Head injury patients with delayed presentation to ED

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Another pearl from EM Lit of Note. Bottom line: Retro review of CT head obtained for trauma divided into <24 hours and >24 hours time of presentation. The delayed presenters had a HIGHER percentage of positive CT and had a similar amount of patients requiring NES intervention.

We discussed this the other day. First Care obtained a head CT on a patient several days after a minor head injury. We presumed it was not indicated. Then I read this paper.

Unfortunately I cannot find in the paper a description of time to presentation. It is grouped into less than 24 hours and greater than. I wonder if the likelihood of positive CT scan decreases as time from injury to presentation increases.

In any event, this poses difficult questions. Should we obtain more CTs on the delayed presenters? They are as likely to have positive findings. In addition, the NICE guideline is 70% sensitive, versus its comforting 98% in the less than 24 hour group.

Would be a good article to discuss for journal club. Would love to see some comments.

Spice/Heroin Reactions

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So I’ve had to encounter my two sickest patients in the holding area within the past 2 weeks or so. One was a reminder from intern year while looking through spice charts, while the other was an actual patient that I had 3 days ago.

We always tend to take the “Tank” patients lightly and overlook them sometimes. I just want to use this as a warning (especially to the interns) that sick patients can also use heroin/ETOH/Spice, so pick up on the small interactions that don’t go right. I’ll try to present these starting with how their chief complaint lead to the final diagnosis.

Patient 1 (intern year)

  • middle aged male
  • CC: Spice OD, Nausea/Vomiting
  • Final Diagnosis: Subarachnoid Hemorrhage
  • Time to Diagnosis: 7 hours

So this guy presented as a spice reaction. This was before spice became as widely spread as it is now, and no one knew what to expect symptomatically (not that there is ANYTHING that is characteristic to spice anyways).

General story from talking with this guy is that he used spice for the first time that night. No significant past medical history. He was on a first date where everything had been going well. He had borrowed some spice from his friend where he used back at his place after dinner. Soon after he started having nausea and projectile vomiting and was acting ‘goofy.’ At that his date called EMS and the date ended.

Exam:

  • Gen: Fully A&O, slightly odd in that he seems incredibly happy to be here
  • CV: RRR
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

This man was like most of our intoxicated patients–a sober re-evaluation. At approximately 2 hours he was still vomiting in the ED, so the medical workup was initiated. Due to his odd behavior with vomiting, we got a CMP/CBC/Tox & CT Head. The night continued busy and I almost forgot about him as I waited for results. Ultimately he never got his CT Head due to being uncooperative but I wasn’t told until hours later. He ended up getting Geodon/Ativan in the ED but instead of calming him down he became more agitated and was no longer oriented. Ultimately getting rolled into room9 to be intubated prior to CT and the final diagnosis was made.

Certain forms of spice that lead to agitation also lead to spikes in blood pressure, and there are a few case reports of significant hypertension occurring after spice use. This guy had the unfortunate case of rupturing an aneurysm after using spice likely from a BP spike. I’m honestly not sure if the outcome would have been any different had I reached the diagnosis sooner — he got repetitive Head CTs and ultimately an EVD on hospital day 3. I didn’t really take him seriously even after I ordered a lab workup. This really changed my perspective on patients being held for intoxication. He spent 1.5 months in the hospital (1 month intubated) before being discharged to rehab.

Patient 2 

  • Middle aged white female
  • CC: Heroin OD got Narcan
  • Final Diagnosis: Cardiogenic Shock
  • Time to Diagnosis: 3.5 hours

This case I handled a bit better (I’d hope after 2 years). Story I could get is that this man had a syncopal episode. Received Narcan PTA by EMS and woke up. In the ED the patient adamantly denies heroin use–states he simply passed out. Luckily I got to him before EMS left, and EMS confirmed reports of bystanders stating opiate use.

