# My wife is dying ...



## SpecialK (Nov 18, 2016)

You are responded to a shortness of breath.  The patient is a 26-year-old female.  Her husband told Control that "it looks like my wife is dying!".

The patient gave birth to her second child about 20 minutes ago but since become very unwell.  Delivery was normal and placenta has passed.  There's about 250 ml of post-partum blood on a towel but all vaginal bleeding has arrested.

It does indeed look like she is making a concentrated effort to die.  She responds to voice, is very pale, skin is mottled and sweaty, she gasps for breath and has had a big vomit on the floor.  The vomit has chunky bits and is very frothy and watery looking.

Obs: BP 80/50, PR 120, RR 30, Temp 36.5°, SpO2 82% RA, BGL 7 mmol/l, ECG sinus tachycardia.

O/E the only significant finding is when you listen to her chest; you hear bilateral sounds are some combination of wheezes and crackles.

1.  Succinctly describe her primary problem? ("she is dying" is obvious and not acceptable!)
2.  Putting lung sounds aside, what does the pattern look like? Is it consistent with the history?
3.  What treatment do you provide?
4.  You're 20 minutes from a secondary hospital and 50 minutes to a tertiary hospital.  Where do you go?
5.  HEMS at the tertiary hospital can come out and back you up.  They have blood and ultrasound.  Do you call for them? Do you want them to come by road or air? What do you do in the meantime?


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## VentMonkey (Nov 18, 2016)

SpecialK said:


> You are responded to a shortness of breath.  The patient is a 26-year-old female.  Her husband told Control that "it looks like my wife is dying!".
> 
> The patient gave birth to her second child about 20 minutes ago but since become very unwell.  Delivery was normal and placenta has passed.  There's about 250 ml of post-partum blood on a towel but all vaginal bleeding has arrested.
> 
> ...


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## SpecialK (Nov 18, 2016)

She did not have twins.  She is G2P2.

The baby doesn't need any medical intervention.  In practical reality, I would happily let dad strap the infant car seat in the front of the ambulance if he wants to go with his wife (which I imagine he would) or he can take both in his car and drive behind the ambulance.

The pattern of her vital signs is, as you said, shock.  What type of shock do you think she has? If you think it is hypovolaemic shock, is the level of shock she has consistent with the history of blood loss we can see? What other causes of shock might she have? What is the significance of her breath sounds? If we take away the fact she has just given birth and consider her presentation in any other person what would you call it?

A second ambulance can be the house in 15 minutes and they are coming in the opposite direction from you i.e. if you head towards hospital they are coming from the other direction.

So you have called for HEMS and they have decided it's faster and best for them to come back you up by road.  They will arrive in 50 minutes because that is how far they are from you i.e. coming from the large hospital.  In the meantime what are you going to do? Are you going to wait for them to come to you or are you going to meet them en-route?

She has not improved; in fact she continues to deteriorate.  She is beginning to develop very small purple spots on her skin.


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## DesertMedic66 (Nov 18, 2016)

My guess would be a PE


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## VentMonkey (Nov 18, 2016)

SpecialK said:


> She did not have twins.  She is G2P2.
> 
> The baby doesn't need any medical intervention.  In practical reality, I would happily let dad strap the infant car seat in the front of the ambulance if he wants to go with his wife (which I imagine he would) or he can take both in his car and drive behind the ambulance.
> 
> ...


Petechial rash, and crackles I don't think a PE is that high up on my differentials. She seems to be in DIC, and in the later stages of an irreversible shock. Her prognosis is poor, but if you're having dad take baby to the ED, we can focus on mom.

Again, what we do in The States isn't really what you may do, nonetheless, this frees up provider wiggle room. I would load mom up and meet the HEMS crew somewhere in between assuming she doesn't code between then and now. Because she only has a certain amount visible doesn't mean it's not hypvolemic, but you definitely got me thinking.

It could be some form of distributive related to something else, I am still not convinced this is a massive PE, though I guess it's possible.

I'll let others continue to chime in on this one...


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## DesertMedic66 (Nov 18, 2016)

For me the first 2 things that came into my head were PE and AFE


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## VentMonkey (Nov 18, 2016)

DesertMedic66 said:


> For me the first 2 things that came into my head were PE and AFE


Elaborate?


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## DesertMedic66 (Nov 18, 2016)

VentMonkey said:


> Elaborate?


For AFE a lot of her symptoms seem to fit. Skin discoloration, respiratory comprise, circulatory comprise, vomiting, pulmonary edema, tachycardia, and that started just after giving birth. If I remember correctly AFE usually occurs during birth or right after birth.


