What EMS Needs To Know About Post-Abortion Care

DISCLAIMER: This blog will be speaking about the medical care secondary to an abortion (spontaneous or medically-induced). Kindly leave your politics and religion in your back pocket for this post. I understand this may make you uncomfortable, but I encourage you to learn so we can better understand and care for our patients.

Let's start with clarifying terminology. Abortion is defined medically as loss of pregnancy. There are spontaneous abortions (miscarriages if <20 weeks or stillbirth if  >20 weeks) or medically-induced abortions (sometimes termed 'elective'). 

Miscarriages occur in 10-15% of all pregnancies (when women know they are pregnant), and 80% of these occur in the first trimester. It is believed that if we accounted for women who did not know they were pregnant, the rate of miscarriage could be as high as 50%. 

According to Guttmacher Institute, 18% of pregnancies (excluding miscarriages)ended in medically-induced abortion in 2017. It's safe to say that abortions are quite common, so let's talk about them!

Let’s look at typical progesterone levels in pregnancy. The corpus luteum produces progesterone until the fetus by way of the placenta can produce enough of its own to sustain the pregnancy, at around 8-12 weeks.

Miscarriages can happen for a variety of reasons; most of the time it is impossible to know the cause. More than likely, a chromosomal abnormality is to blame, but implantation problems or maternal health conditions could also play a role.

Mifepristone is the chemical abortion agent that is FDA approved up to 10 weeks from conception. It works as a progesterone antagonist. Because progesterone is needed to build the placenta, mifepristone causes endometrial shedding and induces bleeding.

Mifepristone is a progesterone antagonist. It causes the levels of progesterone to effectively bottom out, preventing the uterus from sustaining pregnancy.

Misoprostol, a prostaglandin analog, can be used in conjunction and assists in strength and frequency of uterine contractions and dilation of the cervix. As expected, this treatment is very likely to cause severe cramping, bleeding, nausea, and diarrhea. There is a chance the medication will be unsuccessful in removing the entirety of the uterine contents. This places the patient at a large risk for infection. 

Prostaglandins bind to the EP1 and EP3 receptors in the uterus to trigger contractions and dilate the cervix. This is the effect of analogous misoprostol.

The surgical abortion can be performed by vacuum aspiration or by the more invasive dilation and curettage (D&C). It is important to understand what kind of abortion your patient had. Dilation and curettage has a significantly higher risk of infection, hemorrhage, cervical injury (no C-collar needed), and uterine perforation. It is not uncommon that prophylactic antibiotics will be ordered for this patient. 

This is a perfect segue into why we care pre-hospitally. What are we looking for? How can we properly assess our patients, screen for life-threats, treat respectfully?

Let's start with some common concerns…

Infection. If a standard of care is to prescribe prophylactic antibiotics, it's probably a good idea for us to be nervous about sepsis if we get a patient post-abortion. HOPEFULLY, all of these women are instructed to stick to pads to manage the bleeding after their procedures, but be sure to ask them specifically. Using tampons to control bleeding illuminates a huge neon VACANCY sign for bacteria in the female reproductive organs…and check in they will. Next, you should ask about the length and quality of bleeding. Miscarriages and medical abortions  can be incomplete. This could be a source for infection as well.

Keep in mind that most of our experiences with sepsis up to this point have likely been with patients, often geriatric, with comorbidities. It's possible our lower end 100s for these patients is just as alarming as  Grandpa's 130s. Be flexible in your algorithms. Don't delay a sepsis alert if she's 104 degrees can fry a dang egg on her head, is confused, but her heartrate is 102 and her pressure is 110/60. Sorry, lady, you didn't quite make the cut for an alert! Don't do that. Treat your patient. If you need a big room, go get her a big room. 

Hemorrhage.  Bleeding is expected with any type of abortion, of course. Again, ask about the length and quality of bleeding. Disseminated intravascular coagulation (DIC) should be considered in all severe bleeding patients. Look for your signs of shock. 

Mental Health Emergencies. This is a very delicate and personal issue. Abortion and infertility are words so taboo it's as if we worry that saying them too loud will cause a contagion. For many women, this is a very challenging experience. Some could be at an increased risk of domestic violence or ostracization. Be aware of how you communicate with your patients. Try and encourage an environment where they feel they can be honest and detailed with you so you can get a proper assessment. Ensure their privacy and dignity are protected.  