Exam:

  • Vitals: HR 120, RR 16, O2 96%, BP 80/45, T 98.0
  • Gen: Fully A&O, drowsy
  • CV: tachycardia
  • Pulm: CTAB
  • ABD: NT/ND
  • Neuro: CN II-XII intact, motor intact, sensation intact, ambulates without difficulty to bathroom

My initial thought was that he may need some more narcan or that he received a longer acting opiate. The tachycardia was a wild card and didn’t make much sense with the picture. He remained afebrile and temp recheck, so I wasn’t thinking sepsis much at that time. At this point due to the tachycardia not making sense I ordered labs (and a tox for co-ingestants) and thought his BP/HR would improve with fluids.

I reassessed him after bolus #1 and #2 and neither HR or BP improved. Labs returned with an elevated WBC at 19.6. Opiates positive on top but otherwise were unremarkable. EKG sinus tachycardia. CXR and urine unremarkable. At this point even though I had no fever or source I felt compelled to initiate a septic workup and Lactate returned at 7.9.

I was starting to get lost as why this guy was so unresponsive to fluids and O’Brien and I threw the USN to bedside at this point. Turns out he was in acute systolic failure with an ejection fraction of 11%. No history of CHF and also no signs of volume overload on exam except very mild pulm edema. Troponin peaked at 0.5.

He was admitted by cardiology while they trended his status. He went to the cath lab on hospital day 3 with clean coronary arteries. Ejection fraction improved to 60% by time of discharge. Talking with the team today they are still uncertain of the cause.

These are two cases of sick patients being in the holding area. Hopefully, it serves to remind everyone that any patient can be sick.

Interesting Ultrasound

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A late 20s F G4P3003 at approximately 6 weeks gestation by LMP presents with a chief complaint of vaginal bleeding. A few hours PTA, patient states she felt a “gush of blood” with some mild abdominal cramping. VSS. On exam, noted to have a moderate amount of vaginal bleeding per the os. On our bedside ultrasound we note what appears to be a viable IUP with cardiac activity.  However, the uterus appears septate, with half containing the IUP and the other half more hyperechoic/solid in nature. We were concerned for a possible subchorionic hemorrhage and consulted OB/GYN. Our bedside US image is below:

BS US

OB came down with their Cadillac ultrasound and confirmed our findings.  For comparison, here is their much clearer image:

OB US

For this patient, with this large of a subchorionic bleed, the likelihood of her carrying this pregnancy to term was low. They planned to have her follow up in clinic for a repeat ultrasound in 2 weeks to reassess viability. Per our OB colleagues, other things on the differential included a fibroid. However, as this patient had 3 very healthy and rambunctious boys at the bedside with her, OB commented that a fibroid that large would likely have resulted in infertility.

And from UptoDate:

“A subchorionic hemorrhage or hematoma is a risk factor for spontaneous abortion, particularly when it amounts to 25 percent or more of the volume of the gestational sac. A meta-analysis of seven comparative studies found that women having a subchorionic hematoma had a significantly increased risk of spontaneous abortion, compared to women without such findings (18 versus 9 percent; OR 2.18, 95% CI 1.29–3.68). The findings also are associated with an increased risk of placental abruption (4 versus 1 percent; OR 5.71, 95% CI 3.91–8.33) and preterm premature rupture of membranes (4 versus 2 percent; OR 1.64, 95% CI 1.22–2.21). The increased risks of preterm labor and stillbirth appeared to be dependent upon the presence of vaginal bleeding.

Pregnancy outcome associated with subchorionic hematoma also relates to location, with worse outcomes observed for retroplacental hematomas, compared to marginal hematomas. The location, rather than the size, of a subchorionic hematoma may be the most important predictor of pregnancy outcome. Evidence relating to the size of the hematoma and the risk of adverse outcomes is inconclusive.

The only management option for subchorionic hematoma is expectant. There is insufficient evidence regarding whether bed rest decreases the risk of pregnancy loss when a subchorionic hematoma is present. Some clinicians repeat an ultrasound in one to two weeks to confirm fetal viability and assess any change in size of the hematoma, primarily to provide reassurance to the patient. A subchorionic hematoma is not an indication to conduct a diagnostic evaluation for an acquired or inherited thrombophilia.”