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## EpiEMS (Nov 18, 2016)

Shoot - I had a long response that got deleted.

I was thinking PE or maybe DIC...

She's in profound (likely obstructive, possibly hypovolemic) shock and needs rapid transport to definitive care. As a BLS unit, rapid transport and high flow oxygen administration is my best bet - I do need an ALS intercept, and HEMS would be a great way to do it.


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## VentMonkey (Nov 18, 2016)

DesertMedic66 said:


> For AFE a lot of her symptoms seem to fit. Skin discoloration, respiratory comprise, circulatory comprise, vomiting, pulmonary edema, tachycardia, and that started just after giving birth. If I remember correctly AFE usually occurs during birth or right after birth.


For those unfamiliar with this acronym/ term...
http://afesupport.org/what-is-amniotic-fluid-embolism/


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## DesertMedic66 (Nov 18, 2016)

VentMonkey said:


> For those unfamiliar with this acronym/ term...
> http://afesupport.org/what-is-amniotic-fluid-embolism/


This link provides more info into the common signs and symptoms: http://www.mayoclinic.org/diseases-conditions/amniotic-fluid-embolism/basics/definition/con-20035462


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## EpiEMS (Nov 18, 2016)

VentMonkey said:


> For those unfamiliar with this acronym/ term...
> http://afesupport.org/what-is-amniotic-fluid-embolism/



Thanks! Wow...that's the kind of thing I've never imagined would happen. 
1 in 40,000 deliveries in North America...that's quite rare (the conditions we typically worry about seem to all be below 1:1,000 deliveries based on quick Google-fu).


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## VFlutter (Nov 18, 2016)

Agree with AFE, likely still in the first phase. Intubate, volume resuscitate, and pressors/inotropes. Consider HEMS to an ECMO center. There is some evidence supporting "A-OK, Atropine Ondansetron, Ketorolac 

I have seen a few of these and they are some of the sickest patients i've had. 

Great article (From Wash U)
http://www.marchofdimes.org/pdf/missouri/AFE_11-21-13.pdf


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## VentMonkey (Nov 18, 2016)

@DesertMedic66 and @Chase good call. Even if this isn't the cause (I highly doubt it; you guys are on it) good material, guys.


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## SpecialK (Nov 18, 2016)

Chase said:


> Agree with AFE, likely still in the first phase. Intubate, volume resuscitate, and pressors/inotropes



Which inotrope would you use (if you had the choice)? Would you give it as bolus aliquots or as an infusion?

Considering the "pattern" of her shock would you use a different inotrope than you would normally?


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## Carlos Danger (Nov 18, 2016)

SpecialK said:


> Which inotrope would you use (if you had the choice)? Would you give it as bolus aliquots or as an infusion?
> 
> Considering the "pattern" of her shock would you use a different inotrope than you would normally?



Considering the etiology, I would not use an inotrope, I would use a drug that is primarily a vasopressor.


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## VFlutter (Nov 18, 2016)

Remi said:


> Considering the etiology, I would not use an inotrope, I would use a drug that is primarily a vasopressor.



Agreed with vasopressors as primary treatment however I think an argument can be made for inotropes given RV dysfunction is a large component as things progress. However you still may have and under filled LV so benefit may be minimal. I like Epi drips for situations like this, i.e. massive PE.


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## SpecialK (Nov 18, 2016)

Shucks. you blokes are stars .... yes, it was amniotic fluid embolism (AFE).

I'd never heard of it, and this was a real case.  There have been a number of local cases of women with AFE who have made normal recoveries despite dramatic, accelerated and continued deterioration once they received IV adrenaline infusions.   

Here are my thoughts

*1. Succinctly describe her primary problem?*
She has very severe shock

*2. Putting lung sounds aside, what does the pattern look like? Is it consistent with the history?*
The "pattern" of her signs and symptoms looks like hypovolaemic shock from partum haemorrhage.  However, it is not consistent with only 200 or 300 ml of blood loss.  If we *do *consider her lung sounds but put aside the fact she has recently delivered a baby this pattern of shock and her lung sounds screams anaphylaxis in any other patient.  Indeed, there is a large immune component to AFE similar to anaphylaxis.  

*3. What treatment do you provide?*
Well, a little debatable but high flow oxygen and IV access.  If I had blood I would give her blood.  I would also give her an IV adrenaline infusion.

