Unusual OB/GYN Case. Wacha gonna do?

[sevoflurane]

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So... here it goes:

20 y/o otherwise healthy fem. with RPOC (fetal demise) presents to the outpatient side for D&C.

She goes to sleep.

Operation is uneventful.

Post-op vag. pads are bloody... more so than the usual D&C.

VSS.

She is monitored for the next 30 minutes with continued slow bleeding.

OB does a speculum exam, can't see a bleeder... 😕 but she continues to bleed anyway.

Wacha want to do?

 

[scudrunner]

What does RPOC stand for?

How about VSS?

Here is my MS-2 thinking:

Is there any connection between why the fetus died and why she is now bleeding? Any history of coag disorders/factor deficiencies in the family? Is she showing any petechiae?

How are her vitals? Probably should get a CBC, PT/PTT. Not sure what else...

I assume a saline IV is already going, is FFP a good idea at this point?

Also, how about pitocin to clamp off bleeding?

Maybe I'm way off, but hey, that's how you learn, right? 🙂

 

[TexasGas]

retained products of conception

vital signs stable

 

[RT2MD]

How are her vitals? Probably should get a CBC, PT/PTT. I assume a saline IV is already going, is FFP a good idea at this point?

Also, how about pitocin to clamp off bleeding?

Maybe I'm way off, but hey, that's how you learn, right? 🙂

Well... I guess I'll throw my vast M1.5 experience in here...

I agree with scudrunner. CBC, PT/PTT. I would guess that the FFP question would be given by the results of the labs. I don't know how the Pitocin works to clamp off the bleeder, and would love to be enlightened.🙂

How far along was the patient's pregnancy? Would we have to consider an accessory lobe of a placenta? With the speculum exam after a D&C, was the OB just saying they couldn't see blood coming from the cervix, or was it more in depth than that?

I suppose if it was a significant amount of blood loss, we could always go to specials, see if we could find a bleeder that way..

AND, I'll echo this statement: "Maybe I'm way off, but hey, that's how you learn, right? 🙂"

 

[PMPMD]

IUFD makes me think of DIC. Was she oozing from anywhere else?

CBC, coags, fibrinogen, FDPs

T&C for one blood volume's worth of PRBC, FFP, + plt & cryo

Ensure large bore IV access.

Definitive Tx is removal of POCs - allegedly this was already done, if so, she should improve. If not, maybe they left some in there and they're causing the release of tissue factor.

 

[Idiopathic]

Seems fairly straightforward. Diff includes 1)continued RPOC 2)DIC 3)inherent coagulation abnormality

T+S/T+C sent (same thing here), second IV, CBC, coags, fibrinogen. I wouldnt think uterine tone would be the biggest problem here, but would be amenable to a dose of oxytocin, would not consider methergine/hemabate without further uterine exam.

Expect the worst, DIC a real possibility here. Prepare for big transfusion, possibility of underlying infectious process that could complicate hemodynamics...sometimes things that are indolent become aggressive after initiation of anesthesia (Murphys Law?).

Should have made it more complicated by doing regional...force the providers hand with a persistent vaginal bleed under lidocaine spinal...oh and give her a class 4 airway 😉

 

[Idiopathic]

Well... I guess I'll throw my vast M1.5 experience in here...

I agree with scudrunner. CBC, PT/PTT. I would guess that the FFP question would be given by the results of the labs. I don't know how the Pitocin works to clamp off the bleeder, and would love to be enlightened.🙂

How far along was the patient's pregnancy? Would we have to consider an accessory lobe of a placenta? With the speculum exam after a D&C, was the OB just saying they couldn't see blood coming from the cervix, or was it more in depth than that?

I suppose if it was a significant amount of blood loss, we could always go to specials, see if we could find a bleeder that way..

AND, I'll echo this statement: "Maybe I'm way off, but hey, that's how you learn, right? 🙂"

pitocin is an oxytocin analogue, which is released during labor, resulting in augmented uterine contractions and increased uterine tone to prevent postpartum hemorrhage. pitocin is given to both induce/augment labor and after cesarean section, since the maternal response may not be sufficient.

 

[Idiopathic]

i didnt mention uterine perforation but that has to be a big concern here as well, especially in the anesthetized patient. im not sure if you can tell without hysteroscopic exam, but i suppose laparoscopic exploration wouldnt be out of the question if highly suspicious.

