Approach to PE

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

The Kitchen Sink

Fairly early into an overnight shift the radio goes off.  EMS is approximately 6min out with mid 30s male undergoing CPR. Per bystanders, the patient was going running from door to door, banging on doors and yelling for help. Shortly after being taken into police custody he was found to be pulseless. Had been undergoing CPR approx 10 min. King airway in place. No improvement with dextrose and naloxone.

The intern on and myself go to Room 9 to get set up. When EMS arrives about 10 minutes later, CPR is still ongoing and rhythm has been asytole/PEA throughout. The story remains consistent with him going from door to door yelling for help but now there is some variation as to whether he was cuffed and then lost his pulse, was found without a pulse, or if he got into a physical altercation with the neighbor and then lost pulse shortly after arrest. There are no signs of trauma and we elected to not invite additional chaos by calling a Level 1.

CPR is continued. King airway switched out for ETT. Accucheck 250’s. Central venous access and bilateral chest tubes placed with no rush of air or blood. Sats persist at 85% on vent, etco2 is in 60’s. He gets epi q3m. A dose of vasopressin and steroids. Istat has K 5.5. Lactate >20. Received 2-3 amps of bicarb. Received calcium. Upon rhythm checks he was primarily asystole except for 2-3 checks with a narrow pea that would not persist. Each time the ultrasound was placed on his heart there was no cardiac activity. My thought process at this time was that he was either excited delirium that I’m not going to be able to do much about or some kind of ingestion/overdose. We called pharmacy and asked for lipid emulsion. His ETCO2 had remained between 40-60 and we were about 40 minutes out from reported time of arrest. I decided if the lipids were unsuccessful that would be when we would call it.

They arrived about 15 minutes later and were infused. By now his etco2 had drifted down to 10 on the most recent pulse check. No changes occurred and TOD was called.