*4. You're 20 minutes from a secondary hospital and 50 minutes to a tertiary hospital. Where do you go?*
I have a firm preference for going straight to the tertiary hospital.  I would however in this case, considering she is actively dying in a reasonably uncontrolled manner, ring the secondary hospital (via the Clinical Support Officer in Ambulance Control) and ask if they will accept her first or not.

*5. HEMS?*
Yes I would ask for HEMS to come out and back me up but via road.  At the same time as HEMS came towards me I would head towards them and meet en-route rather than waiting at the scene.  There is going to be very limited room to work on this patient in a helicopter and the family cannot go with her.


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## phideux (Nov 22, 2016)

If the HEMS unit is heading your way to intercept, why not just head towards the close hospital to intercept? It is almost the halfway point.


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## SpecialK (Nov 22, 2016)

phideux said:


> If the HEMS unit is heading your way to intercept, why not just head towards the close hospital to intercept? It is almost the halfway point.



Because "hospital" does not always equal "definitive care".  All hospitals are not created equal.

I don't honestly know if this patient is going to be best served going to the secondary hospital, or if it is worth going to the major hospital.  There has been a case series of patients with AFE who despite significant and progressive deterioration have rapidly improved with an IV adrenaline infusion.  

I would respond HEMS (in this case they would come out by road) and start heading towards hospital.  I'd give the secondary hospital a ring via Control to ask them if they wanted her or if it would be best to take her to the tertiary hospital.  Her level of improvement would also guide what I did.  If she was not improving then I would take her to the closer hospital.


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## Alan L Serve (Nov 22, 2016)

She's a-bleedin'.

She may die.

Get in the lines, fill her up, and see if you can't find a few bags of blood. PRBC and FFP. Medicines to help with getting her BP up and the heart to beat a bit nicer.

She's probably a gonner. Search her purse for her credit cards. It'll be fun until you go to jail.


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## SpecialK (Nov 22, 2016)

Alan L Serve said:


> She's a-bleedin'.
> She may die.
> Get in the lines, fill her up, and see if you can't find a few bags of blood. PRBC and FFP. Medicines to help with getting her BP up and the heart to beat a bit nicer.



Where do you think she is bleeding from?
Do you think 200-300 ml of blood loss is compatible with her near moribund state? Doesn't the pattern of deterioration look a bit odd?
Why would you give packed cells and plasma but no platelets? Why not just give her whole blood?


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## Alan L Serve (Nov 24, 2016)

SpecialK said:


> Where do you think she is bleeding from?
> Do you think 200-300 ml of blood loss is compatible with her near moribund state? Doesn't the pattern of deterioration look a bit odd?
> Why would you give packed cells and plasma but no platelets? Why not just give her whole blood?


Years ago a rookie EMT asked me a question.

"Where is the blood from this very hypovolemic patient? I see a tiny amount!"

To which I told the rookie, "The patients bleeds both on the outside _and_ the inside."

Blood is so important, more than simple crystalloids. FFP, PRBC, and platelets. There is even a magic ratio to help with bleeding. Did you know this magic thing? 3:1 FFP to PRBC.

The coagulation factors are in the plasma. The secrets are in the stars.


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## Akulahawk (Nov 24, 2016)

I'm a few days late in responding to this but I read the initial story when it first posted and I thought AFE as well. Given the transport destination variables, I would call for HEMS while I'm still on scene, do what I can, and head toward the closer facility. Their capabilities are likely going to be quite a bit more extensive than I'd be able to offer in my ambulance. If anything, HEMS can rendezvous on the closer facility's pad and take the patient from there to the tertiary facility and if the patient is still trying to die before I can get her going, HEMS is still en-route to their pad and I can go to that closer facility, have them begin stabilizing the patient while waiting for HEMS to arrive, take over stabilization and begin rapid air transport to the tertiary facility.  If she's doing OK and is at least somewhat stable, I might consider a run directly toward the tertiary facility and have HEMS rendezvous with me somewhere on the way.


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## SpecialK (Nov 24, 2016)

Alan L Serve said:


> Years ago a rookie EMT asked me a question.
> "Where is the blood from this very hypovolemic patient? I see a tiny amount!"
> To which I told the rookie, "The patients bleeds both on the outside _and_ the inside."
> 
> Blood is so important, more than simple crystalloids. FFP, PRBC, and platelets. There is even a magic ratio to help with bleeding. Did you know this magic thing? 3:1 FFP to PRBC.  The coagulation factors are in the plasma. The secrets are in the stars.



Let's look at the "big picture".