April Journal Club

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Hey, all,

There is multimedia for this month’s journal club, so I wanted to post it all in one place. The theme will be impossible decisions in the department (eg ED thoracotomy without surgery backup, but we’ve talked about that issue ad nauseum). In my mind, it’s best to think about how you’ll approach impossible decisions now, before they show up overnight on single coverage in the middle of nowhere. Other ideas for discussion are welcome.

Closing the emergency department: EP Monthly, Diversion 1, Diversion 2

Crashing VP shunt patient: Tapping a shunt article, Tapping a shunt video

Epidural hematoma: Burr hole for epidural hematoma article, Burr hole presentation, Video of a burr hole

 

Sepsis-3

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I’m sure you guys have heard about the new sepsis definitions unveiled at the SCCM conference last week which were originally published in JAMA (2016;315(8):801-810); if not you’re in luck because I’ve outlined them for you below.  Keep in mind the sepsis definition has not been updated since most of you were still in high school- or middle school- I’m showing my age, in 2001, with Sepsis-2.

Sepsis-3:

New Terms and Definitions

  • Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection
  • Organ dysfunction: Acute change in total SOFA score ≥2 points consequent to the infection
  • Identification of patients likely to have poor outcomes:
    • ICU Patients: SOFA score ≥2: Overall mortality risk of approximately 10% in a general hospital population with suspected infection
    • ED patients: qSOFA score >2 (SBP < 100 mm Hg, RR > 22, or altered mental status)
      • These patients are likely to have a prolonged ICU stay or to die in the hospital
    • Septic shock: Sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 and a serum lactate level >2 mmol/L despite adequate volume resuscitation
      • Hospital mortality is in excess of 40%
    • The term “severe sepsis” has been abandoned

Zofran

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Well here is the study that has had everyone talking for a while. Good old ondansetron category B now may cause congential malformations in the fetus. This study in the journal Reproductive Toxicology retrosp of 1349 infants concludes a risk for CV defect (septum specifically) is increased to a statistically significant degree. My favorite prior study looked at 608,000 pregnancies and concluded no malformation risk. This is in the NEJM. So I am much more likely to follow the recs of the huge NEJM study.

Now we could do more prospective studies of course to see if ondansetron is causing any true effects. And we can always use the promethazine, prochlorperazine class of drugs in these patients while in the ED or even for discharge. I still love good old extremely evidence-based ginger pills, also B6, diphenhydramine, not eating crap food, etc.

Discussion is welcome.

72 Hour Returns

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Much has been written about ED recidivism. Ryan Radecki at EM Lit of Note has just reviewed another article about returns, this one looking at bounce backs from inpatient services as well. His conclusion is that 72 hours returns should not be used as a quality measure for ED metrics. His complaint is the nonspecific analysis of these returns. When we discuss 72 returns in our didactics, we attempt to focus on the cases from which we can learn how to prevent discharge of inappropriate patients. We are discussing shifting more toward discussing less cases with well defined take home points as we enhance didactics. Take a look at the Radecki commentary and if interested, the growing body of literature. If anyone is especially interested, a solid admin project / scholarly project would be to analyze our 72 returns over a longer period than a month. Drs Coleman and Platt presented a poster at CORD when we presented the Room9ER poster years ago.

Essay Contest

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Hey guys its that time of year again for the Spears Essay Contest. See details below. We have had some finalists in the past. Inside information: not many people submit essays, you have very good odds.

Entries Due March 7!
The 2016 Richard Spear, MD, Memorial Essay Contest
Win $$ and get published in Louisville Medicine!

GLMS physician members, GLMS in-training (residents and fellows) members and all University of Louisville medical students are invited to enter this year’s Richard Spear, MD, Memorial Essay Contest. Cash prizes will be $1,500 for the winner in the practicing and retired physician category and $750 for the winner in the physician-in-training and medical student category.

