AM and there were a number of Admin-type staff wearing yellow vests – not a good sign.  We had been asked to form a team to fly into the camp and evacuate the injured in helicopters commandeered from the local gas company.  Time was critical – so we grabbed the Parry packs, all the pre-packed gear we have in store and headed off to the airport – 2 docs (myself and Dr Seb R-D – my registrar) and 3 nurses.  We were joined by a crew of volunteer SES workers, 2 policemen and the local St John’s ambo vollies.

The brief was vague – at least 1 dead, one critically head-injured and about 25 – 30 other injuries.  Port Hedland airport was out of action and RFDS could not land nearby.  We sat through a weirdly boring helicopter safety briefing whilst our brains turned over the possibilities!  Then there was a bit of argy-bargy with the Police and other agencies about who should go in and what gear we should take.  Interesting how people’s priorities are set by their perspective – one Police officer wanted to take a box of 50 body bags…mmmmm, maybe not a high priority!  After a bit of ‘negotiation’ we took off and saw just how much water a cyclone can dump – the desert looked like a swamp overnight!

About a mile out of the camp we could see the debris of buildings scattered over the desert.  Landing was a bit scary – still gusts up to 100 kph!  We landed a good 10 hours post impact so the workers had moved all the injured to – the cool rooms of the kitchen block – they were the strongest standing buildings!  There was not much lighting, the walls were damaged / off and the floor was wet. The Pilbara sun had come out and it was getting humid.  We were taken straight to the man with the head-injury, stepping over the other injured people.  For me, this was worrying – am I focusing on one at the expense of the other potentially bleeding patients?

The critical man had been struck in the head by debris and then been lucid, apparently helping other victims.  He then became drowsy and LOC.  He had a large temporal scalp injury and had been vomiting – blood in the airway.  Breathing but was gurgling secretions, no suction available.

At this point we decided to divide the team – triage the other patients whilst we tried to stabilize A, B and C in the critical man. This is the time where you just have to trust your team – one cannot do all, you need a team to divide and conquer.

I won’t bore you with the next 10 hours of what seemed like constant chaos at the time, but here are a few choice moments and lessons learned from working in an extreme environment with little resources.

Our patient had lots of blood in the airway and we had no good suction. As soon as you slide in the laryngoscope blade the bulb is coated in blood and all looks dark! My tip – have 3 or 4 laryngoscopes at hand and use the first few to find the landmarks, suck what you can then quickly replace the blade with a new, fresh one to light up the cords

My mate was struggling to get an IV in this patient – and I needed Sux to get the airway in. So we went for the intraosseous gun into the tibia. Unfortunately the gun didn’t go right through the cortex…Doh! So he asked for a hammer – being a mining camp, a large hairy man brought in a 2 foot sledge hammer! This has to go down as one of the more surreal moments in my career. There was Seb attempting to ‘tap’ in an IO needle with a massive tool. In retrospect we could have gone for the IM or SL injection. But it worked!

After tubing and stabilising the head-injured man we had a dilemma – we needed to get him out ASAP, but that would mean one of the team leaving and using precious resources before we really knew how bad the rest were. So as the senior Doc, I decided to send the more junior Doc out with the severe patient and stay behind to sort the rest. Don’t know if this was the right call, but we had to decide quick. Seb did a great job after a 2 minute tutorial in ventilating the head-injured patient. (Note: never keep the muscle relaxant in your top pocket.)

So the next challenge – sorting out 20 odd patients with a range of injuries / symptoms – all roughly as bad as one another, no obvious crashing patient. A bit tricky to allocate triage… We sorted them into – ‘spinal precautions’ vs. ‘walkers’ as a good number had mechanisms and symptoms that suggested spinal injury. We immobilised those with ?spinal injury and then triaged the others. More helicopters were incoming – so we had to decide who to send next.

Light – we take this for granted in our bright, white hospital environs. Having to work in the dim light of a commercial cool room was an eye-opener! Get the patients into a well lit area, this sounds obvious, but it takes some doing in the real world of a disaster. However, it makes all the other work so much easier. So many cues we take from visual information when clinical exam is all you have to go on in the field.

I wanted to get IV access into anyone who looked like they might have a risk of bleeding – just in case. However, puting 2 large-bore IVs into 20 people is not as easy as you might think, especially when you are crawling in the dark and have to jump over people to get to others. We ED docs take the IV trolley for-granted. It is really tricky to carry enough gear to do all this in quick time and safely dispose of the sharps. My Tip: pre-pack specimen bags with all the gear you need for 2 drips. Take it to the “bed”side and have a small sharp container in the other hand. This might sound obvious, but it took me an hour to figure it out!

