Tag Archives: MedicoLegal

Wound prophylaxis – Should lip lacs get antibiotics (and few others)?

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During my review for 72 hour returns we had a through and through lip laceration come in that returned with a wound infection a few days later.  This prompted me to look up current recommendations as I’m pretty sure that I haven’t been giving antibiotic prophylaxis for this.

Searching literature, Tintinalli and UpToDate…… Most superficial wounds do not require prophylaxis, however, through and through lip lacerations were an area of uncertainty and debate….

Tintinalli  – “matter of provider preference.”

UptoDate – no clear clinical evidence to say that these wounds should receive antibiotic prophylaxis , however, due to the pathogens of the oral cavity, they recommend prophylaxis.

Current literature – Review article in 2008, Annals of Emergency Medicine, Mark DG et al – review of studies do not show a statistically significant benefit; however, the only double-blinded randomized control trial showed a trend toward benefit in patient’s that were compliant with therapy.

Some other stats – Rate of infection in wound treated in the ED (Tintinalli)

Head and neck 1-2%

Upper extremity 4%

Lower extremity 7%

Oral wounds – 9-27%

If giving prophylaxis then Pen VK or Clindamycin is recommended for 3-5 days.

For other oral wounds, <1cm, no need to close. Close if large gap susceptible to food getting trapped, and counsel on good oral hygiene.  Dental and OMFS usually recommend d/c with chlorhexidine gluconate oral rinse (0.12%) (Peridex) and will have patients swish and spit after meals to keep the wound from contamination with food particles.

My take away from this is strongly consider antibiotic prophylaxis with through and through oral wounds as they are higher risk for infection with oral flora; however, not an absolute must based on the current evidence.  Be sure to emphasize good oral hygiene, and as always, close follow up with good return precautions.

Other wounds to strongly consider prophylaxis due to increased risk for infection are mammalian and human bite wounds, crush injury, puncture wounds, and wounds with either fresh or salt water contamination, or patients who are immunocompromised, asplenic, advanced liver disease, associated edema (according to the IDSA).

Open fractures and wounds with joint capsule violation should receive antibiotic prophylaxis.

Reminder: Update Tetanus and simple lacerations do not need antibiotic prophylaxis.

Primum Non Nocere

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First, do no harm.  Sounds easy enough, but have you ever ordered a “screening CT?”  Have you ever been “better safe than sorry?”  We’re all aware of the nebulous risk of radiation from the imaging we order, we know that getting stuck for blood hurts, and sometimes medications have side effects, but what happens when the results of tests themselves are the things harming patients?

This article does a great job exploring this question.  I’ve also found patients much more receptive to my explanations as to why I’m not ordering the thing they think they need since reading this and spending some time thinking about it.  There are definitely times when my honest indication for ordering that Head CT is “patient wants it…” but in general this article has pushed me a little closer to the minimalists’ corner.

Overkill – Atul Gawande

Poor Lonely Repeat Troponin – posted by Bertolotti and Huecker

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We have noticed more and more this culture in our ED of obtaining an initial ECG, an initial troponin, and then waiting 2 or 3 or 6 hours to obtain a second troponin only and then discharge if negative.

I dove into the literature and wrote this post to address the SECOND ECG AT TIME OF SECOND TROPONIN as part of a rule out strategy for low risk ED patients.

I will not even address the fact that people are not obtaining a 2nd ECG at time 20-30 minutes from the first. This is on UpToDate, in ACC guidelines, in ACEP guidelines. It is simply standard of care to obtain an early, repeat ECG on anyone you remotely suspect of having ACS. I harp on this in lectures and have posted on it before. I also will not be talking about hs-Troponin (high sensitivity troponin). Many articles and FOAMed commentaries have covered hs-Trop, and we do not have this test at UL. So please do not think you can rule out all comers with 1 troponin, because you need the hs-trop to even consider this.

This post relates to the issue of a repeat ECG at time 2hr or 3hr (I am not a 6 hour guy, I like the 2 or 3 hr depending on symptom time frame). Don and I discussed the 2nd ECG phenomenon and he said it is just our culture at UofL, hence inspring our Room9ER post. Well we need to change the culture.