Essay Contest Themes: All entries must be original, unpublished writing intended solely for publishing in Louisville Medicine. Essays must be pertinent to the following themes*:

1. Practicing and Retired Physician Category
“How Medicine Has Changed Me”
– or –
2. Resident/Fellow/Medical Student Category
“Social Media in Medicine”
 
*If you are a practicing or retired physician member, you must choose Category 1. If you are a resident, fellow, or medical student, you must choose Category 2.


Length: 800 to 2,000 words. 

Format: Do not put your name on any page of your essay. Instead,include a separate cover letter with name, entry category, essay title and contact information. This allows judges to be blinded to author names.

Deadline: Monday, March 7, 2015.


Submission: Send via email as an attachment to Aaron Burch ataaron.burch@glms.org.  Email submissions are highly preferred, but if not possible, send entry by fax to 502-736-6341 or by mail to 

101 W. Chestnut St., Louisville, KY 40202.

The winning essays and Medical Writing for the Public Award will be announced at the annual GLMS Presidents’ Celebration and published in the July issue of Louisville Medicine. 

Finally

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I am quite excited about this study but sad I was not the one to publish it. Out of South Florida, a study of 72 patients who received a NONCONTRAST CT Abdomen for various locations of abdominal pain.

Excluded were: trauma, pregnant, surgery in past 30 days, pain more than 3 days, MD discretion (thought usually to be suspicion for vascular emergency), unable to be reached for 7 day follow up, would not consent, unstable, suspected renal stone (as this is already the standard of care), known cancer, BMI < 18. Sounds like a lot of exclusions but this pared the population down to the general population of patients in whom I would consider the noncontrast CT abd for nonspecific abdominal pain. Notice suspicion for appendicitis was not an exclusion, many studies have shown minimal benefit to oral contrast in appendicitis. They also did not exclude very acute abdominal pain (ie using a minimum number of hours of pain).

The results: 0/72 patients had a missed diagnosis on the initial noncontrast CT. 3/72 had repeat contrasted studies which added little. Of the 31 patients discharged, no one had surgery, death, or repeat CTs done.

This is obviously a small sample at one hospital. Selection bias can be a factor, as MD discretion was an exclusion. I would love to see more studies like this, possibly RCTs. As more and more centers get the higher resolution CTs, we should see less and less contrast given for CT of the abdomen and pelvis.

Humanity

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This is a commentary on this article by a resident reflecting on life, trauma, and death. The  resident’s self-reflection is a nice read and something with which we can all identify. But the “meta-reflection,” if you will, is something we do not usually get to see in our EM journals. We read one or two essays in each Annals, sometimes in Academic EM and in JEM. I tend to read these first or tear them out and hold them until I can read in a quiet room and really concentrate on them. And I do my own reflecting on the themes and ideas presented by that person.

The commentary article describes the difficulty in a self-analyzing essay. The schizophrenia and detachment involved in presenting your own thoughts in this way. Dr Ratzan reviews some of the (sadly few) accomplished physician writers and their themes. William Carlos Williams was a poet/writer and physician. Richard Selzer, a retired Yale surgeon, is still living and I hope still writing. His books are so rich and he is so talented a writer that I can hardly read more than 20 pages at a time. Brilliant physician writers are rare but essential to the humanity of our profession.

And emergency medicine in particular, with its intensity and ?necessary detachment, might need this humanity more than any other specialty. I recommend we all read something either in the medical humanities, or something seemingly unrelated to medicine. You might think the literature or the book of humor or the young adult futuristic death competition book is non-medical. But connecting, or reconnecting, with that part of yourself that is separate from the ED will make you a better doctor and healer.

It can become trite to say feelings are important, we need to have empathy, there is a human side to this job of ours, etc. And it is a difficult jump from reading a feel-good essay to the next day walking into the room of a patient with fibromyalgia and trying to channel that empathy you were just reading about. But trust me, if you make an effort to do this you will appreciate your patients. Good advice I read from a Brazilian shaman: “remember that the world does not revolve around you.” you have to really think about that to understand. Try to picture the world through literally through other people’s eyes, makes yourself and your troubles seem smaller.