 

[RT2MD]

pitocin is an oxytocin analogue, which is released during labor, resulting in augmented uterine contractions and increased uterine tone to prevent postpartum hemorrhage. pitocin is given to both induce/augment labor and after cesarean section, since the maternal response may not be sufficient.

Thank you, I knew about it being an oxytocin analogue, but hadn't correlated the increased uterine tone preventing hemorrhage. I appreciate it. 👍

 

[sevoflurane]

As usual this forum is full of rockstars. Great job to the med students who stepped up to the mic. And you both are right... this is a LEARNING forum so there are never stupid questions or answers. Your answers were both excellent.

Idio's response is spot on. Can't get much past this long horn... 👍

Pitocin, Methergine or Cytotek or combination should be given to try and attenuate/stop bleeding. In addition, a speculm exam followed by ultrasonography (r/o perf, retained products) should be performed.

DDx:
Perforation
Retained products
Trauma to vagina/cervix
Bleeding disorder

USD and speculum exam were negative....

So what we did:

First thing:

😀



Back to the OR for second look under GA/relaxed patient.... Access = 18G x 2 in a 55kgmer. We could've placed a central line/a-line at any point but we chose to wait as we knew it could be placed in seconds flat and we were doing alright with 18G's.

Continued bleeding, and bleeding, and bleeding...

PT/PTT/INR/FIBRINOGEN/CBC/BMP/ABG + FDP's would help secure the diagnosis....

On with the case....

Still, no central access or A-line at this point... Oozing at PIV sites, lab draw sites....

Blood in the field looks coolaid like... none of the nice looking dark clots you look for after giving protamine after coming off bypass.... coolaid, coolaid, coolaid... oozing cooliad at IV sites....

Mainly Nitrous going through PVC (this is my partners case... I was just helping and prolly woulda given a bit of special K, but that's neither here or there) .4-.5 MAC.

This is DIC from release of tissue thromboplastin until proven otherwise folks.

Labs come back: Platelets go from 360 > 60, fribrinogen 66, PT and PTT are 19 and 36 (I expected higher). Hgb down to 6.

VSS pretty normal throughout besides a little tachy.

5 units of blood, 5 FFP, 2 Cryo, 5 Platelets all going in before we get these labs back.

Questions:

1) What is the role of antifibrinolytics....i.e. amicar/txanexamic acid in a patient like this... oozing patient who is loosing blood?

2) Any hesitation is placing a central line or a-line?

 

[Idiopathic]

great questions for residents

 

[scudrunner]

Questions:

1) What is the role of antifibrinolytics....i.e. amicar/txanexamic acid in a patient like this... oozing patient who is loosing blood?

2) Any hesitation is placing a central line or a-line?

I'm obviously not a resident, but...


1) To stop the consumption of coagulation factors and platelets...?

2) Seems like there would be- she's already oozing from the IVs, so you don't want to go making any more holes to bleed from before regaining hemostasis. But, when would it be indicated in a situation like this?

 

[btbam]

TXA seems like a great idea to me. It's given at my training institution in cardiac cases to help with this "oozing" problem post-bypass. Assuming hemodynamically stable, I would hold off on invasive access.

 

[Idiopathic]

amicar could be given but another drug needs to be given with it/before...what?

id have no problems putting in a big line/a-line. mortality/morbidity in this situation is very high and if you cant keep up with replacement you have no shot.

 

[Doctor4Life1769]

As usual this forum is full of rockstars. Great job to the med students who stepped up to the mic. And you both are right... this is a LEARNING forum so there are never stupid questions or answers. Your answers were both excellent.

Idio's response is spot on. Can't get much past this long horn... 👍

Pitocin, Methergine or Cytotek or combination should be given to try and attenuate/stop bleeding. In addition, a speculm exam followed by ultrasonography (r/o perf, retained products) should be performed.

DDx:
Perforation
Retained products
Trauma to vagina/cervix
Bleeding disorder

USD and speculum exam were negative....

So what we did:

First thing:

😀



Back to the OR for second look under GA/relaxed patient.... Access = 18G x 2 in a 55kgmer. We could've placed a central line/a-line at any point but we chose to wait as we knew it could be placed in seconds flat and we were doing alright with 18G's.