Pain Control. I have been on a truck with medics who have uttered "of course it hurts, what were you expecting to happen when you got an abortion?" and have withheld pain medications. Please, if you take nothing away from this blog, don't be that guy. It's like being the guy who slams the narcan "to ruin their high". It doesn't look good on you. Strangely enough, it's actually not our job to judge our patients, only to treat them and listen to them. Look, I'm not going to sit here and convince you their pain is real just as I shouldn't have to do that for someone whose arm is hanging out of the socket. All I'm saying is if someone is in misery in your bus and you are withholding medication because you disapprove of the mechanism that caused their pain, you should probably just go home.

Embolism. Don't forget there is a small risk of amniotic fluid embolism which can cause severe respiratory distress or cardiovascular collapse. 

Although not often thoroughly covered in traditional education models, comprehensive post-abortion care is imperative to help prevent life-threatening complications and long-lasting psychological trauma. Miscarriages occur in 10-15% of all pregnancies, and 25% of women are expected to have an abortion before turning 45. The odds of treating a patient after the termination of a pregnancy are high; will your standards of quality of care be as high? 





Shallow Hal-dol by Natalie Zink

In a world where Ketamine rules all FOAMed, services without access to this “miraKle drug” often get left out of the conversation on safe chemical restraint. So, Ketamine Warriors, I humbly ask that you imagine for a moment that you don’t have your secret sauce, and you must rely upon……BENZOS AND ANTIPSYCHOTICS.

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I will leave the “favorite benzo flavor” out of today’s discussion and instead shoot for a dissection of a fairly popular prehospital/hospital antipsychotic agent, Haldol. 

Before this past May, I never had access to haloperidol. Knew of it and its general characteristics, of course, and heard a couple “B52!!!”s yelled out in the ER but never had an opportunity to use it. This made for an uncomfortable Natalie when I learned 5mg Versed and 5mg Haldol IM was our chemical restraint concoction of choice, so I dove into the research. 

I must be honest here: I didn’t really like what I found. Long onset, sketchy side effects, significant half-life…..not my ideal characteristics for a sedation agent. Then, add on anecdotally how many patients list Haldol as an allergy because they had such adverse reactions-not thrilling news for someone often administering this drug before we are even able to get a name, much less a full medical history, due to excited delirium, tox, or just downright combativeness. So, allow me to make my case for why we should be taking much more care and consideration before grabbing for the haloperidol as a first line drug…


Indications: Excited delirium, agitation, psychosis, vomiting, chronic hiccups 

Mechanism of Action: Strong antagonist of Dopamine receptors (D2) AKA inhibits dopamine’s effects

Contraindications: Parkinson’s Disease, hypersensitivity. 

Yes, you read that right. Head injury is not a contraindication to Haldol. Go on and take y’all’s mind-blown selves to the research suggesting no harm in intermittent administration to TBI patients, and holler if you need me.

Side Effects: Extrapyramidal symptoms (Parkinson’s-esque), restlessness, worsened agitation, spasms, drooling, dystonia, hypotension, nausea, vomiting, vision changes, irreversible dyskinetic movement syndrome (especially in elderly women)

Really Scary Side Effects: QT Prolongation > Ventricular Arrhythmias >Sudden Cardiac Arrest

Onset: For IM injections, 20 minutes ‘til peak effects in average population, 34 minutes in schizophrenic

Half-life: Almost 21 HOURS 

Mechanism of Metabolism: Lipophilic and hella metabolized by the liver (only ~1% of original drug in the urine)

Drug Interactions: 

  • Lithium: Cause extrapyramidal symptoms, encephalopathy, coma
  • Tricyclic Antidepressants: Decrease metabolism/elimination of TCAs
  • Quinidine, Buspirone, Fluoxetine: Increase Haldol serum levels
  • Carbamazepine, Phenobarbital, Rifampicin: Decrease Haldol serum levels
  • Warfarin: Increase warfarin serum levels
  • Acyclovir: Increase Haldol serum levels
  • Metformin: Decrease efficacy of metformin
  • Insulin: Decrease efficacy of insulin

So, why does haloperidol work?

The best working theory we have for the positive symptoms of schizophrenia is an over-production of dopamine in the mesolimbic system. That’s to say that the hallucinations, delusions, agitation, aggression, disorganization reside……right here 

The part of schizophrenia that we typically want to treat and control in a prehospital emergency setting is acute agitation and aggression; therefore, BOOM we want that pathway to cool its dopamine jets, which Haldol achieves. 

So then, what’s your problem, Nat?