The patient you are seeing in the ER is likely having the worst day of his month or year or even life. Try not to forget that. Happy Thanksgiving.

The EKG in Palpitations

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Late 20s female w CC of chest discomfort and palpitations, n/v x 1 days. No recent illness, no fever/chills/diarrhea. Says the episodes come on abruptly and last less than a minute. No h/o early cardiac disease or early death in family. Says she feels short of breath with the episodes and her chest feels tight. Denies tunnel vision. Denies syncope but feels like she could pass out. ROS o/w positive for anxiety (grad student). Denies T/ETOH/D. Social history o/w irrelevant. No allergies. Only medicine is OCP. Exam is unremarkable (heart normal, lungs clear, appears well).

What would you order on this young patient with this complaint? How would you document it?

I have recently seen a few charts in this and similar patient presentations that gave me pause. I’ve seen workups from EKG alone to the full cardiac rule-out and everything in between. The only true unifying theme, and I think rightly, the most important test is the EKG (aside from a pregnancy test).

And most of the charts have a documented EKG. Ok. No problem there. Below is an example of a chart documented on a <30yoF patient with Palpitations…

 

Normal_ECG

“NSR, Rate 85, Normal P waves. No S/T wave changes. Normal QTc. No ischemia. No EKG for comparison. “

 

The problem with this? Aside from a few parts, it is mostly irrelevant to the life or limb threatening abnormalities that we are looking for in the EKG. Sure, it will bill just fine, but I worry that there a few among us who aren’t SPECIFICALLY looking at the EKG in the palpitations patient for common causes of palpitations. I mean, really, how many of us see MIs present as palpitations?

 

So what should you look for in an EKG in a palpitations patient?

  1. Rate (tachy or brady or no?)
  2. Blocks
  3. HOCM
  4. Brugada
  5. AVRD
  6. Prolonged QT (cong. QT) or Short QT (why?—AVRD)
  7. WPW
  8. Ischemia

 

Now lets talk about the EKG abnormalities found in each:

HOCM—About 90% of HOCM pts have an abnormal EKG. Remember, these are often young folks, so their ekg should be pristine. The etiology is a hypertrophic septum, so characteristic LVH is seen (V4R wave is “off the chart”), as well as deep, narrow q waves laterally. Occasionally flipped, broad T-waves are seen. There is also an apical variant that shows GIANT TWI in septal and lateral leads… you’ll know it if you see it, it looks grossly abnormal. But HOCM itself can be much more subtle. Look for Q waves and LVH then listen to their heart and refer to cardiology for an echo. Both of the below are pretty obvious, the second one is the GIANT TWI i was talking about. Not a lot of things do that.

time 4 hours HR 84

HypertrophiccardiomyopathyapicalvariantYamaguchisSyndrome

Brugada— 50% familial, most present >20yo but can be seen at birth. In brugada, you’re looking at leads V1-3, looking for a Right bundle branch block and either “coved” (st elevations with long, flat ST-segment that looks like a ski-slalom) or the “saddle type” (which is way less common and looks a lot like, well, a saddle. But remember there is STE there too which makes a side of the saddle, then the T-wave makes the other side of the saddle. This sometimes looks like a STEMI, except in a patient without chest pain and then you notice the saddle shaped concave ST segment and the CC and family history and you can smile because you didn’t activate the cath lab. Also, these patients can have EKGs that show brugada pattern SOMETIMES and not other times. Look for the ski-slope and the saddle. Hop aboard this saddle and you’re going to need a defibrillator, as anti-arrythmics don’t change mortality much….

14_minutes_QRSd_146ms_p_2_Amps_bicarb_axis_167

255v62n11-13145482fig1

This image says there are 3 types. OK, well, that’s true and all but seriously, it’s still a saddle, so you shouldn’t be led astray.