This happened 20 minutes ago.  In that relatively short time, she developed profound and severe shock which the husband says came on very quickly.  She also has severe difficulty breathing and upon listening to her chest, we hear something like wheezes with crackles.  Given this information and her presentation, the pattern of her shock is really a bit odd don't you think? Does hypovolaemic shock usually present like this; i.e. with such a fast onset including severe difficulty breathing and a wheezy chest? No.  What does? Anaphylaxis (or in this case, an anaphylaxis-like reaction).

We cannot say for sure she is not bleeding somewhere (unless of course you can do USS) but given the above I'd be leaning towards hypovolaemia not being the cause of her problem.  It might be, but what is going to be more important, i.e. what is going to likely be fatal if we do not treat it, is the anaphylaxis-like reaction she is having.  There have now been a number of cases of AFE where despite profoundly rapid and continued deterioration the patient has made a normal recovery once receiving IV adrenaline.

And yes, I am aware of 3:1 ratio for FFP to PRBC.  My question is why you are going to give her plasma (which contains fibrinogen) but no platelets? And do you honestly want to piss-arse around carrying frozen plasma and red cells? Wouldn't it just be so much easier and more sensible to carry whole blood like a number of services are now doing?


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## MonkeyArrow (Nov 24, 2016)

Alan L Serve said:


> Blood is so important, more than simple crystalloids. FFP, PRBC, and platelets. There is even a magic ratio to help with bleeding. Did you know this magic thing? 3:1 FFP to PRBC.


The most recent literature states that a 1:1:1 ratio of PRBCs to Platelets to FFP is best in trauma patients. While not a trauma patient, the reason you transfuse those patients is due to hypovolemia, the same mechanism you are proposing to transfuse for in this patient.


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## Alan L Serve (Nov 24, 2016)

MonkeyArrow said:


> The most recent literature states that a 1:1:1 ratio of PRBCs to Platelets to FFP is best in trauma patients. While not a trauma patient, the reason you transfuse those patients is due to hypovolemia, the same mechanism you are proposing to transfuse for in this patient.


Trauma is not medically sick.

Very different mechanisms.

Like black magic vs dark magic. Similar, yet different.


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## VFlutter (Nov 24, 2016)

This lady sounds very early in her presentation and likely in the first phase which predominantly is obstructive shock. I doubt she has progeessed to DIC and hemorrhagic shock at this point in time. The hypoxia and cardiac collapse kill most AFE before they even get to the second phase.


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## Akulahawk (Nov 24, 2016)

Chase said:


> This lady sounds very early in her presentation and likely in the first phase which predominantly is *obstructive shock*. I doubt she has progeessed to DIC and hemorrhagic shock at this point in time. The hypoxia and cardiac collapse kill most AFE before they even get to the second phase.


I agree that she seems to be in this phase. My suspicion is that the closer hospital probably doesn't have the ability to crash patients on to ECMO and probably has the ability to transfuse large amounts of blood (whole or 1:1:1 components) to get her through the DIC/Hemorrhagic phase.


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## Alan L Serve (Nov 24, 2016)

Akulahawk said:


> I agree that she seems to be in this phase. My suspicion is that the closer hospital probably doesn't have the ability to crash patients on to ECMO and probably has the ability to transfuse large amounts of blood (whole or 1:1:1 components) to get her through the DIC/Hemorrhagic phase.



The chances of her dying,
using 1:1:1,
Grow like a fetus in womb.


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## VFlutter (Nov 24, 2016)

Alan L Serve said:


> The chances of her drying,
> using 1:1:1,
> Grow like a fetus in womb.



I'm not sure I follow your rationale. This is not a coagulopathic issue.


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## Alan L Serve (Nov 24, 2016)

Chase said:


> I'm not sure I follow your rationale. This is not a coagulopathic issue.


DIC or bleeding=coagulopathy


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## VFlutter (Nov 24, 2016)

Alan L Serve said:


> DIC or bleeding=coagulopathy



My argument is that she is not currently in DIC. Although DIC is a part of AFE it is usually later in the presentation, to which ~60% never survive to.


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## ERDoc (Nov 26, 2016)

Alan L Serve said:


> She's a-bleedin'.
> 
> She may die.
> 
> ...



Except for the fact that clinically she looks nothing like hypovolemia.


