Case Study: An OB Catastrophe

The following is a case simulation involving a patient initially encountered in Labor and Delivery. While the initial encounter occurred in a specific setting, this particular case will evolve and include transitions to various specialty areas over the healthcare continuum. Specialties Critical Case Study

Updated:  

Case Study Objectives

  1. Present a simulated case as it evolves over time.
  2. Encourage open discussion from nurses that represent a variety of specialties.
  3. Promote learning based on the:
    • details of the case
    • evaluation of the data
    • known interventions in order to provide holistic care
  4. Recognize maternal morbidity and mortality as a serious public health issue facing the world.

Introduction

The initial presentation that will proceed is meant to set the tone for the next set of events that will occur. I would like to preface by saying that this particular part of the case is where I have no actual nursing experience so I encourage colleagues who work in this specialty area to chime in with their responses.

Let's keep this lively, but also make sure we are respectful of each other.  Remember that we work in different hospitals and protocols may be different.  Also, be aware that while the following scenario seems "garden variety", it will get more "exciting" as we move along.

Case Specifics

History / Presentation

EJ is a 32-year old, Gravida 4 Para 2, at 34 weeks and 2 days gestational age. She has no chronic medical problems but admits to current tobacco smoking since age 17.  She says that she has been trying to quit and has cut back her smoking to 2-3 cigarettes a day.  She lives with her husband and two children ages 3 and 5 in a 2-bedroom apartment. 

She receives prenatal care at an urban Federally Qualified Healthcare Center (FQHC).  She previously worked as a server at a restaurant but has become unemployed for a couple of months due to restaurant closures from the coronavirus pandemic.  She has good family support from her parents and her husband, RJ, who is a delivery truck driver.  She is insured through her husband's coverage. 

Today, she called her Women's Health Nurse Practitioner (WHNP) when she experienced a gush of watery fluid from her lady parts while playing with her children.  She was told to come to OB Triage at the nearby Tertiary Medical Center Antepartum Unit.  Upon presentation, she was seen by the OB Triage nurse who found her anxious but well-appearing. 

Vital Signs

  • Temperature: 36.7 degrees C
  • Heart Rate: 84
  • Respiratory Rate: 16
  • Blood Pressure: 112/74
  • O2 Saturation: 96% RA
  • Fetal Heart Rate (FHR): 140

Physical / Pelvic Examination

An OB-Gyn resident saw EJ and performed a physical examination that revealed clear, pale yellow, odorless fluid leaking out of her endocervical canal with pooling in the lady partsl vault.

Diagnostic Studies

The OB-Gyn resident performed ultrasonography which revealed:

  • oligohydramnios
  • a fetus that is small for its age, without birth defects, in no distress
  • a placenta that does not cover the cervix

Recommendation

The OB-Gyn team recommended admission to the Antepartum Unit.

Diagnosis

At this point, EJ's diagnosis seems obvious but you are welcome to state it in your response to the thread.

1 - As EJ's nurse, state some assessment findings that would make you concerned. 

2 - As the nurse in that unit, what laboratory tests and monitoring procedures would you anticipate in this case, and why?

Specializes in L&D, OBED, NICU, Lactation.
9 minutes ago, klone said:

Okay, I know labor dude and I are on the same page. I'm going to diagnose this patient with an AFE (amniotic fluid embolism). Even though it's rare, the hallmark sign that that is what is going on is this:

This is typically how an AFE presents: at or around delivery of the placenta, the woman will suddenly feel unwell, nauseated, SOB, or express an impending sense of doom. 

The treatment (as labordude alluded) is immediate administration of the medications known by the acronym A-OK (atropine, ondansetron, and ketoralac). 

AFE will usually quickly develop into DIC, which is why she suddenly hemorrhaged once she became unresponsive. 

Other than A-OK protocol, treatment is supportive - blood products, volume expanders, treatment for cardiac arrest, transfer to ICU. Mortality is around 50-80%. And this is where I tag the ICU nurse. Baby's born, I'm outside my wheelhouse now. I'm happy to assess her  Bakri q2h, but that's about it. ?

There is a FASCINATING book called "37 Seconds" which is a woman's firsthand account of surviving AFE (and KNOWING before she even went into labor that she was going to die in childbirth - she spoke at the 2017 AWHONN annual conference in New Orleans).