So you have put in 40 IVs into 20 patients and you want to give fluids. You have no way of documenting or recording how much fluid each patient has received. So here is what you need: 1 magic marker. You just write a big “1″ on the first bag, then when you change the bags you write “2″ on the next bag…. This sounds simple, too simple for our huge doctor brains, it really beats trying to remember the ins and outs of 20 people! This trick is so simple I have taken it back to my ED / anaesthetic practice. When you are doing a big case, or a massive transfusion – it is gold, at a glance you can look and see where you are up to.

So how do 3 nurses keep an eye on 20 odd patients scattered around a wrecked building? They can’t – this is what I observed. I was keen to keep up frequent pulse / BP / RR etc on the injured, so that we might detect occult bleeds / shock etc early in the injured. But that takes serious manpower. So I thought we could enlist the help of the un-injured folk who were there trying to help. I line each patient up with a “buddy” and gave instructions to stay and feel the pulse, watch for new symptoms / distress – and let us know if anything changed. Sounds like a good idea? Maybe not. I think I underestimated the effect this trauma had on the workers. I think half an hour later and about 50% of the “buddies” ha all excused themselves – they were not coping

There was one chap – fit looking guy who was not in the original group of “patients”, he admitted to a few bangs and scrapes. He had a few episodes of syncope towards the middle of the day. I was sure he was probably bleeding or worse. We have him IV fluids and kept a close eye on him, flew him out on the next transport…. he turned out to have a coincidental chronic leukemia with a Hb in his boots. I certainly didn’t pick the anaemia clinically, and in the context wasn’t looking for it!

Of the serious blunt trauma – there was a chap with a left upper quadrant injury / left flail chest. To look at he had a crushed left lower rib-cage. I got to him and put in IVs, gave some morphine for pain, and got a quick medical history. This guy was lucky – he had had his spleen removed a year prior for what sounded like a low platelet count. I could have kissed him – I was sure he was gonna have a splenic injury when I saw his chest, he did well from a lung point-of-view.

So after working solid for a few hours in a hot, sweaty, stressful situation we all get a headache, and a burning desire to pee. Not sure about you , but I don’t think straight with a full bladder and moderate dehydration. If you are in this scenario – pee and drink – you have to do it. I think I kept putting it off for paranoid ideas that I would leave for a minute and something bad would happen!

One woman was killed prior to our arrival, she was crushed by a building. Once the dust had settled on the injured, I was asked to certify her death by the Police in attendance. I was surprised as to how meaningful this act was to the other survivors. Not sure if it gave some “finality” to the other victims or in some way validated the grief they were feeling. The disaster courses always talk about resource allocation – don’t waste time on the unsalvageable – but I think there is a place for this once the situation is under some control. No evidence for this as usual, just my gut-feeling

So those are my “pearls” from TC George.  I would love to hear what you have to say, and hear your war stories and what they have taught you.   Dr Seb R-D has returned to be my Reg once again and I will be posting his lessons from this day soon.

Back to Sepsis soon

Casey

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Sepsis Ib: Maybe Lactate is more like a Surg review for RIF pain…

Filed Under: Critical care / ICU, Emergency, General Practice, Surgery, Useful Evidence by Casey Parker — Leave a comment
June 25, 2011

Those of you who read Sepsis I may have been amused by my attempt to compare lactate to a Pap smear – OK, it is a long bow (?in the running for the Agincourt Award).  But my point is, we just don’t do enough lactates in the typical ED to try and catch all the subtle / early, hypoperfused septic / SIRS patients.  So I have another analogy that I hope will be familiar to all the GPs and ED folk out there…

You are working in a medium-sized ED and have just seen a 15 yo boy with 12 hour history of (R) lower quadrant pain, nausea and not much else.  His obs are pretty normal, mum thinks he might have had a fever earlier.  There is no other diagnosis likely on exam – however when you feel his belly  it is not convincing for peritonism – no guarding, rebound or mass, just a bit tender to deep palpation.  You know he might have an early appendicitis, but you also know that a good number of these fizzle out to nothing overnight.  So what to do?