  1. We aren’t always administering this drug to schizophrenic patients. Yes, sometimes, we find the classic clear-cut case or patient we are familiar with who maybe missed their monthly injection. However, most of the time, we are dealing with complex cases in high-stress situations. I so hope we have all joined the school of thought that severe agitation is indeed a medical emergency, and a fragile, dangerous one at that. We must think swiftly about the safest plan for ourselves, our crew, our patients, and any bystanders. I won’t be discussing defusing or other methods of restraint here, just making a point that urgency in stopping the acute problem of agitation is our first priority on these calls. If the patient is hypoxic, we give oxygen. If they’re hypoglycemic, we give sugar. Yet, if they’re combative, they get an antipsychotic? Interesting. 
  1. Haloperidol is not an effective rapid sedative. Like I just said, in order to move forward in the treatment of this patient, we have to bring them from a Level 10 to at least a Level 6. Why wait 20 minutes (or 34!!!!) to get there? Further delaying the ability to fully assess, not to mention treat this patient. Some of y’all’s services don’t have anywhere near those transport times, so, I mean, you’re welcome to the ER staff, but I still have a clinically agitated dude who is further stressed by my bright, moving, terrifying machine with pokey things. That does not make for excellent care. 
  1. It lasts way too long. I mean waytoo long. A half-life of 21 hours is absurd. For comparison, the half-life of midazolam is about 2 hours. If we have an adverse reaction, just hold on to your hats; we have a BIT until this stuff is cleared out. 
  1. Finally, my real beef with the stuff….it’s not ONLY affecting the mesolimbic pathway!

Let’s go to the nigrostriatal tract to see what I mean.

Big stuff is going on here…like 80% of the body’s dopamine, NBD. But it’s ok; it’s not like that dopamine is involved in anything important. OH WAIT. MOTOR PLANNING. Without that, well, you kinda...

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Pseudo-Parkinson’s-type extrapyramidal symptoms can occur from the antagonism of the dopamine receptors like dystonia, akathisia, and tardive dyskinesia. Those symptoms can range in severity from tense muscles and restlessness up to difficulty swallowing and breathing. Me no likey. Think about it, though, Parkinson’s patients take Carbidopa to treat their symptoms and increase their dopamine. We are doing the opposite. It can be a bummer. I do wonder if part of the role of the Benadryl in the common B52 cocktail (Benadryl, 5mg Haldol, 2mg Ativan by the way) is to guard against the extrapyramidal symptoms. My literature review was lacking in rationale for it other than generic sedative effects. Anyone care to weigh in?

Now, over to the tuberoinfundibular tract…

Dopamine in the tuberoinfundibular pathway inhibits prolactin release from the pituitary gland. Therefore, inhibiting dopamine increases prolactin. This causes discharge from the breasts and a decrease in estrogen and testosterone which affects fertility, sex drive, and eventually bone density. Also, fairly uncool symptoms for somebody who ended up being a tox patient had we been able to discern that earlier and withhold a dopamine antagonist.

BONUS: Guess what else is really fun! GABA receptors (multipurpose inhibitors in da’ brain) MODULATE Dopamine receptors! So, activating GABA receptors suppresses dopamine receptors. Guess what enhances GABA receptors?! Benzos! So essentially when we 5x5, we are just straight up Hoovering these folks’ dopamine right on out of their mesolimbic systems. Rock on.


Look, Haldol is a very effective First-Generation Antipsychotic medication for schizophrenia. So far, the literature hasn’t shown increased efficacy of Second Generations (atypical antipsychotics) over First. Haloperidol is the affinity champion on dopamine receptors while Second Generations tend to also antagonize serotonin receptors. The atypicals(i.e. risperidone, olanzapine, clozapine, quetiapine, aripiprazole, ziprasidone), while having a decreased risk of extrapyramidal symptoms, tend to cause more metabolic side effects like weight gain and hyperglycemia. Again, our prehospital purpose is treating time of behavioral crisis, and haloperidol has been proven to be a successful sedative.

On the other hand, I cringe at the thought of Haldol being used as a first line without consideration for its pharmacokinetics. While successful, it is not a simple sedative. It doesn’t really suit the prehospital environment because of its long onset, and it doesn’t suit the average non-dopamine rich patient. If anything, its administration to a non-schizophrenic patient makes me a little worried about airway difficulties from extrapyramidal symptoms, especially when given in conjunction with a respiratory depressant. 

Who knows? Maybe someday I’ll eat these words, but I’m just not too crazy about this stuff being used as a broad sedative (as I’m sure my sass alluded to). I have just one more question…is there still room on the Ketamine train, guys?














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