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## Carlos Danger (Nov 26, 2016)

The pathophysiology of AFE is interesting. I just read a CEU thing on it recently. For one thing, amniotic debris is found in something like 30% of tested parturients, even though only 1 in 10,000 or fewer develop the AFE syndrome. No idea what actually causes the syndrome. The initial phase can appear primarily obstructive (d/t what is essentially pulmonary artery spasm), vasoplegic, or coagulopathic and can happen at any point from late pregnancy to several days postpartum.  Presenting symptoms can be anything from a headache or mild SOB to nearly instant vascular collapse. The "A-OK" cocktail apparently really works, and reduced mortality significantly in the retrospective analyses. Aside from the A-OK cocktail, treatment is simply supportive.

Probably no role for blood replacement, at least not until the later coagulopathic stages.


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## Alan L Serve (Nov 26, 2016)

ERDoc said:


> Except for the fact that clinically she looks nothing like hypovolemia.


Roses are red,
Violets are blue,
She looks like,
Someone who has hypovolemia


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## ERDoc (Nov 26, 2016)

Alan L Serve said:


> Roses are red,
> Violets are blue,
> She looks like,
> Someone who has hypovolemia



Sure, except for the fact she is not losing any volume.  All of her H&P points to a cardiac/resp cause.


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## Alan L Serve (Nov 26, 2016)

ERDoc said:


> Sure, except for the fact she is not losing any volume.  All of her H&P points to a cardiac/resp cause.


My friend,

We will agree to disagree.


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## ERDoc (Nov 26, 2016)

And you, my friend, will kill the pt


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## Alan L Serve (Nov 26, 2016)

ERDoc said:


> And you, my friend, will kill the pt



And you, 

my friend,

are my dearest friend.


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## Handsome Robb (Nov 26, 2016)

It sounds like Lupus to me. 


Sent from my iPhone using Tapatalk


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## SpecialK (Nov 26, 2016)

Alan L Serve said:


> Roses are red,
> Violets are blue,
> She looks like,
> Someone who has hypovolemia



Ask yourself ... do patients with hypovolaemia normally present with a rapid onset of very severe shock?  If her normal blood pressure is for example 120 (assuming she has not developed maternal HTN) then for her BP to now be 70 or 80 means it's about a third less than normal which is a large change in such a short amount of time assuming her blood volume is normal (and indeed, don't pregnant women get an enlarged circulating volume anyway?).

We cannot say for sure without opening her belly up or doing USS, but there are a number of factors which point away from hypovolaemia:

(1) The very fast onset.  The husband said it happened 20 minutes ago when the ambulance first arrived; so if it took the ambulance 10 minutes to drive there, then in reality, it happened 10 minutes after she gave birth.  He told Control it looked like "my wife is dying" so presuming she looks pretty much the same as she did then when the ambulance first arrived, she hasn't progessed much.  This means she went from essentially being well to critically unwell in a very short space of time (a few minutes).

(2) The lack of visible blood.  Granted bleeding can be internal; she would have to lose a litre or more I imagine in one go to look this sick from hypovolaemia in such a short space of time.  I didn't mention it but I'd also give her some IM oxytocin and do fundal massage as well as IV fluid in case she had uterine haemorrhage.  In this case, if that is done, she doesn't improve.  That would further point away from hypovolaemia.

(3) Her lung sounds.  This is the "clincher" that points strongly towards an anaphylaxis-like reaction.  If we "put aside" the fact she is pregnant and has just given birth, anybody else who has a history of severe shock which came on very rapidly and wheezy lungs screams at the top of their, well wheezy lungs, "anaphylaxis" no? Surely you must agree?

The balance of risk here, as well as all other things we are doing to her, is giving her some adrenaline no? If can't hurt, and it might be the thing which saves her life? Which in this case, it was!


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## Alan L Serve (Nov 26, 2016)

SpecialK said:


> Ask yourself ... do patients with hypovolaemia normally present with a rapid onset of very severe shock?  If her normal blood pressure is for example 120 (assuming she has not developed maternal HTN) then for her BP to now be 70 or 80 means it's about a third less than normal which is a large change in such a short amount of time assuming her blood volume is normal (and indeed, don't pregnant women get an enlarged circulating volume anyway?).
> 
> We cannot say for sure without opening her belly up or doing USS, but there are a number of factors which point away from hypovolaemia:
> 
> ...



Yes, my friend.

For the reasons I described, above.

Have a blessed evening. I'm going to study HVAC now.


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## ERDoc (Nov 26, 2016)

Alan L Serve said:


> And you,
> 
> my friend,
> 
> are my dearest friend.