  1. Send him home with mum and get another look at his abdo in the AM, “return if worse”
  2. Admit under the Surgeons for essentially the same management, the Surgeon will review in he AM
  3. Consider investigations: FBP, CRP, or even the nebulous ?appendix USS
  4. Find a keen surgeon who will just whip out his appendix and ask questions later

Appendicitis can be subtle, hard to diagnose in some.  In others it is screamingly obvious – fever, rebound, localising RIF tenderness.  My point is this – we are good at the obvious ones, easy to diagnose and satisfyingly pus-ridden appendixes are removed.  However most surgeons will tell you that if every appendix they remove is purulent / perforated – then they are probably not doing enough(early) appendectomies!  You have to remove some normal appendixes to ensure you are “catching” enough of the nasty ones (this is controversial, but the principle applies – see review).

OK, now back to sepsis screening in ED.  You identify the population of patients who meet the criteria listed in Sepsis I.  These are the people in whom the probability of sepsis is high enough  for you to justify the minor cost / inconvenience of a panel of bloods (including a lactate).  The lactate result then allows you to further stratify the risk with some objectivity.  See review of its uses.   So stratification might look something like this

  • Lactate normal (<2): can be managed as per usual, ID source of sxs, outpatient management
  • Lactate 2 – 4 : at risk, needs close observation, micro samples and empirical Abs, repeat lactate after initial intervention
  • Lactate high (>4):  needs urgent resuscitation, micro, empirical ABs.  This group has a high 28-day mortality independent of the presence of shock. see Mikkelsen et al

The goal here is to identify the subtle ones – the ones that you might have otherwise sent home.  If every ABG / lactate you order comes back positive – you likely have sent home somebody in early septic shock!  You need to drop your threshold for ordering a VBG to the point where you have a decent ‘negative rate’ so you are not missing the early sepsis.  So doing a lactate is a bit like asking the Surgeons to review the ?appendix – the smart surgeon stratifies the risk of perforation / complications against the risk of removing a “normal appendix”.  However, doing a lactate is infinitely easier, cheaper and less invasive than an appendectomy.  BUT, missing an occult sepsis is very bad.  So you have not much to lose and all to gain.  Oh, and the surgeon might use time as a “diagnostic tool”  BUT this may not be such a great idea when it comes to ?Sepsis as we shall see as we progress through this series.

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Sepsis I: why lactate is like a Pap smear.

Filed Under: Clinical Cases, Emergency, Internal Medicine by Casey Parker — 2 Comments
June 23, 2011

This is the start of a series of posts on sepsis, I hope to cover the following topics in the coming weeks:

  • I :  Sepsis: screening and diagnosis
  • II : Antibiotics – what and when
  • III : Identify the source and control it if you can
  • IV :  Fluid and inotropes in sepsis

So here is the case for discussion – this is a real ED case from Broome last month.

39 yo woman with type-2 DM on insulin and metformin.  Presents to ED with fever, vomiting and vague (L) lower abdo pain for 12 hours.  States she feels thirsty, looks uncomfortable. No cough, URTI, no diarrhea.  Recently treated for UTI by GP, no urinary sxs since.

Triage obs @ 08:45 am : p=135/min,  BP = 119/73, T = 39.5, RR = 20.

Physical exam = tender (L) lower abdo, ENT / chest clear.   U/A = 2+leuks, 2+ blood.   BSL 8.4

Seen by RMO who recognised she was sick, IV access bloods and 2 L of normal saline.  Bloods sent:

  • FBP – mild lymphopenia
  • CRP = 19
  • UEcr / LFTs  all normal.  Bicarb 26
  • VBG – pH 7.27; pCO2 56; BE 1.9;  HCO3  28;  lactate 4.7
  • Blood cultures sent

On review a few hours later – patient feeling a bit better.  USS of abdo /pelvis – no findings to explain LIF tenderness.

Remained unwell with headaches, fever, tachycardia.  Repeat bloods for VBG were done – now looking more normal, acidosis corrected and lactate down = 1.9.  (What does “lactate clearance mean?” in this scenario)  So what happened?  Case D/W senior docs and…

Discharged home….  then represented later that night with same symptoms, rigors.  Admitted and commenced on IV ceftriaxone and gentamicin @ 22:00 (~13 hrs post triage).  This is not Broome ED’s finest moment, a possible near miss.  So how could we do better?

