Alright, picture this: you are sitting at work waiting for the next call, when the crew working opposite of you returns from an incident. The other crew walks into the lounge to join you, but you notice they have a look of solemn defeat on their face. When you ask them what’s wrong they tell you they just cared for a female with postpartum hemorrhage, and they had no idea what to do. At first you think to yourself, “how could that be?!” But then go on to realize that if you are being honest, you don’t really know either. Did we skip that chapter??
Here is the case:
You are dispatched to a private residence (Paramedic/EMT crew configuration) for a female patient who gave birth at home and is now hemorrhaging. When you arrive on the scene, you see a 33-year-old female patient lying supine on the bed in a second-floor bedroom, being tended to by two midwives. The patient is awake but thrashing about and acting erratically. You see a birthing tube in the bedroom, filled with bloody water, as well as multiple large blood saturated dressings.
The midwives inform you that the patient gave birth approximately one hour ago, without complication, to a full-term gestation baby, who is in another room with the father. The midwives report that EMS is not needed for the baby. The midwives go on to explain that following the baby’s birth, the patient began to hemorrhage. Due to the hemorrhage, the midwives performed a fundal massage and administered 1,000ml of normal saline via a peripheral IV, to no prevail. After an hour of fundal massaging, the midwives decided that additional care was needed, and contacted 911.
Let us pause there for a minute…
Now, if you are like me, my first thought was to blame the midwives! But, when I really thought of it, I am not sure they did anything differently than I would, at least initially. Should they have called 911 sooner? Sure, I think we can all agree on that. But, from a basic care perspective, I am not sure there is anything that the average EMS crew would do differently, despite this case being anything but basic...
When I reflect on my EMT education (14 years ago) and my paramedic education (10 years ago), I genuinely don’t remember learning about postpartum hemorrhage (PPH). Perhaps we did, but I don’t recall it; my bona fide thought was “did we skip that chapter?” As an EMS Educator, I believe we inadequately prepare EMS clinicians, during their initial education, to care for a mother in distress post childbirth. Our mental models include such an emphasis on the antepartum and intrapartum catastrophes that exist, such as placenta previa, abruptio placenta, prolapsed cords, limb presentations, neonatal resuscitation, etc, that we spend all our time focusing on them, and by the time we get to postpartum maternal emergencies, we don’t have anything left to say. The conversation usually ends with, “if the mother begins to hemorrhage, forcefully massage her fundal abdomen and the bleeding will stop.” Cool, sounds easy enough! But is that really it? What if the bleeding doesn’t stop? I can only speak for me, but I don’t ever remember anyone talking about that, and I would venture to guess most readers don’t either.
The American College of Obstetrics and Gynecology defines PPH as “cumulative blood loss greater than or equal to 1,000ml, accompanied by signs and symptoms of hypovolemia within twenty-four hours of the birthing process.” I love this definition because it is simple and to the point: bleeding post birth accompanied by shock. I can totally picture this! Massive blood loss, altered mental status, tachycardia, tachypnea, hypocarbia, and finally, hypotension (remember this is a late sign!)
Back to the show…
After speaking with the midwives, the EMS crew begins to assess the patient at which time she remains awake, but is speaking incoherently and thrashing about the bed. Upon first glance, it would appear she was seizing, but further evaluation would indicate she is just restless.
Let’s pause again, shall we?
Awake, speaking incoherently, and restlessness. This is shock! Shock is defined as inadequate tissue perfusion. Just three words, but they mean so much. Remember that shock is much like plumbing: if you had a leak from your bathroom sink, the problem would be interrogated down to the pipes, the pump (the sink itself), or the physical water coming into the device.
Perfusion in your body is much the same. If a patient is experiencing shock, they are either experiencing a pipe problem (distributive), a pump problem (cardiogenic/obstructive), or a volume problem (hypovolemic/hemorrhagic). In the case of our patient, she is experiencing the latter.
Hemorrhagic shock occurs when blood loss from a traumatic injury or otherwise, exceeds the requirements of cardiac output.
CO = HR x SV
Every time your heart beats, it releases blood from the left ventricle, used to perfuse the rest of the body, via the aorta. This is referred to as stroke volume. Moreover, as we are all aware, our heart is continuously beating to maintain not only perfusion, but homeostasis. If the amount of blood released from the heart per beat (stroke volume) is multiplied by the number of times the heart beats per minute (heart rate) the product is cardiac output, which expresses the amount of blood released from the heart per minute.