Continued bleeding, and bleeding, and bleeding...

PT/PTT/INR/FIBRINOGEN/CBC/BMP/ABG + FDP's would help secure the diagnosis....

On with the case....

Still, no central access or A-line at this point... Oozing at PIV sites, lab draw sites....

Blood in the field looks coolaid like... none of the nice looking dark clots you look for after giving protamine after coming off bypass.... coolaid, coolaid, coolaid... oozing cooliad at IV sites....

Mainly Nitrous going through PVC (this is my partners case... I was just helping and prolly woulda given a bit of special K, but that's neither here or there) .4-.5 MAC.

This is DIC from release of tissue thromboplastin until proven otherwise folks.

Labs come back: Platelets go from 360 > 60, fribrinogen 66, PT and PTT are 19 and 36 (I expected higher). Hgb down to 6.

VSS pretty normal throughout besides a little tachy.

5 units of blood, 5 FFP, 2 Cryo, 5 Platelets all going in before we get these labs back.

Questions:

1) What is the role of antifibrinolytics....i.e. amicar/txanexamic acid in a patient like this... oozing patient who is loosing blood?

2) Any hesitation is placing a central line or a-line?

Here's a stab.

1. If bleeding were to continue despite above treatment, and the dx of hyperfibrinolysis is made (fibrin split products seen? sorry my internet is really crapping out so can't see initial post w/o taking 20 mins to load), I would go ahead and give it. It will stop bleeding quickly in a pt with increased fibrinolysis. It would also decrease the need to add more FFP, which has its own issues.

2. Coagulopathy is a relative indication. Not sure on this, could still do it

Just my .02

 

[Doctor4Life1769]

amicar could be given but another drug needs to be given with it/before...what?

id have no problems putting in a big line/a-line. mortality/morbidity in this situation is very high and if you cant keep up with replacement you have no shot.

Give with heparin due to clot formation?

Sounds good with the line, thanks for clarifying.

 

[Idiopathic]

ill try not to step on sevo's toes but you should heparinize before amicar. (edit: WHEN YOU ARE TREATING DIC)

since there is no surgical bleeding, i would anticipate amicar/etc. improving this situation as clotting factors are transfused. i have seen this save someones life in exactly this type of case (actually it was DIC from an AFE when i was a med student.)

that lady walked back into the hospital 1 month later to show everyone pics of her kid. i would anticipate that scenario having close to 100% significant morbidity and at least 25% mortality, so it was a big win and coagulopathy was completely uncontrolled prior to that intervention.

 

[Doctor4Life1769]

ill try not to step on sevo's toes but you should heparinize before amicar.

since there is no surgical bleeding, i would anticipate amicar/etc. improving this situation as clotting factors are transfused. i have seen this save someones life in exactly this type of case (actually it was DIC from an AFE when i was a med student.)

that lady walked back into the hospital 1 month later to show everyone pics of her kid. i would anticipate that scenario having close to 100% significant morbidity and at least 25% mortality, so it was a big win and coagulopathy was completely uncontrolled prior to that intervention.

I don't have much experience with all this yet. However, how quickly does Amicar work (since you said give heparin before rather than with)?

 

[btbam]

Also, maybe someone already said this but we would order a D-dimer for suspected DIC right?

 

[Idiopathic]

Also, maybe someone already said this but we would order a D-dimer for suspected DIC right?

horribly nonspecific test, guaranteed to be positive in many situations. i would never order this test under any circumstance.

although the textbooks say it can be useful in the dx of DIC, you likely would have your answer before the results of this test were back

 

[sevoflurane]

Thanks for taking the lead on the discussion idio. That was exactly what I was going for.

You see, as a medical student and in early residency, I never really understood coagulation... I memorized the intrinsic pathway and extrinsic pathway and it's idiosynchrinoisms, but I really didn't have the depth...

Back then it was 2D and not full flowing....

😀


I am certainly no expert.... and really... it's not all that black and white... There is enough coagulation stuff around you can have a subspecialty in hematology right?.

Anywho...

I thought this was a good case for the MS's and some residents that may want to bring some depth to their knowledge. This is a very simplistic view of coagulation, but I believe it is better to start from afar with this subject and then work your way in + clinical scenarios always makes learning more fun IMHO.

So here it is....