This is where I compare screening for sepsis to a Pap smear (hang in there, it is a weird comparison but stay with me).  As GPs we look at women’s cervixes all the time and we screen them for cervical neoplasia using Pap smears.  However, there was a time before Pap smears when we just looked at women with a symptom – eg. PV bleeding and did a spec to look for cervical changes / cancer etc.  I am sure most of the referrals to the Gynae yielded a positive result – but a lot of women with subtle changes / CIN were missed in the asymptomatic early stage of disease when intervention would have helped.  This is the basis of any screening tool: screen an “at risk” population with a sensitive test to find those who potentially have pre-clinical disease.   So back to sepsis:

Screening at triage uses a set of criteria to define the “at risk” group of patients.  The following criteria are used in other centres:

  • Fever (>38) OR suspected infection
  • pulse > 90
  • RR > 20
  • systolic BP < 90
  • Any change in mental status
  • SpO2 < 92 % on RA
  • Immunocompromised: steroids, chemo, uncontrolled diabetes
  • Invasive devices, surgery or procedures recently

So if you have 3 or more of these criteria you are into the high risk group and you automatically get the screening tool = bloods including a venous or arterial lactate sample, cultures, FBP, CRP, UECr, LFTs, Coag profile.  Lactate is either <2   OR  > 2.  (If > 4 then resuscitation should be commenced ASAP.)

You then get early review by a senior doctor to commence septic source identification workup: cultures, urine, CXR, any other pus, LP if indicated.

The goal is to expedite this process so that empirical or directed anitbiotic therapy can be delivered ASAP (door-to- ABs time minimised)

So that is screening in a nutshell.  Identify the “at risk” patients, do basic bloods + lactate then decide on appropriate therapy / Investigation.  The plan is to remove idiosyncratic decision making around the sick patient and streamline the process from triage to diagnosis / treatment.

I imagine that the “at risk” group will be in the 100 per month in my ED, then the lactate + patients will be ~5 % of those, ie. I am happy with a 1 in 20 pick up to maximise sensitivity and not miss any true positives.

Let me know if this sounds crazy…. evidence to follow

 

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Clinical Case 015: Septic Surprise

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine, Obstetrics by Casey Parker — 7 Comments
June 17, 2011

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)

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Are you an Occasional Intubator?

Filed Under: Anaesthetics, Emergency, General Practice, Pearls and Pitfalls, Pharmacology, Specialist Tips, Useful Evidence by Casey Parker — 3 Comments
June 14, 2011

If you are a reader of our comments sectio, you will know about Dr Minh Le Cong – RFDS Doc from Cairns who is one of the most enthusiastic teachers I have come across in the ether.  If you want a sample of his pearls of wisdom – go to my post on Preoxygenation Pearls and check out the comments section.

One of his passions is teaching airway skills to GPs / occasional intubators.  He also loves debunking medical mythology and dogma – and he has taken aim at the classical Rapid Sequence Intubation (RSI) and cricoid pressure.

So if you are an occasional intubator, or just would like to know what all the controversy is about – Minh has allowed us to put up his lecture on the topic.

The Occasional Intubator for Broome Docs blog

Check it out  – let me, and Minh know what you think.  I am sure there are some Anaesthetists out there who have something to say?   Casey

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Blind drunk – unilateral

Filed Under: Emergency, General Practice, Internal Medicine by Casey Parker — 1 Comment
June 13, 2011

Do you have a Breakfast Club in your ED.  In our ED it is commonplace to see 2 – 3 drunk, head-injured patients sleeping it off and having “neuro obs” until the cornflakes and tea are served – followed by spontaneous discharge.  This “ward round”is usually pretty mundane, sometimes a few sutures etc.

But last week I saw something new – blindness, acute left eye loss of vision following a punch to the head (not a first time attender).  This made me ponder the possible differentials.  External exam was pretty much NAD, so what is the cause?  This is the list I came up with for this scenario:

Retinal detachment, vitreous bleed, traumatic cataract, occult foreign body, lens disloation, post-traumatic optic neuropathy, vascular injury / dissection (carotid or vertebral), transient cortical blindness, retrobulbar haematoma…  as you can see a big differential, anyone else think of any causes not obvious on exam?  In terms of probability the first 3 (underlined) are the big ones.

Anyway – I have a confession – I am pretty crappy with an ophthalmoscope.  So in this situation I reach for the linear high-frequency US probe.  If you have never done this – it is the easiest USS in the book, just plonk the probe on the upper lid and waft it up and down.

from

This image is from the guys at Ultrasound Village.  Check out their site and courses.

Shows the typical retinal detachment – floating retina anchored at the disc posteriorly.  Acutely htis will move as the patient moves the globe, however after a while it tends to fix in one place.  Can be differentialted from a vitreal bleed by asking the patient to look up and down and checking the änchor point”is fixed at the disc – not floating / or rolling.