This is where I was going. The presentation screams this to me. AFE, especially the rapid cardiorespiratory collapse, neurologic symptoms, moving into DIC and left ventricular dysfunction. The low platelets and low fibrinogen are hallmark and I bet that EJ would high fibrin split products if that lab value was present too. The upside is that AOK is really effective IF AFE is recognized and the meds are given quickly. They are easy to keep available and can be kept together in an AFE kit.

Specializes in OB-Gyn/Primary Care/Ambulatory Leadership.
Just now, JKL33 said:

So AFE then DIC then MODS...

?

Yep!

Specializes in OB-Gyn/Primary Care/Ambulatory Leadership.

Here's a great presentation on the use of A-OK protocol for AFE. Sadly, many nurses and even OB providers are unfamiliar with this treatment protocol.

https://www.arkansascrnas.com/wp-content/uploads/2017/11/AOK-for-AFE-HANDOUTS-no-references.pdf

Having never really seen the DIC >> MODS part manifest right before my eyes I really didn't think that all of this would happen in such close succession, I guess? The AFE causing arrest, sure. But her heart and liver are in big trouble now...maybe brain too.

 

Specializes in OB-Gyn/Primary Care/Ambulatory Leadership.

That's why it has such a high mortality rate.

Also I realized earlier that my comment about not suspecting AFE because of oligohydramnios doesn't make much sense, since obviously everyone's membranes are already ruptured at the point we're talking about. ??

Specializes in ACNP-BC, Adult Critical Care, Cardiology.

@klone, you could have presented this case! haha

This is obviously a made up case and was inspired by an actual case I encountered and we as a whole team of providers and nurses decided that the diagnosis was amniotic fluid embolism (AFE).

AFE is very rare as was mentioned and in fact some Obstetricians have not encountered it in practice and only know of it from case reports and textbooks. The range of case reports in the literature is 1.9 to 6.1 per 100,000 deliveries (1).  It is also a clinical diagnosis based on the presentation and after eliminating all other possible explanations.  I painted a "typical" presentation here because I am more interested in discussing the case than to confuse...but, there sure are atypical cases that have been reported.

Proposed Pathophysiology:

Not well understood but based on hypothesis that entry of amniotic fluid into the maternal systemic circulation carrying with it fetal cells and antigens creates an abnormal hypersensitive immune response.  This leads to vasodilatation and procoagulation somewhat similar to how we explain the systemic inflammatory response in septic shock.  This further creates capillary leaks leading to pulmonary edema, increased cardiac workload, and disregulation of the coagulation/fibrinolyisis pathway leading to DIC.

There is a proposed diagnostic criteria by the Society of Maternal Fetal Medicine and the Amniotic Fluid Embolism Foundation in order to gather more research data on these cases (2).  These are:

  • sudden onset of cardiopulmonary collapse
  • DIC
  • Onset during labor or within 30 mins of placental delivery
  • absence of fever

I am glad you OB guys brought up the A-OK protocol which I didn't mention in the case because that will be a dead give-away.  What I also found interesting in my readings was that autopsy of women who met the diagnostic criteria didn't always reveal amniotic fluid components in their pulmonary circulation. This was previously thought as the main insult that leads to AFE.

References:

(1) Knight M et al, Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations. BMC Pregnancy Childbirth (2012).

(2) Clark SL et al, Proposed diagnostic criteria for the case definition of amniotic fluid embolism in research studies. Am J Obstet Gynecol (2016).

Next steps?

I would like to delve deeper on EJ's ICU management but I'm hoping for responses from the ICU nurses. BTW, if this wasn't such a classic AFE, what other things could have happened?

Specializes in ACNP-BC, Adult Critical Care, Cardiology.
15 minutes ago, JKL33 said:

Also I realized earlier that my comment about not suspecting AFE because of oligohydramnios doesn't make much sense, since obviously everyone's membranes are already ruptured at the point we're talking about. ??

That's OK, sometimes we speak out our thoughts and then we realize, oh wait a minute, I take it back LOL.

Specializes in ACNP-BC, Adult Critical Care, Cardiology.
On 9/6/2020 at 8:21 PM, JKL33 said:

Having never really seen the DIC >> MODS part manifest right before my eyes I really didn't think that all of this would happen in such close succession, I guess? The AFE causing arrest, sure. But her heart and liver are in big trouble now...maybe brain too.