If you want to boil coagulation into one sentence it is this:

Coagulation is the balance of the force between fibrin (think of it as clot) and plasmin (think of it as clot buster).... One is like Luke Skywalker the other is like a Sith Lord.

In our bodies, because of many inhibitors and activators of coagulation, the force (coagulation) is in balance... and we need it this way... too much of either is bad = bleeding or thrombosis.

When DIC ensues (release of tissue thromboplastin), this balance is altered and you get systems getting activated in both arms... running amuck... THERE IS CLOT FORMATION AND FIBRINOLYSIS OCCURRING BOTH AT THE SAME TIME. So you get the manifestations of DIC....

Bleeding AND Clotting both simultaneously.


So what do the antifibrinolytics TXA /ACA do...???

They prevent the conversion of plasminogen to plasmin. Plasmin is a clot buster right?... Well if you are inhibiting the clot buster...then you are affecting the balance toward creating clots>>>>> and hence it's application in preventing blood loss in the heart room and in spine cases...

What does it mean in relation to DIC?

DIC has micro and large vessel thrombosis + bleeding. This thrombosis is exactly what causes the loss of fingers, toes, entire extremities, portal vein circulation, cerebral circulation.... DVT's, PE's and so on and so forth....
The excessive fibrinolysis causes excessive bleeding... Either one= Badness.... you bleed and deposit thrombus both at the same time.

YOU SEE THE PROBLEM with antifibrinolytics?... oozing may get better with ACA, but it can also cause a fatal sagital sinus thrombosis due to a coagulation state that favors deposition of CLOT.

YOU MUST BE CAREFUL.

Again, I'm no expert, but Idiopathic is right in prompting you to use heparin IF the clinical scenario is such that antifibrinolytics are being considered:

As for the central line/a-line thing.... well, this is more straight forward:

If they need it, put it in.

If they don't, then avoid it.

After we dropped her off in the ICU, she got a central line and over 12 hrs. probably donated a good 200 cc's into a pack full of 4x4's...


🙂

 

[scudrunner]

Great post sevo, thanks for taking the time to teach us graaas-hoppaahhs.

Would love to see more cases posted, for whatever level, by whomever, they're all fun to read at the very least.


Although I have to say, those pictures of necrotic baby appendages kind of tug at my heart strings. Sad situations right there.

 

[sevoflurane]

It's reality bro... and that's why I think we need exceptional physicians entering our field. 🙂

It's not just pent, sux, tube.... There is more.

 

[scudrunner]

It's reality bro... and that's why I think we need exceptional physicians entering our field. 🙂

It's not just pent, sux, tube.... There is more.

Absolutely.

 

[Ketafol20]

Anyone want to give recombinant Factor 7a?

 

[beavis]

Sevo, this type of thread is one of the main reasons I keep coming back to this forum. Thank you.

Beav

 

[deleted9493]

I am a big fan of TEG, even though it's not used in the ORs at my home institution. It certainly well-demonstrates the dysregulation of coagulation/fibrinolysis in DIC...


http://ceaccp.oxfordjournals.org/content/7/2/45/F3.large.jpg

 

[Idiopathic]

Anyone want to give recombinant Factor 7a?

if she is about to exsanguinate and nothing else is working, maybe. this case sounds a little more manageable with 5/5/5/2 of products and a seemingly stable patient.

also, remember the main problem here is not the inability to form clot, rather, as sevo said, its an imbalance between the native clotting system resulting in an INCREASED ability to clot and break down clots. VIIa has been noted to help in refractory cases, but Im not sure there is much to hang your hat on there until all the clotting factors are used up and you cant form any new clot.

 

[Ketafol20]

if she is about to exsanguinate and nothing else is working, maybe. this case sounds a little more manageable with 5/5/5/2 of products and a seemingly stable patient.

also, remember the main problem here is not the inability to form clot, rather, as sevo said, its an imbalance between the native clotting system resulting in an INCREASED ability to clot and break down clots. VIIa has been noted to help in refractory cases, but Im not sure there is much to hang your hat on there until all the clotting factors are used up and you cant form any new clot.

First of all, I don't have a lot of experience with rfVIIa as probably is the case with most everyone here.

Idio, you are right, it is a "last resort" treatment. But rfVIIa still needs the usual clotting factors (thrombin, fX, and platelets) present in order to be effective.