In my practice the US has made eye assessment sooo much easier.  I reckon I can confidently exclude a detachment using US much easier than with the scope, and with the US you can get right around to the anterior part of the retina – I find tis impossible with the opthalmoscope.  You can also see a FB easily and the blood in a vitreal bleed is easy.  I have not seen a lens dislocation with this – so cannot comment.

Anyway my patient had the classic left-eye-blind ((R) handed assailant) of a traumatic retinal detachment and she was seen by the visiting Eye guys – unfortunatley she had had this for a bit longer than she was originally letting on and there was little chance of a fix

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To Breech, or not to Breech. That is sometimes the question…

Filed Under: General Practice, Obstetrics, Pearls and Pitfalls, Useful Evidence by Casey Parker — Leave a comment
June 12, 2011

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

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Clinical Case 014: “That’s not a knife….”

Filed Under: Anaesthetics, Clinical Cases, Emergency, Surgery, Useful Evidence by Casey Parker — 3 Comments
June 10, 2011

So this is a typical Broome case.  As always – I will not sugar-coat it for you , just a blow by blow description of how it rolled out. Oh, and this one has a happy ending

30 yo. woman presented via ambulance after being stabbed in the left chest (through the axillary tail of her breast).  Seen at 3AM, primary survey all OK, a bit drunk though.  Secondary survey – single stab wound only, explored under local – could not see any penetration through the intercostals, though difficult to say clinically. portable CXR = no pneumothorax, no effusion. No FAST scan done.  Admitted to the ward for observation, IV fluids and surgical RV in AM.  Obs were not normal, but steady overnight.  Hb 134 g/l on gas.

The next AM, complaining of abdo pain, now some shoulder tip pain on the left.  Repeat formal CXR – no PTX, small effusion left costophrenic angle.  I was on for anaesthetics – so called for pre-op review to explore the wound further.  P= 120/min, BP = 110/50, RR = 25/min, feeling sick / vomited.  Hmmm…. not good

I decided to put in a big IV and send bloods for repeat Hb, VBG, cross match etc…the surgeons opted for a CT to look into the cause of the abdo pain – ? occult visceral injury.  So off to the “doughnut of death”

So the VBG comes back: lactate is 4.2 So – something is up, not perfusing her organs as one might hope.  Meanwhile in CT they have found a large amount of blood in the left upper quadrant, a small left chest effusion but no clear source for the bleeding ? spleen.  Clearly she needs some volume resuscitation – the plan is “Haemostatic Resuscitation“, check out the link for an awesome lecture on this topic.  Bottom line – lots of salty water is a bad thing for a bleeding patient, you gotta give some red stuff and products.

So without further ado we whiz her off to OT for a laparotomy, she does pretty well on induction / RSI, art line, central line, IDC and so on.  We now get the formal Hb back – it is 59 g/l (Doh! not good) and we start the packed-cells.  I called for some FFP to give and well – we don’t have platelets.  Of course the lab want us to document ‘coagulaopathy’ before thawing the FFP.  This is one of my pet peeves – in the 60 minutes they take to thaw the FFP, we will likely be in the deep end of ‘coagulopathy’.  Can’t they just trust me, we need some FFP! (See Emcrit podcast on Massive transfusion for details)  My guess was we were dealing with a concurrent blunt trauma to the spleen.

Well, there was a hole in the diaphragm, about an inch lateral to the left ventricle, this wound continued through the following structures: left lobe of liver, lesser omentum (the source of the ongoing bleed), pancreas and just stopped short of the renal vein/artery. The spleen was intact!

At this point I started to get a bit nervous – I had been ventilating the patient for an hour and was starting to think – there must be a lung injury here, is she gonna blow a pneumothorax?  So what to do?  I got out the USS and took some intercostal views to look for a PTX.  None to be seen.

USS has been shown to be more sensitive and specific than supine CXR in trauma – see this review of the literature

So they got control of the bleeding and we got our PRBCs and FFP in and by the time we were closing she had a Hb of 100 and was peeing like a trooper.  We decided to fly her out – the pancreas injury is not one we wanted to “observe” in our little hospital – if she got sick from this we would be in a lot of trouble.  On follow-up all was well – no further surgery required.

The local con’stab’ulary popped in later to say they had found a very long, fishing knife at the scene – my estimate was that it had to be 40cm from the skin wound to the pancreas!