In the average adult, cardiac output is approximately 6L/minute. But, when a patient begins to hemorrhage and lose blood volume, the heart says “uh-oh! I need to fix this so my cardiac output doesn’t drop!” The heart has two options at this point: 1) add more volume 2) increase the heart rate.
Unfortunately, option one would be most beneficial, but cannot be done due to the hemorrhage in question, so that’s out. Because increasing the stroke volume aspect of the equation isn’t an option, the heart’s only choice is to compensate for the volume loss by beating less forcefully, at a faster rate, thus allowing the body to maintain some sense of perfusion and homeostasis for a time. Hmmm… the heart is compensating to make up for missing volume? Wow. Almost sounds like that’s why we call it compensated shock!
A hemodynamic evaluation of the patient revealed a heart rate of 140bpm, a respiratory rate of 28 breaths per minute with diminished tidal volume, a blood pressure of 100/60mmHg, an SPO2 of 91%, and an ETCO2 of 24mmHg, in addition to the altered mental status. A physical examination revealed that the patient “appeared to be no longer bleeding.”
If we were to break down these vital signs, I am not sure that we would discover anything surprising. The patient’s tachycardic and tachypneic, which makes sense due to the increase in her acidotic state due to the volume loss. They patient is also hypoxic due to the lack of blood flow to the lungs and ineffective gas exchange in the alveoli, and hypocarbic from the acidosis. No shock there. But what about her blood pressure? Is it low? Sure, it’s not great, but I honestly don’t think it’s that bad for someone who apparently lost a significant amount of blood! BUT, buyer beware…
Blood pressure is the last vital sign to change in shock. The tipping point from compensated shock to decompensated shock is when the patient becomes hypotensive. Hypotension occurs when the heart says “I can’t keep up this rate anymore” and begins to slow down. Be cautious not to fall into the normotensive-ish trap, thinking the patient isn’t ill.
So, what do we do? How do we determine how far along the compensation pathway the patient is? That’s where shock index enters the game. Shock index is a mathematical expression during which the patient’s heart rate is divided by their systolic blood pressure. Often expressed as:
The premise of shock index is vey simple: your heart rate should never exceed your systolic blood pressure. If it does, your heart is working way too hard (compensating). If the quotient of the shock index equation is 0.7 or less, it is representative of the patient being less likely to experience shock at the present time. However, if the shock index exceeds 0.8, it is more likely the patient is experiencing shock and requires resuscitation.
In the case of our patient, the shock index is 1.4, clearly indicative of shock requiring aggressive resuscitation. With all of the above in mind, I will tell you that I personally do not put all my eggs into the shock index basket. I believe I should not necessarily need an equation to tell me whether or not the patient in front of me is sick. BUT, I am a huge proponent of utilizing the shock index to assist my clinical decision making on those patients where I am unsure based upon my physical exam, or in any patient I wish to quantify my thinking about whether or not the patient is in shock. All-in-all, shock index is terrific. Use it! But don’t let it replace a good assessment.
Okay, so we have dissected the shock, but what happens during PPH anyway?
The “Four T’s” of PPH:
1. TONE: Uterine tone can be suboptimal in context of atony or bladder distention.
2. TISSUE: Retained tissue can include products of conception including succenturiate lobe or abnormal placentation, as well as retained blood clots from an atonic uterus.
3. TRAUMA: Trauma of the genital tract can include vaginal, cervical, and/or uterine injury such as lacerations, extensions, uterine rupture, and/or uterine inversion.
4. THROMBIN: Thrombin includes pre-existing or acquired coagulopathy.
In the case of our patient, which “T” do you think she is experiencing? Remember, at the time of EMS arrival there is evidence of significant blood loss, but the patient appears to be no longer hemorrhaging.
Given the presentation, I am inclined to believe the patient is suffering from a tone and tissue problem. History would suggest the patient did not sustain any trauma precipitating her hemorrhage, nor does she have a history of pre-existing coagulopathy. It is possible (and likely) she has become coagulopathic due to her hemorrhage and associated acidemia from shock, but not due to an underlying clotting disorder. As a result, it is most likely that the patient suffered an abnormal separation of tissue within the uterine walls, associated with poor uterine tone, which resulted in uncontrollable hemorrhage. In addition, it is important to note that a lack of visible hemorrhage does not rule-out internal hemorrhage. Moreover, in the case of this patient, it is imperative that we recognize that a lack of hemorrhage is not necessarily correlated to a lack of severity; it simply could mean a lack of available blood volume to hemorrhage.