It is also quite expensive, about $6000 for a 70 kg pt.

Just thought this was a good thread to discuss rfVIIa.

 

[imfrankie]

So... here it goes:

20 y/o otherwise healthy fem. with RPOC (fetal demise) presents to the outpatient side for D&C.

She goes to sleep.

Operation is uneventful.

Post-op vag. pads are bloody... more so than the usual D&C.

VSS.

She is monitored for the next 30 minutes with continued slow bleeding.

OB does a speculum exam, can’t see a bleeder... 😕 but she continues to bleed anyway.

Wacha want to do?

This case so reminds me of a case I had while a resident. I had already had a couple coronary spasms because the young healthy girl had trismus on induction, wouldn't open her mouth, the sux wouldn't work, another stick wouldn't work--then the monitors went out. This is the days when attendings weren't around cause they were either in the office/lab writing papers, or home sleeping at night. So finally I get her intubated and it looks/sounds like the tube is in the right place. (Capnograph is still dead) Hope she's not an MHer. THEN the OB resident and attending are fiddling around, time is passing...I'm thinking, let me just get through this Lord. So time drags on and red stuff seems to be filling up the plastic bag drape hanging at the butt. I ask nicely, "everything okay?" Then the left coast OB lady gives me the "EVERYTHING IS FINE DOWN HERE, YOU JUST WORRY ABOUT THE ANESTHESIA" Well, okay, yeah. She kept bleeding and bleeding. Dammit, I'm alone up in the OB suite. Urrrr. Now I'm sweating under the drapes, trying to get a real IV. Where's the blood, somebody run these labs, quit stroking the surgeon and get me some products, fluid, a new monitoring system. X PRBC / Y FFP /Z Cryo / some plateletts and my own elevated troponins later the girl finally gets out of the OR and to some real monitoring in the ICU. I will never forget that. NEVER TRUST THE SURGEON, ALWAYS VERIFY. Oh man.

 

[RT2MD]

Great post sevo, thanks for taking the time to teach us graaas-hoppaahhs.

Would love to see more cases posted, for whatever level, by whomever, they're all fun to read at the very least..

Couldn't have said it better, Love these cases... I can't wait until I get into clinical years!

Thanks to everybody for their posts! 👍

 

[Idiopathic]

First of all, I don't have a lot of experience with rfVIIa as probably is the case with most everyone here.

Idio, you are right, it is a "last resort" treatment. But rfVIIa still needs the usual clotting factors (thrombin, fX, and platelets) present in order to be effective.

It is also quite expensive, about $6000 for a 70 kg pt.

Just thought this was a good thread to discuss rfVIIa.

good point, i guess what im trying to say is that you usually would consider VIIa when you have an inherent coagulopathy, such as what may result from poor number or function of clotting factors that you cant replace quickly enough with transfusion or that are simply not working well enough, such as after bypass, etc. Here that is not the case, at least initially. Eventually you may get into the scenario where you are just feeding THE OOZE, and that may be the time to consider VIIa. It is very expensive and thrombogenic as well, so we have seen blood vessels clot off, new bypass grafts go down, etc. after giving it, but people usually stop bleeding.

 

[dhb]

Labs come back: Platelets go from 360 > 60, fribrinogen 66, PT and PTT are 19 and 36 (I expected higher). Hgb down to 6.

This is the problem i have with DIC: how are you coagulating if you have no coagulation???

I've never seen a true DIC: embols + bleeding

Much more common is the classic dilution coagulopathy which is almost always paired with a higher consumption of factors due to the bleeding taking place.

 

[Stank811]

Interestingly just used factor VII today

5yo moyamoya PMHX of sickle cell disease complicated by CVA in 09 currently being treated with exchange transfusion requiring chelation secondary to iron overload who had b/l synangiosis yesterday and was an emergent add on this morning secondary to subdural hematoma. Coags off the top of my head at the start of the case were PT 19, INR 2.1, PTT 88, D-dimer 3.4, Plts 120, Fibrinogen 137 ....so after giving ffp, plts, cryo, prbcs with no resolution of bleeding and oozing at surgical site pt was given 90ug/kg x2 as loading dose and within 10-15min bleeding significantly slowed at surgical site. Case finished with pt sedated and tubed in the unit stable but I will have to wait and see how the patient wakes up. But thought the case was a good example of how quickly factor VII worked for us to help control bleeding intraop and hopefully our pt wont have any of the dreaded side effects of the drug.