No, I am the ER doctor that has to try to salvage what is left of this poor women when you finally get her to the ER



SpecialK said:


> Ask yourself ... do patients with hypovolaemia normally present with a rapid onset of very severe shock?  If her normal blood pressure is for example 120 (assuming she has not developed maternal HTN) then for her BP to now be 70 or 80 means it's about a third less than normal which is a large change in such a short amount of time assuming her blood volume is normal (and indeed, don't pregnant women get an enlarged circulating volume anyway?).
> 
> We cannot say for sure without opening her belly up or doing USS, but there are a number of factors which point away from hypovolaemia:
> 
> ...



All good points.  Keep in mind what has just happened to this woman.  She had a huge, firm object (the baby) forcefully pushed through a small passageway (the cervix and vagina), creating a nice open pathway with little resistance to the flow of blood.  The only other pathway out of the uterus is the fallopian tubes which are very small and provide significant resistance to blood flow through them.  There is no way this woman lost enough blood through her tubes to account for the degree of shock she is in.  The only other natural pathway is out the cervix/vagina and we know she hasn't lost enough blood there.  Now we have to think of some disasters that may have happened that has caused hypovolemia.  The only one really would be a uterine rupture.  There is no reason to think uterine rupture in this case.  The baby delivered with little easy, there no risk factors and she is not having any abd pain that is out of the ordinary.  You also wouldn't see the resp issues with a rupture that quickly.


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## Alan L Serve (Nov 28, 2016)

ERDoc said:


> No, I am the ER doctor that has to try to salvage what is left of this poor women when you finally get her to the ER



I pray you will forgive me, 
my most lovely friend,
in that I don't believe you to be,
as ER doctor.


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## Akulahawk (Nov 28, 2016)

Alan L Serve said:


> I pray you will forgive me,
> my most lovely friend,
> in that I don't believe you to be,
> as ER doctor.


We're lucky to have this ER Doctor as a member of our forum. While there are occasionally things that he says that we may disagree with, consider that in this case, the majority of the members here are posting things that are pretty much inline with each other, leaving you as the outlier. Clearly you maintain that this patient is hypovolemic. If this is the case, where's the source of bleeding? Think about something here since this is your position: If this patient truly had suffered massive blood loss within 10 minutes of giving birth to the point where SBP pretty much is in the tank starting off with basically a normal BP, wouldn't this patient still be hemorrhaging massively and likely have exanguinated within 20 minutes? I haven't heard of anyone suffering such a massive injury where their blood pressure drops to some horrifically low number within minutes who is still alive and conscious 20 minutes later. Bleeding like that just doesn't magically stop like someone turning off a spigot, no it trickles to a stop because there's nothing left to leak out. 

Harken back to your earliest EMT training when you were taught about the various types of shock. This patient is essentially suffering one of those types of shock and it _isn't_ a hemorrhagic/hypovolemic shock. 

Another way to think about this is: what would happen to your blood pressure if someone suddenly constricted your pulmonary arteries and veins to, say, 1/3 their usual diameter? Remember that this means a sudden and significant decrease in blood _flow_ through an important part of the circulatory system...


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## VFlutter (Nov 28, 2016)

Alan L Serve said:


> I pray you will forgive me,
> my most lovely friend,
> in that I don't believe you to be,
> as ER doctor.


 
So let's say you have a patient who is a few days post op from an Exp. Lap who was recently diagnosed with a DVT and now presents like this lady. Do you solely assume they are in hemorrhagic shock from an intra-abdominal catastrophe or do you maybe consider a massive PE with obstructive shock?  

I am not sure this is even worth the argument.


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## SpecialK (Nov 28, 2016)

Alan L Serve said:


> I pray you will forgive me,
> my most lovely friend,
> in that I don't believe you to be,
> as ER doctor.



Are you honestly that poorly educated you can't see the difference between hypovolaemia and other causes?  I honestly can't think of what else it could be so I'm really not sure?

Let me try to help you understand, again

(1) This young woman gave birth normally and  twenty minutes later you are on-scene where she is in profound, severe shock.
(2) If it took 10 minutes for you to respond, and two minutes for the husband to go through Control, that is 12 minutes
(3) So in reality, this all happened over the space of about eight minutes
(4) The husband told Control it looks like "my wife is dying" so this came on very rapidly (see 3. above)
(5) There is no external bleeding and about 200 ml of blood on a towel, 200 ml of bleeding doesn't cause profound, severe shock
(6) Her chest sounds wheezy (or at best approximation - could be crackles in there too).  This is the "sinch" that it is not hypovolemia. 
(7) Combining the degree of shock she has, the very rapid onset and her lungs all combine to point away from hypovolaemia.
(8) If you had any other patient who had not just given birth and had this degree of shock and a wheezy chest you would, I hope, think anaphylaxis
(9) AFE is a known condition with a large degree of anaphylaxis-like response and the "total scenario" fits with this.