Her heart findings could be explained by the pattern on the echocardiogram that suggests Stress-Induced Cardiomyopathy (hypokinesis in the mid to apical segments).  Some patients end up with biventricular failure.  

Venous thrombosis and embolization is seen in DIC and can involve various organs including her liver. Her INR elevation is obviously from DIC but could also be from insult to the liver from the hypotension, congestion, etc (aka shock liver), hence, the triple digit transaminases. Bili rises with bleeding. 

The brain infarcts are odd right? why would she have that? This is a real question because we always think of embolic strokes as arterial rather than venous.  Does DIC also lead to arterial embolization? I don't know, unless maybe she has PFO that allowed the clots to cross it and go to her arterial circulation.

Specializes in ACNP-BC, Adult Critical Care, Cardiology.
1 hour ago, labordude said:

This is where I was going. The presentation screams this to me. AFE, especially the rapid cardiorespiratory collapse, neurologic symptoms, moving into DIC and left ventricular dysfunction. The low platelets and low fibrinogen are hallmark and I bet that EJ would high fibrin split products if that lab value was present too. The upside is that AOK is really effective IF AFE is recognized and the meds are given quickly. They are easy to keep available and can be kept together in an AFE kit.

I've also read that in some AFE case reports, the patient had some kind of aura...a feeling of impending doom...like they said "I think I'm gonna die" and then the event happens.

Specializes in ACNP-BC, Adult Critical Care, Cardiology.
3 hours ago, klone said:

?

There is a FASCINATING book called "37 Seconds" which is a woman's firsthand account of surviving AFE (and KNOWING before she even went into labor that she was going to die in childbirth - she spoke at the 2017 AWHONN annual conference in New Orleans).

How interesting.  The case we recently had (not EJ) is a woman who survived AFE as well and is neurologically intact (even after looking blue and lifeless during CPR).  Her accounts of events leading to her ordeal and during it send chills up our spines but I can't say it here for privacy reasons.

Isn't the most appropriate term for this condition now considered "Anaphylactoid Syndrome of Pregnancy?"

I believe circulating fetal cells are now thought to commonly pass to the mother during delivery, but only an extremely tiny fraction of women experience this catastrophic process;  this terminology stresses the excessive immunologic response thought to underlie this syndrome.

ICU nurse tagging in:

As DIC is probably better understood as a cluster of related coagulopathies, (which may account for her arterial emboli) serial ROTEM/TEGs will likely be helpful in determining blood product/factor replacement.  In terms of her on-going management, aside from managing her DIC and uterine hemmorhage with restrictive transfusion targets, much of her treatment will be supportive in nature.

Her neuro prognosis is poor; arterial thrombi plus a 30-minute low-flow time during the resuscitation suggest severe cerebral hypoxia. Serial neuro exams and sedation vacation as typical.  She may benefit from EEG to assess for non-convulsive status epilepticus as a contributor to her poor mental status.  Heparin would generally be indicated for cerebral thrombi (and pro-coagulopathic DIC) but is contraindicated here given uterine hemorrhage. Maintaining normal MAPs would be other major goal here.

Given the extensive insult and CPR time, her pressor requirements are relatively modest.  Her right heart works well, so the elevated CVP is likely due to extensive volume resuscitation, and some pulmonary hypertension, combined with high intrapulmonary pressures from her vent settings. 

Her epi is currently at a predominantly ionotropic dose, so, with her now adequate BP; her norepi could be slowly weaned as tolerated with Epi titrated based on serial TTE, or she could be transitioned to a more pure inotrope. 

At this point, volume status is tenuous; she is likely intravascularly overloaded, but with risk for repeat bleeding; so as long as her kidneys are semi-functional it's way too early to make any aggressive moves on this front.  This leaves her lungs stuck.  Her pulmonary compliance and p/F ratio are consistent with ARDs, but her ABG shows only a very mild respiratory acidosis. Maintain settings and wean as tolerated; if we're splitting hairs she doesn't need an FiO2 of 134, so her PEEP could probably be weaned slightly.

Kidneys remain a big question mark; her UOP and BUN/Cr should be watched for ATN. Much of the rest: her lactic acidosis, transaminitis, etc should be trended for now as they will likely resolve as the rest of her clinical picture improves. Oh, and give her some nutrition-given her pressor needs trickle feeds and GI ulcer prophylaxis should suffice.