 

[proman]

Interestingly just used factor VII today

5yo moyamoya PMHX of sickle cell disease complicated by CVA in 09 currently being treated with exchange transfusion requiring chelation secondary to iron overload who had b/l synangiosis yesterday and was an emergent add on this morning secondary to subdural hematoma. Coags off the top of my head at the start of the case were PT 19, INR 2.1, PTT 88, D-dimer 3.4, Plts 120, Fibrinogen 137 ....so after giving ffp, plts, cryo, prbcs with no resolution of bleeding and oozing at surgical site pt was given 90ug/kg x2 as loading dose and within 10-15min bleeding significantly slowed at surgical site. Case finished with pt sedated and tubed in the unit stable but I will have to wait and see how the patient wakes up. But thought the case was a good example of how quickly factor VII worked for us to help control bleeding intraop and hopefully our pt wont have any of the dreaded side effects of the drug.

This patient likely has an acquired Factor 8 inhibitor, which is what NovoSeven was originally labelled for. Have the hematologists check for that? It's commonly seen in hemophiliacs who require frequent transfusions.

 

[W222]

This is sorta an aside, but is it just me or do terrible things seem to happen on OB floors? I mean, I have seen way too many acreta/percretas, uterine atony, DIC, C-hys sections, horrific airways, etc. I think sometimes people forget that even though they are in the hospital for a joyous occassion, their bodies are still in a state of physiological disarray and C-sections are surgical procedures. I hate when the OBs look at you after the kid is out with a "what the hell is going on?" look, I have nightmares of these days.

 

[Stank811]

My staff actually mentioned factor VIII deficiency after factor VII worked so quickly and since there was very little change with FFP, plts, and cryo but did not bring up the acquired factor VIII deficiency which is something I will have to read up on but sounds promising. We did get a heme consult but just checked the EMR and they have not left a note yet so it will be interesting to see what they come up with.

 

[Arch Guillotti]

Back to the OR for second look under GA/relaxed patient.... Access = 18G x 2 in a 55kgmer. We could’ve placed a central line/a-line at any point but we chose to wait as we knew it could be placed in seconds flat and we were doing alright with 18G's.

I have seen a situation like this one time so far as a resident also on OB. It was a mighty struggle to place the art line, we were lucky to get it in

 

[Arch Guillotti]

This is the problem i have with DIC: how are you coagulating if you have no coagulation???

I've never seen a true DIC: embols + bleeding

Much more common is the classic dilution coagulopathy which is almost always paired with a higher consumption of factors due to the bleeding taking place.

DIC is ugly and you will know it when you see it, oozing from everywhere.

 

[dhb]

DIC is ugly and you will know it when you see it, oozing from everywhere.

To the best of my knowledge for DIC you need thrombo-emboli + coagulopathy.
Oozing is just coagulopathy to me.

 

[sevoflurane]

This is the problem i have with DIC: how are you coagulating if you have no coagulation???

I've never seen a true DIC: embols + bleeding

Let me just preface my response with this: I spent a good 3 months of ICU time at a big center that did more liver transplants than any other center in the US at the time. We had our share of coagulation issues, sepsis, ARDS, etc. We also had a massive burn unit. I have lived thorough the years where APC was very popular and have seen undeniable DIC many a times. Exceptional experience.

Again, I'm no expert, and I'm only here to share my thoughts on the subject:

Let's start looking at the forest and ask some questions:

Why would a perfectly healthy 20 y/o going in for a routine D&C have this type of bleeding? I mean D&C's are straight forward cases right? People shouldn't die from D&C's.... unless you don't know what you are doing.

If the speculum exam and USD were both negative in relation to perforation, lacs, trauma.... then WHY would this young lady with a starting platelet count of 360 continue to bleed...??? When I asked OB what he had seen he responded with: "No definitive single point of bleeding, just red, juicy tissues with a constant trickle from everywhere". Let me add that the obstetrician in the OR can take out a uterus robotically likidy split. He is very good.

Now... when you go to the books, is there any special mention of DIC in relation to obstetrics? The answer to this question is absolutely. It is at the very top of the list of conditions associated with DIC after sepsis and malignancy.

Why?