So how do we fix this? Sure, we could continue with the traditional fundal massage, and I certainly would. In fact, I would encourage it! But remember, if it hasn’t worked for the midwives for the last hour, it’s highly unlikely it will begin working more successfully just because you’re doing it. Furthermore, if any attempt to reestablish uterine tone was going to be successful, it would have been! We need to change it up and do something different. What are our other options?
Volume Replacement- Blood Products
Volume replacement is a solid start and certainly one of the things this patient is in need of, but what should we use? As it turns out, as shocking (pun intended!) as this may seem, it is best practice to replace blood volume with… well, blood volume! Personally, I would try to make a move toward low titer O whole blood products (LTOWB). But if packed red blood cells (PRBC) are all you have please give them; some blood is better than no blood! The upshot to LTOWB products are simply that we can give more volume in whole blood (500ml) whereas with PRBCs we can only administer about 350ml. Moreover, LTOWB also allows us to administer platelets and plasma, in addition to red cells, to promote clotting and homeostasis.
If you don't have access to LTOWB and are administering component therapies such as PRBCs or plasma, this is still incredible and I highly encourage it! Like I said, some blood is better than no blood! However, if you are administering components such as PRBCs and plasma, consider also administering calcium gluconate or calcium chloride for hypocalcemia that will occur from exposure to the citrate preservative in the blood.
I would be remiss if while talking about blood products, I didn't touch on the logistics of matching blood types and Rh factors. Let's break it down:
Red blood cells have antigens on their surface that define blood cell identity:
A Antigens- Blood Type A
B Antigens- Blood Type B
A/B Antigens- Blood Type AB
No Antigens- Blood Type
Whatever antigen you have, you have antibodies AGAINST the other antigens:
Blood Type A- Anti-B antibodies
Blood Type B- Anti-A antibodies
Blood Type AB- No antibodies
Blood Type O- Anti-A and Anti-B antibodies
With this in mind, Blood Type AB can function as the universal recipient, whereas Blood Type O can function as the universal donor. In the hospital setting, in a controlled environment with time permitting, patients are typically crossmatched to receive blood components which align with their appropriate blood type. Unfortunately, in the EMS environment as well as within the realm of high stakes resuscitation, it is not feasible, practical, or responsible to have access to blood components for every blood type. This would be incredibly expensive, not to mention accrue a significant amount of unethical waste. Therefore, Blood Type O is used in these situations. But, O blood is a scarce and precious resource that must be cherished and used with responsibility and advocacy.
Now that we have the typing out of the way, what about all of this positive (+) and negative (-) stuff? We see it all the time, patients will be recorded as having A+ blood B- blood, O+ or O- blood, etc. But what does this actually mean?
The +/- following a blood type signifies the presence (+) or absence (-) of the Rhesus (Rh) protein in the red blood cell, which is a contributor to the maintenance of the erythrocyte membrane. A patient is considered Rh+ if the Rh protein is present on the red blood cell, whereas if there is an absence of Rh protein on the red blood cell, the patient is considered Rh-. Approximately 85% of the population is Rh+!
Patients who are Rh+ can receive Rh+ or Rh- blood. However, patients who are Rh- can produce Anti-D antibodies against the Rh+ factor, if exposed. Therefore, Rh- patients should ideally (key word) only receive Rh- blood. However, O- blood is always in such short supply that it is not feasible for it to be stocked in every ambulance, helicopter, and resuscitation bay. As a result, the use of Rh+ blood components, specifically O+ PRBCs, is common practice in all patients, even those who are Rh-.
Wait a minute, didn't I just say to give Rh- patients Rh- blood? I surely did... in a perfect world! Here's the deal, the only true resuscitative concern is in Rh- women of child bearing age who receive Rh+ blood. If an Rh- woman of child bearing age receives Rh+ blood, there is no harmful effect on the patient. BUT, the patient could potentiallyt develop Anti-D antibodies against Rh+ blood. If this were to occur and the patient were to become pregnant with an Rh+ baby, the Anti-D antibodies against the Rh+, passed to the fetus from the mother, could cause hemolytic anemia in the infant.
With all of this in mind, in the spirit of our topic of PPH, here is how I like to think about it: if the mother dies from hypovolemia, it will never matter if she develops Anti-D antibodies. In the unlikely event you encounter an Rh- female patient of child bearing age in hemorrhagic shock, from PPH or otherwise, and all you have is Rh+ blood components, GIVE THEM! Better to treat the patient for the risk of Anti-D antibodies and future hemolytic anemia of her children than to have her die of hemorrhagic shock.