Now I didn’t want Geralds to cherry-pick an article to try to rebut me on this, so I went down a rabbit hole of ACS rule out, nSTEMI, HEARTS, TIMI and cardiac markers.

If your attention span is reaching its limit here is the bottom line:

All rapid rule out tools and their validation studies involve at least a SECOND ECG with the repeat troponin. HEARTS, ACC/AHS guidelines, TIMI-based rule outs, etc.

I was early to drop the CK and CK-MB on initial and repeat marker testing in favor of solely the troponin, but dropping the ECG is irresponsible. And is not evidence-based.

Below are many quotes and a figure, then a letter to the editor, from various sources. It was actually somewhat difficult to find in the methods exactly when or even if a repeat ECG was done. Much of the time, the ECG done at time of 2nd trop was not even the 2nd ECG, as mentioned above. “Serial ECGs” is the rule. It seemed as though the repeat ECG(s) were implied in the study, and that the research question was simply timing a troponin.

 Dr Huecker composed most of this post because Dr Bertolotti is so excited about and diligently preparing for Research Day. 

Enjoy, and please post comments! 

  

— Patients with probable or possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals (see Section 2.2.8). (Level of Evidence: B)

— The c-statistic of troponin only was 0.70. With addition of the ECG the c-statistic improved significantly to a value 0.78, with a likelihood ration test p-value of <0.001

— Anderson et al. JACC Vol. 50, No. 7, 2007 ACC/AHA UA/NSTEMI Guideline Revision August 14, 2007:e1–157                                                                                                    If the initial ECG is not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs, initially at 15- to 30-min intervals, should be performed to detect the potential for development of ST-segment elevation or depression. (Level of Evidence: B)

— ACEP (What will be used for or against you in court, as the case may be)

Acute Coronary Syndromes (Non–ST-Segment Elevation – Adult)

Critical Issues in the Evaluation and Management of Adult Patients with Non–ST-Segment Elevation Acute Coronary Syndromes (September 2006)

Complete Clinical Policy on Non–ST-Segment Elevation Acute Coronary Syndromes (PDF)

Scope of Application. This guideline is intended for physicians working in hospital-based emergency departments (EDs) or chest pain evaluation units.

Inclusion Criteria. This guideline is intended for adult patients presenting to the ED with suspected non–ST-segment elevation acute coronary syndromes.

Exclusion Criteria. This guideline is not intended for pediatric patients, patients in cardiogenic shock, or patients with injury on the initial 12-lead electrocardiogram (ECG).

Critical Questions

  1.  Are serial ECGs useful during the ED evaluation of patients with suspected acute coronary syndromes?
  • Level A recommendations. None specified.
  • Level B recommendations.Perform repeat ECG or automated serial ECGs during the ED evaluation of patients in whom the initial ECG is nondiagnostic for injury and who have symptoms consistent with ongoing or recurrent ischemia. No recommendations can be made in regards to the exact timing of repeat ECGs. Studies suggest that 30 to 60 minutes after baseline may be a reasonable time interval for repeat ECG. 
  • Level C recommendations. None specified.

— Letter: Re: “Troponin-negative chest pain”—a diagnostic evasion?

This brief article is well written and I agree the diagnostic label of ‘troponin negative chest pain’ is unhelpful. However the article repeats some common misconceptions which require correction.

Firstly, the article implies that the majority of patients attending hospital with chest pain have an acute coronary syndrome. This is absolutely not the case – in fact most patients with suspected acute coronary syndrome do not have it. (1) Often patients receive a label of acute coronary syndrome and this is later corrected by the cardiology registrar or consultant on call – although by then it may be too late to change the patient’s perception that they have ‘had a heart attack’.

Secondly, there appears to be a misunderstanding of the value of troponin testing. Troponin assays are positive when there has been myocardial necrosis. They do not give any information about the mechanism of myocardial necrosis – a positive troponin can indicate acute coronary syndrome, but may also occur in heart failure, prolonged arrhythmia, sepsis, pulmonary embolism and many other situations. (2)

Similarly, a negative troponin does not absolutely exclude a cardiac cause for symptoms – nor does it mean the patient is necessarily in a low risk group. (3) Patients with unstable angina, dynamic ECG changes, but negative troponin should be considered as having a similar risk of mortality and morbidity to those with a normal ECG but a positive troponin.