• AFE
• Fetal Death in Utero (direct release of tissue factor)
• Abruption Placentae
• Preeclampsia/Eclampsia

Let's ask some other questions:

Why would FDP's (cleavage of fibrin monomers) and D-dimers (cleavage of fibrin-fibrin bonds) be MARKEDLY elevated in somone who is otherwise perfectly healthy and now is showing us signs of bleeding? Doesn't this lab value test for the BREAKDOWN of fibrin clot? If you are replacing 1:1:1 + cryo, should there be breakdown of clot in a non DIC patient? It seems to me, that in a healthy individual who is bleeding, evolution would dictate clot formation, not marked fibrinolysis/consumptive coagulopathy.

1:1:1 + cryo is not hemodilution.

Although, I do agree that FDP's and DD's are not generally useful in hospital patients, I do find them useful in otherwise healthy 20 y/o's with no past medical history.

DIC is fibrinolysis and fibrin/thrombin formation occurring both at the same time. This doesn't mean that every case has clinical evidence of purple fingers + bleeding from mucous sites. Sometimes the overwhelming picture is clot, sometimes it's bleeding and sometimes it's both. I've seen all 3 of these. It is a spectrum of coagulation dysfunction, and it's clinical manifestations vary. I mean... there is such a thing as chronic DIC in patients with malignancy right?

One of the big differences between DIC and Primary fibrinolysis is platelet count and it's rapidity of decline. When was the last time you had a platelet count go from 360 to 60 in a of couple hours?

This by itself is extremely unusual. I'll do a routine Mitral/Aortic valve and won't see anywhere close to this type of decline.... and we are talking about pump runs which inherently cause platelet activation. You'll def. loose platelets, but it is unusual for it to be this dramatic with starting platelet numbers above 350 in otherwise routine cases.

Lastly, you had to be there. The oozing at IV puncture sites and mucous membrane sites is very characteristic of DIC. You'll recognize it when you see it.

Hopefully you will at least think of it as ACA and TXA are both indicated in primary fibrinolysis and could be a death sentence to a patient with DIC.

FWIW, I don't ever give antifibrinolytics to patients I suspect might have DIC... I'll get an intraoperative hematology consult and let them make the call.

🙂

 

[proman]

To the best of my knowledge for DIC you need thrombo-emboli + coagulopathy.
Oozing is just coagulopathy to me.

Proof of thrombosis isn't required to make the diagnosis of DIC, or the term I prefer, consumptive coagulopathy. You aren't seeing the clots because they are forming in the microvasculature, causing a microangiopathic hemolysis. It's a histologic finding, but rarely there will be life-threatening thrombosis (hepatic or adrenal vein thrombosis, purpura fulminans, etc). Thrombosis isn't a part of the criteria of DIC:

1) Thrombocytopenia
2) Abnormal coagulation
3) Low fibrinogen
4) Evidence of fibrinolysis (FDP)

 

[proman]

FWIW, I don’t ever give antifibrinolytics to patients I suspect might have DIC... I’ll get an intraoperative hematology consult and let them make the call.

Agree. Your best available resource is your blood banker. They are a wealth of knowledge and can facilitate mobilizing the lab and blood bank.

 

[dhb]

I prefer, consumptive coagulopathy.

I prefer that term too

 

[Arch Guillotti]

Lastly, you had to be there. The oozing at IV puncture sites and mucous membrane sites is very characteristic of DIC. You’ll recognize it when you see it.

Yes, you will know it when you see it.

 

[Ketafol20]

good point, i guess what im trying to say is that you usually would consider VIIa when you have an inherent coagulopathy, such as what may result from poor number or function of clotting factors that you cant replace quickly enough with transfusion or that are simply not working well enough, such as after bypass, etc. Here that is not the case, at least initially. Eventually you may get into the scenario where you are just feeding THE OOZE, and that may be the time to consider VIIa. It is very expensive and thrombogenic as well, so we have seen blood vessels clot off, new bypass grafts go down, etc. after giving it, but people usually stop bleeding.

It's not surprising that new grafts clot off with rfVIIa since it is the insulted endothelium that VII requires to activate the coagulation cascade. I am not certain but I believe it is more rare for the native uninsulted vessels to clot off. It is however, nice that the surgically insulted vessels (or trauma) are the most active sites of VII. I'm sure someone will correct me if I am off base here.