AVRD- What the what? AVRD stands for arrythmogenic right ventricular dysplasia, and basically their RV gets filled up with fat and cartilage during development. This is not so good. These folks may have exertional chest pain (it’s a cardiomyopathy). And, because it’s a structural heart disease, most of them will have EKG abnormalities (~90%). The most specific finding is an EPSILON wave, which is a little puny looking bump after the QRS that looks like a little P wave but is out of place and behind EVERY QRS. These are hard to catch, so you HAVE TO LOOK FOR IT IN PARTICULAR! Also, remember, not every Osborne wave is AVRD (is the patient hypothermic?) Occasionally this will make the QT interval short, but it isn’t reliable. Other, less specific findings are TWI in V1-3 that looks like a juvenile pattern… but remember juvenile pattern should go away when the patient becomes less juvenile. So if they have TWI in percordial leads an they are >20 and have palpitations or syncope… PANIC. No, but really, they probably have AVRD. And the syncope was probably VTACH. But they’re good now, right? Give them a defibrillator too.

avrd_figureone-2

 

Oh, crap. That’s what happens when you send the patient home without looking for AVRD.

 

ARVC

Congenital Prolonged QT-– Ok, so a bit of an update to our usual shortcut “half the R-R rule,” in Academic Emergency Medicine in October 2015, some folks published a retrospective review of some cases of EKGs with prolonged QT and non prolonged QT, and found that our quick half the RR interval thing is about 88% sensitive (r/o prolongation) but only 53% specific. Which ain’t terrible, but its also not super good (12% aren’t ruled out). Of course, what the study failed to highlight but is written and useful is that the ½ RR rule is 100% sensitive (in this study) if the HR was >60. So my take is, if they are brady, calculate it yourself, and if not, 1/2RR is good to go. Which is what I think most of us do anyway. Three cheers for studies confirming our guesses!

Screen Shot 2015-11-08 at 5.44.26 PM
WPW—Not much to say here. You know this. And you damn well should be documenting it. That PR interval is short because your patient is dying for you to find his delta wave.

Wpw

ACS– Well, this is what we do.

Blocks- P before every QRS, QRS after every P. Intervals.

 

So… how should you be documenting these EKGs? With the same attention to the life and limb threatening abnormalities you are looking for on your history (early family death) and exam (murmur?). I can’t say what is right or not, but below is how I would document that EKG on our patient from earlier (NSR, rate 85, No STE/D, No TWI, no definite EKG evidence of WPW/AVRD/CongQT/blocks/HOCM).

Cheers.

 

Images:

https://meds.queensu.ca/central/assets/modules/ECG/Normal_ECG.bmp

http://hqmeded-ecg.blogspot.com/2014/06/history-of-hypertrophic-cardiomyopathy.html

http://www.doctorshangout.com/photo/hypertrophic-cardiomyopathy-apical-variant-yamaguchi-s-syndrome

http://hqmeded-ecg.blogspot.com/2013/05/brugada-pattern-induced-by-tricyclic.html

http://www.revespcardiol.org/imatges/255/255v62n11/grande/255v62n11-13145482fig1.jpg

http://www.geneticheartdisease.org/jpegs/avrd_figureone.jpg

http://www.heartpearls.com/wp-content/uploads/2009/07/ARVC.jpg

http://www.crkirk.com/thumbnail/arrhythmias/images/svt/ECG_WPW.htm

Another abdominal pain

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I had a patient in her 30s that presented with 1 day hx of N/V and diffuse abdominal pain that was most severe in her epigastric and LUQ and radiated to her back.  She had PO intolerance since the pain started the night before. Past medical hx was significant for R nephrectomy that she states is because her “kidney wasn’t working right”. Pt says that this pain feels just like the pain she had from that kidney.

PE: VSS, afebrile. She is curled in the fetal position and yells anywhere you touch on her abdomen but states that the worst pain is when I press her epigastrum and LUQ. She has a large RUQ scar from her nephrectomy. No CVA ttp, negative murphy sign.