So, whilst nothing is ever 100% in medicine, and we can never say "never", we can look at the balance of risk vs benefit in how to proceed.  I'd give her some fluid, IM oxytocin and do fundal massage because she _might _have internal PPH but it doesn't look like it.  However, the risk of doing so is quite low especially as the placenta has delivered.  Critically, and I cannot express how significantly critical this is, I would also give her IV adrenaline because her clinical presentation screams "anaphylaxis".  She is so shocked I doubt IM adrenaline would absorb very well and would take too long anyway.  You could give it to her via dilutional aliquots or you could run as an infusion.  I would personally run it as an infusion.  

There have been a number of (unpublished) cases of patients with AFE who have been near-death only to make completely normal recoveries once they have received IV adrenaline.  Some have also received blood but I don't think that is life-saving, certainly if I had blood I would give it to her initially instead of abnormal saline (abnormal in the sense she hasn't lost it) but I'd also give her IV adrenaline.


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## VentMonkey (Nov 28, 2016)

I have no qualms about admitting that this scenario has been quite the educational endeavor for me.


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## NysEms2117 (Nov 28, 2016)

VentMonkey said:


> I have no qualms about admitting that this scenario has been quite the educational endeavor for me.


i'm learning all types of shiyte. including i have to learn a lot more... a lot lot lot more...


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## VentMonkey (Nov 28, 2016)

It makes complete sense, but is yet quite remarkable in regards to the cascade of events that the obstructive (clot) shock has caused such a patient; good scenario.


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## SpecialK (Nov 28, 2016)

VentMonkey said:


> It makes complete sense, but is yet quite remarkable in regards to the cascade of events that the obstructive (clot) shock has caused such a patient; good scenario.



I'd say more she has distributive shock (as we see in anaphylaxis),

I had honestly never heard of AFE until I saw this case.  If I had seen this patient prior to knowing about it; I would gone down the route of PPH and done as above; I also like to think my clinical decision making is "good enough" to recognise she was having pseudo-anaphylaxis and give her some adrenaline however I can't say for sure because we'll never know.

But as you say, yes, it makes perfect sense.


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## ERDoc (Nov 29, 2016)

Alan L Serve said:


> I pray you will forgive me,
> my most lovely friend,
> in that I don't believe you to be,
> as ER doctor.



You're right, I'm not but I did stay at a Holiday Inn once.


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## SpecialK (Nov 29, 2016)

ERDoc said:


> You're right, I'm not but I did stay at a Holiday Inn once.



Negative marks for being a d!ck and using an American joke I had to look up.

Do you normally call yourself an "ER doctor"? In Australasia it's normally "emergency medicine XXX" e.g. registrar, consultant (specialist), physician.  To us saying "ER Doctor" is like a Cardiologist calling himself a "ward doctor" cos he sees pts in the cardiology ward.

Anyway, here's a good article on AFE https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823093/

Dr Google tells me there are some moves to rename this "anaphylactoid syndrome of pregnancy" which is more befitting and will hopefully mean reduced mortality if people think of the it in terms of the primary treatment being adrenaline, not volume loading or giving treatments for PPH.


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## StCEMT (Nov 29, 2016)

SpecialK said:


> Dr Google tells me there are some moves to rename this "anaphylactoid syndrome of pregnancy" which is more befitting and will hopefully mean reduced mortality if people think of the it in terms of the primary treatment being adrenaline, not volume loading or giving treatments for PPH.



So question for any and all. I follow what you mean with it resembling anaphylaxis and using epi, what I found on Google was saying the same thing about it resembling that. So why is the A-OK treatment plan what I see recommended instead? Unless your article goes into detail Chase and I don't remember, admittedly I didnt have time to read it all when I opened it. Epi makes sense, but the lit says A-OK had good outcomes in many cases and is what I have seen multiple times since following this.


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## SpecialK (Nov 29, 2016)

StCEMT said:


> So why is the A-OK treatment plan what I see recommended instead?



Atropine 1 mg for vagolysis (needed?)
Ondansetron 8 mg to block serotonin receptors and for vagolysis
Ketorolac 30 mg to block thromboxane production

Src: http://www.marchofdimes.org/pdf/missouri/AFE_11-21-13.pdf

I had to look up what ketorolac was; I don't think it's used locally.  The two patients that powepoint talks about are different; they were both in cardiac arrest.