 

[DipriFan]

TEG provides a wealth of info, fast. You can see evidence of qualitative platelet function, factor deficiency, primary fibrinolysis all within 30min of running a sample.

 

[sevoflurane]

Problem is, most community hospitals don't have TEG's. 🙁

We also had to do a dry run/calibrate our TEG before using it adding time to your results. I don't know if this is the norm however.

Other than that... TEG's are da bomb when it comes to coagulopathy. 👍

 

[Sullivan]

I'm coming to this thread late, but it is such a great discussion of such an important topic, I wanted to add my two cents regarding transfusion and heme lab testing (I'm an attending in transfusion medicine FYI):

1. Regarding TEG: TEG has a place in evaluation of coagulopathies, but its strengths and weaknesses have to be kept in mind. For obstetric patients I am consulting on, I find its greatest strength is evaluating for the presence of hyperfibrinolysis. This helps guide the use of antifibrinolytics (like Amicar) more specifically. It is also useful in giving qualitative information regarding a patient's overall hemostasis. But be aware that the TEG is just that: qualitative. If you have an abnormal MA, or a prolonged r value, how many units of platelet or plasma do you give? (hint: I don't know either). You want to give as many blood products as you need, not more than you need, and for that reason the more quantitative measures seen in other lab testing are more valuable. All you need for making transfusion decisions in this patient are Hct/Hgb, plt count, PT, and Fgn levels, and those should be drawn ASAP as soon as you recognize an obstetric patient is bleeding excessively. I recommend drawing those labs q30 minutes for as long as the bleeding emergency is going on.

2. From my experience, and from what is seen in the literature, the DIC hemorrhage you see in obstetric patients very often manifests with hypofibrinogenemia. The drop in fgn will outpace the drops you see in clotting factors (seen by an abnormal PT). The practice challenge is this: it may take a while (30 minutes+, depending on your lab) to determine low fgn, and then it takes 30+ minutes to thaw/pool cryo. For this reason, when our OBs/OB anesthesiologists call an obstetric hemorrhage to our transfusion service, we immediately start thawing cryo and send it up with the other blood products so that they can have it on hand when they see low fgn labs or the patient has massive hemorrhage. Sometimes the product is wasted, but it winds up being needed more often than not, and will save us transfusing other products in higher volume because of not treating the underlying fgn problem. In the OPs patient, the fgn of 66 is much more concerning to me than the plt count of 60, and is the first aspect of her coagulopathy that should be addressed.

3. Use of NovoSeven (rFVIIa) is a last resort in obstetric patients because of the thrombotic risks, and should only be used when a. the patient has failed transfusion therapy (including cryo) to the tune of 10-12 RBCs and 10-12 plasma and is facing either hysterectomy or death. An important point of NovoSeven, and all clotting factors, is that their enzymatic activity sharply drops off as the patient becomes more acidotic, so if you use it in a patient with a pH of 7.0, you'll only have about 25% of FVIIa activity. So before using NovoSeven, try and correct acidosis and be sure you've transfused enough clotting substrate (fgn, plts, plasma) to be sure it has something to act on. The patient should be closely watched for 24-48 hours for thrombotic complications. We use NovoSeven very rarely (less than five times in the last ten years) and we have a heavy caseload of very complicated obstetric patients. We favor use of Amicar more frequently in these patients.

For folks who may be interested in more in-depth reading on management in this patient population, I'll refer you to the California Maternal Quality Care Collaborative: http://www.cmqcc.org/ob_hemorrhage They have put together an excellent best-practice toolkit for the management of obstetric hemorrhage.

 

[Ignatius J]

So... here it goes:

20 y/o otherwise healthy fem. with RPOC (fetal demise) presents to the outpatient side for D&C.

She goes to sleep.

Operation is uneventful.

Post-op vag. pads are bloody... more so than the usual D&C.

VSS.

She is monitored for the next 30 minutes with continued slow bleeding.

OB does a speculum exam, can’t see a bleeder... 😕 but she continues to bleed anyway.

Wacha want to do?

So she is post-op and VSS? That's the important part right there.

Get some coags and an H/H and call the primary team to let them know about it. Try and get good access in case infusion is necessary.

It's not rocket science, here. She's stabile and that's what we care about in the PACU.