Volume Replacement- Crystalloid
“BUT JONATHON, all I have is normal saline!” That’s okay but I would encourage you to proceed with caution. By all means some (keyword) normal saline volume replacement is better than none at all, but more is not better! There was a time when we would administer as much normal saline to patients as we possibly could, bragging about giving multiple liters to a single patient. Unfortunately, the literature would suggest this is bad practice. In fact, it is even discouraged! Not only does normal saline not replace any of the components the patient is losing, but it is also highly acidic only leading to worsened acidemia in large volumes. NOTE: isotonic solutions such as lactated ringers or PlasmaLyte are more favorable, but should be given conservatively.
Tranexamic Acid
In the hemodynamically stable and non-shock patient, when a wound occurs, platelets travel to the site of the injury, and fibrin is created to bind the platelets together, resulting in a solid clot. Plasminogen is then converted to plasmin which breaks down fibrin to prevent excessive clotting. Unfortunately, in the patient experiencing severe hemorrhage, this process may allow for excessive bleeding before the bleeding can be controlled, most often surgically. Because of this, there was a void of pharmacologic options to help mitigate the risk of untimely hemorrhage, hence the birth (2 for 2 in the pun department!) of Tranexamic Acid (TXA).
Let’s be clear, TXA is not a new medication, it is simply new to the prehospital environment within the last decade; TXA has been utilized in operating theatres and obstetrics for nearly fifty years! In the patient who receives TXA, after platelets go to the injury site and fibrin begins to bind the platelets together, TXA blocks the conversion of plasminogen to plasmin, therefore the fibrin clot is not broken down and clotting continues. This allows for clotting to continue and promotes hemorrhage slowing. However, it is important to note that TXA is not a wonder drug; TXA works best when it is used with other resuscitative mediums, such as blood. Furthermore, TXA does NOT stop bleeding! TXA prevents already existing bleeding from getting worse. Don’t confuse this!
Hypothermia
I would be remiss if I didn’t mention the challenges posed by hypothermia.
What do we know? The more acidotic you become, the more coagulopathic you are, and therefore subsequently hypothermic. In short… keep these patients warm! Hypothermia management is a drag, because it often means making us warm as well. But, if it means saving a life, I think we need to do it, and I personally believe we are really bad at this. I know I am! The last thing I want to be is sweaty (I tell everyone I was made for environments with Wi-Fi and air conditioning!), so I often overlook the simplistic act of turning on the heat in the ambulance, but it’s really important.
Don’t make this step harder than it needs to be: warm environment, warm blankets, hot packs, foil blankets, bear huggers, fluid warmers, blood warmers, etc. are all amazing options. What’s even better is a combination thereof! Use them!
Oxygen
Remember our definition of shock? “Inadequate tissue perfusion.” A primary component of perfusion is oxygen! If perfusion is inadequate, likely also are the oxygenation requirements. Don’t worry about the SPO2 reading. If they are in shock, they should receive high flow oxygen therapy. Period.
So where does this leave us?
Continuation of fundal massage
Blood administration (Components or LTOWB)
Crystalloid Administration
TXA administration
Active and passive rewarming
Oxygenation!
This is fairly straight forward. The basic management of PPH, if done well, is really reflective of standard hemorrhagic shock management utilized in trauma. But what about some other things? What about off label things you may need to try if punting is the only option?
Hemabate
If we have made it to this stage in the game to control the hemorrhage, we are having a really bad day. However, as emergency medicine and critical care professionals, we all know that sometimes these "really bad days" exist, and we have to break the glass for medication we don't use often.
Hemabate (Carboprost Tromethamine) is an oxytocic prostaglandin which can be used for the management of PPH that has been refractory to the conventional management tactics we have discussed. Hemabate works by stimulating myometrial contractions in the gravid uterus to provide homeostasis at the site of placentation.
Hemabate is administered intramuscularly, typically in doses of 250mcg, with subsequent repeating dosing three hours following the initial dose.
Methergin
In addition to Hembate, sometimes patients with refractory PPH benefit from the administration of Methergin (Methylergonovine). Methergin is an ergot alkaloid which facilitates the increase in rate and force of contraction.