Twitt
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Clinical Case 013: Big in Japan

Filed Under: Clinical Cases, General Practice, Internal Medicine by Casey Parker — 1 Comment
June 8, 2011

Ok, here is the case this week.  Sorry – another tragic one, these seem to be the ones that stick in my mind.

32 yo Japanese woman on a working holiday around Australia.  She is thin, fit and well. No recent illness, travelling in Australia for a year working in the hotel industry mainly.

She presented to ED late one night with a persistent cough – dry, non-productive, irritating cough. No fever, dyspnoea, recent URTI or VTE risk of note.  Seen by the senior nurse and given a course of amoxicillin with advice to see GP for follow-up.  All is well.

3 weeks later – represents to ED with ongoing cough, no change with Amoxil or subsequent course of roxithromycin from GP.  PNA result from GP – no significant viruses or pertussis, not Mycoplasma either.  Now states she has been experiencing some exertional dyspnoea.  On examination – nothing to find, chest clear, ENT all fine.  Obs all normal, except for mild hypoxia on RA.  ABG showed asubtle A-a gradient.  The ED doc decided she needed to be admitted for a work-up in the AM.

So, next day – CXR done, not much to show – maybe some faint increased opacity in lower lung fields – reported as normal.

Spirometry was normal – no sign of obstructive or restrictive changes, decent peak flows.

Bloods showed a normal white cell count, mild anaemia and normal CRP.  Only anomaly was a slightly elevated Ca++.

Quaternary survey (the Med Student went and saw the patient!): no new changes, though the student swore she could feel a single 1 cm LN in the lower jugular chain, this was ignored by yours truly….

So – being the type of guy I am, I decided to use time as a diagnostic tool and put her on some ABs.  Give it 24 hours and see if she is any better.  The next morning – she was definitely not better, now becoming uncomfortably hypoxic – SpO2 in the low 90s in RA, despite being well to look at, cough persisting and becoming more continuous – still no sputum.  So I did what we usually do when faced with uncertainty – order a bunch of tests – a Medicare funded “fishing expedition”: repeat the bloods, ABG and see.

So all this showed the same, but the hypoxia was worse.  Back at the bedside the patient was now notably SOB on sitting in bed.  So we decided to open the PE can of worms – a CTPA was ordered…

Q: is there a PE

A:  no

 

So what did the report say?

Bilateral perihilar lymphadenopathy, some reticular changes in the lung fields.  Highly suspicious for sarcoidosis.

 

 

 

So, great – a diagnosis, made sense – young woman, not looking infectious, slight Ca bump – could be sarcoidosis – after all it is at the bottom of every Int. Med Differential Diagnosis list…

So we discussed the case with the Resp Physician in the south who said: good, send her down for a bronch etc.

However… she got more SOB, started to become tachypnoeic at rest.  Oxygen applied, but still in mid 90s on 8 L/min, empirical nebs not helping.  We decided to try some NIV to see if we could get her fit for transfer without intubation.  The BiPAP machine helped for a while but after a few hours she became increasingly hypoxic.  Not looking great.  ABG showing hypoxia with low normal PCO2.

Unfortunately her respiratory failure increased and we decided to move to Resus and intubate.  Relatively straightforward intubation, however her BP did crash with drugs and change to ventilator.  Over the next hour, her oxygen requirements / PEEP increased and the gases got worse.

An NGT was inserted (as per usual) and surprisingly we got some frank blood up the tube – no good explanation for this could be found.

Despite our best efforts she became markedly hypoxic and eventually went into PEA, all the usual resus insued with no return of circulation.

The post-mortem showed – large ulcerated, bleeding gastric carcinoma with extensive metastasis including widespread lymphangitis carcinomatosis. And the malignant lymphadenopathy extended into the mediastinum and the supraclavicular chain.

1) Common things are common – however, common things in Japan are common in Japanese people. The rate of gastric Ca in Japan is high – 5 times that of Australia.  You have to appreciate the context and background of the patient in front of you.  I am sure that mild anaemia in Japan would prompt a gastroscopy ASAP, the same way PR bleeding makes us think colon Ca.

2) Sometimes the radiology report can be wrong – my quick review of the literature showed that it is really not too hard to call lymphangitis something else – eg. sarcoidosis.  I am no radiologist, I rely heavily on the report for interpretation – however if what you are seeing clinically doesn’t really equate with what the report says – then you might want to keep an open mind.

3) Sometimes the Medical Student is right. I know – radical idea, but our students sometimes are so fastidious and honest that they see things that we don’t, or that we do see but explain away in our heads.  Just like the emporer’s new clothes!

Twitt
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