At this time my differential included pancreatitis vs PUD vs gastritis vs pyelonephritis
Labs come back with lipase wnl, no WBC, UA with a lot of epithelial cells and a few WBC. Acute abdominal series xray is wnl

I reassess patient after dilaudid and zofran and she states nausea has resolved but still has severe epigastric/LUQ pain. On reexamination the rest of the abdomen is nontender. The amount of pain she is experiencing in her epigastrum/LUQ concerns me and its not pancreatitis based on the lipase so I order a CT abd/pelvis and I put in the ordering comments “diffuse abdominal pain most severe in epigastric and LUQ”.

The radiologist walks over to the department to tell me that the patient has appendicitis and her appendix which is thickened and with fat stranding is in the mid right abdomen instead of RLQ hence the atypical location of her pain. My assumption is that the reason her appendix is so high is from scar tissue secondary to her transabdominal nephrectomy.

I post this to remind everyone that while the RLQ is the most specific place to have pain from appendicitis, the pain can be anywhere (previous abdominal surgery (in this case), retrocecal/pregnancy, etc).

Approach to PE

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Hey all,
I got the privilege of going to ACEP last week in Boston. When I got the schedule one of the lectures that stood out to be was a PE lecture by Jeffrey Kline. Some of you may recognize the name but if not, he is an attending at IU with a special interest in thromboembolism. He is very active on twitter at @klinelab and wrote the Thromboembolism chapter in Tintinalli’s. After talking about PE last month and specifically approach to PE in the pregnant patient, I thought a summary of the key points would make for a worthwhile post.

The first question in the discussion of VTE should be ‘who actually needs to be tested?’ If someone comes in complaining of recent chest pain or dyspnea, PE needs to be included in the differential. If they are not complaining of those recently and have normal vitals (at all times) then you don’t need to go chasing down a clot that isn’t there. If the patient does complain of those then some sort of documentation is required to show you considered a PE. Even stating ‘I think PE is unlikely because of X, Y and Z’ would likely be enough. Now if your pretest probability is anything other than very low, some combination of wells, perc, Geneva should be applied. I like the following algorithm which I think Kline discussed on EMRap towards the end of last year.
algo

Following that algorithm helps cut down on the number of ct scans you’ll order, cuts down your false-positives, radiation exposure, and contrast induced nephropathy without increasing the number of significant PE’s that you miss.

As far as the pregnant patient, I think everyone knows to start with the lower extremity ultrasounds in hopes of an answer that would let you initiate treatment. However, when that is inevitably negative, there is also an algorithm for that scenario that incorporates a trimester adjusted d dimer.

algopreg

The other main takeaway from this talk was the disposition change on some of the low risk patients. Dr. Kline said he has sent about 70 patients home from the ED after being diagnosed with PE. To stratify who falls into low risk, you can apply the sPESI or HESTIA score as well as who is at low risk of bleeding.

–Simplified PESI-if any +, pt is NOT low risk:
age greater than 80
history of cancer
history of chronic cardiopulmonary disease
pulse greater than 100
BP less than 100
O2 sat less than 90

–Hestia-pt CAN BE considered low risk if
BP greater than 100
No thrombolysis needed
No active bleeding
02 sats greater than 90
Not already anticoagulated
No other medical or social reason for admission
Cr clearance greater than 30
not pregnant, no severe liver disease

For these people they’ll initiate rivaroxaban or apixaban in the ED and send them home with a prescription. The only failures they’ve experienced are people who returned requiring additional pain management. Has anyone done this or considered it? The majority of our patient population would not satisfy these requirements or, frankly, be reliable enough to consider outpatient management, but what about people working in the community with a different population?

Lastly, we all know to look for S1Q3T3 on the ekg to raise suspicion for PE but the odds ratio is only 2.06. Inverted T’s in V2 and V3 have odds ratios of 6.94 and 7.07 respectively, and are the most SPECIFIC ekg finding in pulmonary embolism