Unlike Hemabate, however, Methergin may be given orally in an outpatient setting to assist in patients who continue to bleed post child birth, but are not at risk for significant hemorrhage and volume loss. Oppositely, Methergin may also be given intravenously as a loading dose of 0.2mg, followed by oral administration in varying doses for patients in need of significant resuscitation.
Hemostatic Agents
This is a category I find interesting. When Stop the Bleed was incepted in 2015, hemostatic agents took center stage in the fight against hemorrhage control. “Pack the wound,” we told everyone who would listen. We know it works! Unfortunately, in doing so we have created a mental model that we should not be packing natural orifices if we can avoid it, and as a result we have potentially, although inadvertently, created a stigma that a vaginal opening should not be packed with hemostatic agents. This recommendation comes on the heels of safety, much for the same reason we shy away from packing abdomens: it’s such a large space it cannot be controlled effectively. While this remains true, we are getting to the bottom of our algorithm and are into the territory where we must punt or the patient will die. In speaking to an emergency physician about this matter, she informed me of the following:
“… it is equivocal whether or not the use of hemostatic agents in the vaginal canal works in PPH. But what I do know is that PPH kills patients; that’s not the least bit equivocal. If I had no choice, I’d pack the vagina without hesitation.”
I think this is actually quite the prolific statement: is packing the vagina ideal? Definitely not. But neither is placing a COPD patient on a ventilator and we do that all the time. When in doubt, pack it!
Aortic Compression
Everyone practices medicine a little bit differently. With that in mind, I will be honest, I think if I had a patient in profound shock from PPH that was circling the drain, I wouldn’t do any one of these interventions we explored… I would try to do all of them simultaneously! Undoubtedly, I am going to keep aggressively fundal massaging while giving blood, TXA, oxygen, and warming. I would even go as far to say that I would pack the vagina with hemostatic gauze. But if all else fails, we could try to take control of the patient’s aorta.
In 1994, Riley et. al published "External Abdominal Aortic Compression: A Study of a Resuscitative Manoeuvre for Postpartum Hemorrhage," in the Journal of Anaesthesia and Intensive Care. (PMID: 7818062) During this study, the authors found that manual aortic compression of a patient in postpartum hemorrhage yielded a statistically significant reduction in heart rate from baseline, therefore reducing the rate of hemorrhage. As a result, the authors concluded that manual aortic compression may permit time for resuscitation, treatment, and transport to be instituted, and should be considered in cases of the most severe postpartum hemorrhage.
With this in mind, I found aortic compression to be an interesting concept, and last on the intervention list for a reason. Before we go down this road it is important to note that aortic compression is a point of no return. If you move to aortic compression, it means that all else has failed, or at least been ineffective, and it’s the last option before the patient dies. Furthermore, there is the possibility of significant long-term ramifications for the patient if not done correctly or haphazardly. So again, I say, proceed with caution…
As much as doing a thoracotomy or inserting a REBOA catheter in the ambulance or helicopter would be convenient, it isn’t practical, which leaves us with manual compression. To do so, place your fisted hand in the patient’s abdomen, between the umbilicus and groin. After placement, compress as hard as possible, and do not release pressure. Doing so, will diminish aortic flow by compressing the abdominal aorta between your fist and spinal column, to reduce hemorrhage distal to the occlusion.
Unfortunately, as you might imagine, maintaining significant force in this position, specifically in a moving aircraft or ambulance, is exceedingly challenging not to mention unsafe. However, if done correctly, although it is not a permanent solution, it may work as a placeholder to buy the patient some time.
Disposition Decision Making
Finally, I think it’s important that we create an appropriate mental model for disposition selection in the PPH patient. It goes without saying that, if possible, this patient should be transported to the closest appropriate facility with obstetric surgery capability. However, if you believe the patient is imminently dying, transport to the closest emergency department, is the most appropriate. Any emergency department has more blood availability than you. Any emergency physician can control an aorta invasively. But most importantly… any emergency department has more minds than you. In the ambulance or aircraft, at best, it’s you and your partner. In the emergency department there are many more resuscitationists able to bring tremendous insight to the discussion. Mental models are key, and sharing them is a necessity.
All-in-all, I think we owe PPH more attention than we give it. Although our scenario is entirely fictious, it is becoming more and more prevalent with the increase in home births. Despite the fact that those who facilitate home births are astute professionals, sometimes things still go wrong, and when they do, there is a small newborn child begging you to save their mommy.
PPH matters. Move the needle; don’t skip the chapter.
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