Based on the presentation of this young woman my most important aspect of treating her would be IV adrenaline as an infusion.  I guess atropine and ondansetron are part of the ambulance formulary so could technically administer them for this.  It's not exactly written in the CPG but it'd still be permissible under the discretion to deviate from them.


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## ERDoc (Nov 29, 2016)

SpecialK said:


> Negative marks for being a d!ck and using an American joke I had to look up.
> 
> Do you normally call yourself an "ER doctor"? In Australasia it's normally "emergency medicine XXX" e.g. registrar, consultant (specialist), physician.  To us saying "ER Doctor" is like a Cardiologist calling himself a "ward doctor" cos he sees pts in the cardiology ward.



LOL.  Yes, I call myself an ER doctor.  Most people in the US would be confused if I said I was an Emergency Medicine attending physician.  A lot of people here still think ER docs are just other specialties that work extra shifts in the ER.  I always get asked what I really want to do or what my real job is.  There is a small movement to call us emergontologists, which I think is just stupid.


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## Shrimpfriedrice (Dec 1, 2016)

I follow everything that was discussed so far. I'm sure someone can clarify this for me. So obstructive, hypovolemic, and anaphylactic shock were mentioned, but not cardiogenic. Granted she is fairly young however pregnancies take quiet the toll on the human body. I remember seeing a video of a young mother who developed cardiomyopathy that began in the 1st pregnancy and worsened in the second requiring her to receive a pacemaker.

With that said the onset of symptoms where fairly quick, i'm just suprised no one dug for more of a history? I know normally we probe for a more detailed history before providing possible differentials. Am I missing something?


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## DesertMedic66 (Dec 2, 2016)

Shrimpfriedrice said:


> I follow everything that was discussed so far. I'm sure someone can clarify this for me. So obstructive, hypovolemic, and anaphylactic shock were mentioned, but not cardiogenic. Granted she is fairly young however pregnancies take quiet the toll on the human body. I remember seeing a video of a young mother who developed cardiomyopathy that began in the 1st pregnancy and worsened in the second requiring her to receive a pacemaker.
> 
> With that said the onset of symptoms where fairly quick, i'm just suprised no one dug for more of a history? I know normally we probe for a more detailed history before providing possible differentials. Am I missing something?


What questions would you ask to dig more into the history of this patient? All of her symptoms fit AFE, if you hear hoof beats that doesn't mean there is a zebra.


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## SpecialK (Dec 4, 2016)

Shrimpfriedrice said:


> I follow everything that was discussed so far. I'm sure someone can clarify this for me. So obstructive, hypovolemic, and anaphylactic shock were mentioned, but not cardiogenic. Granted she is fairly young however pregnancies take quiet the toll on the human body. I remember seeing a video of a young mother who developed cardiomyopathy that began in the 1st pregnancy and worsened in the second requiring her to receive a pacemaker.



Cardiogenic shock would present similar to this; i.e. hypotension and signs of poor perfusion which she has.

The "sincher" as to this not being cardiogenic shock is the lack of an immediately identifiable cause _*and *_her wheezy chest.  The most common causes of cardiogenic shock are VT and AMI.  Her ECG is unremarkable for MI and is sinus tachycardia.  It would however likely be incredibly uncommon for such a young person with no history of disposing factors, such as family history, viral carditis etc, to develop cardiomyopathy.

The distinction however for ambulance personnel is not clinically significant.



Shrimpfriedrice said:


> With that said the onset of symptoms where fairly quick, i'm just suprised no one dug for more of a history? I know normally we probe for a more detailed history before providing possible differentials. Am I missing something?



Yes.  You are missing that developing further differentials will not change your treatment in a clinically significant way.

The two most important diagnoses not to miss here are (a) active antepartum haemorrhage, and (b) anaphylaxis, or anaphylaxis like syndrome.

We have very good evidence to point us away from antepartum haemoorhage (see my earlier post).

The diagnosis often depends upon the history, but in this case, a detailed history is inappropriate as the patient has an immediately life threatening problem and we've got enough of a history to combine with physical findings to come up with a diagnosis.


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## Summit (Dec 5, 2016)

Alan L Serve said:


> Have a blessed evening. I'm going to study HVAC now.



HVAC might be a good way to go observing your reactions here. More lucrative at least...


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## Alan L Serve (Dec 6, 2016)

Summit said:


> HVAC might be a good way to go observing your reactions here. More lucrative at least...



I am joining the Cult of HVAC. It pays better and, my friend, the ducts don't complain! Join us.....


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