Troponin assays should generally be considered a prognostic, not a diagnostic test, and should be used in conjunction with the patients history and ECG – never alone.

 

Stop Traffic

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Hey guys some of you were lucky enough to hear my friend Olivia Mittel and her guests educate our group in didactics. She presented information on human trafficking. This is a real issue and many of us have likely discharged a trafficking victim back into a terrible situation. Please read this Annals of EM article for more information very relevant to EM doctors.

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.

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

 

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.

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

NEXUS in the Elderly

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Hopefully everyone is using the NEXUS criteria or the Canadian C Spine rule in evaluation of patients who have undergone neck trauma. Those familiar with both know one major difference, age criteria. NEXUS does not use age, Canadian C spine does. Using both rules together, like PERC with Well’s, increases sensitivity at expense of specificity.

Well here is a study on falls in the elderly (i.e. low mechanism which is another difference between NEXUS and Canadian) and application of NEXUS. Turns out, probably shouldn’t be using NEXUS in patients over 65. Liberally scan these folks, radiation is less of a concern, and the cost is justified due to morbidity of missed injuries. And of course do not bother with plain films (in adults).

Chest Pain Admission Dilemma

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Hey guys here is an interesting article with actual patient oriented outcomes related to admission for chest pain.

Several take home points:

1. From highest quintile of admission rate to lowest (81% to 38%) the rate of MI and death went up by 3.6 per 1000 and 2.8 per thousand. This correlation implies that when you admit more patients you save lives.

2. It is VERY IMPORTANT to note the patient population. These are Medicare patients with average age of 71 years. So we ARE NOT talking about low risk chest pain ED patients.

3. Even though it looks impressive to save these lives, the NNT or number needed to admit to prevent one MI is 250 and to prevent one death is 333. Thats a lot of admissions. And admitting geriatric patients is often not a good thing for them. May be why the decrease in deaths is less than the decrease in MIs. They were dying because of a hospital acquired infection or deconditioning or something else.

4. It is striking to see how different the practice patterns are at different hospitals regarding admission of a fairly homogenous cohort of patients.

Appreciate any further comments.

Just get a walking O2 sat

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In patients with some suspicion for PE, even with a negative d dimer, I have often ordered a walking O2 sat and HR. This was not really evidence based, but maybe now could be. Below is the abstract for a prospective cohort study of patients known to be with and without PE. Interesting data even if only 114 patients. Cannot get full text yet.

Take home point. Combined sensitivity of HR increase of 10 BPM AND Sat decreased of >/= 2% was 100%.

ie if HR does not go up by 10 or more AND sat does not drop by 2 or more they are very unlikely, based on this small study, to have a PE.

 

 

CJEM. 2015 May;17(3):270-8. doi: 10.1017/cem.2014.45.

Ambulatory vital signs in the workup of pulmonary embolism using a standardized 3-minute walk test.

Amin Q1, Perry JJ1, Stiell IG1, Mohapatra S1, Alsadoon A1, Rodger M2.

Author information

Abstract

OBJECTIVE:

Diagnosing pulmonary embolism can be difficult given its highly variable clinical presentation. Our objective was to determine whether a decrease in oxygen saturation or an increase in heart rate while ambulating could be used as an objective tool in the diagnosis of pulmonaryembolism.

METHODS:

This was a two-site tertiary-care-centre prospective cohort study that enrolled adult emergency department or thrombosis clinic patients with suspected or newly confirmed pulmonary embolism. Patients were asked to participate in a standardized 3-minute walk test, which assessedambulatory heart rate and ambulatory oxygen saturation. The primary outcome was pulmonary embolism.

RESULTS:

We enrolled 114 patients, including 30 with pulmonary embolism (26.3%). A ≥2% absolute decrease in ambulatory oxygen saturation and an ambulatory change in heart rate >10 beats per minute (BPM) were significantly associated with pulmonary embolism. An ambulatory heart rate change of >10 BPM had a sensitivity of 96.6% (95% confidence interval [CI] 83.3 to 99.4) and a specificity of 31.0% (95% CI 22.1 to 45.0) forpulmonary embolism. A ≥2% absolute decrease ambulatory oxygen saturation had a sensitivity of 80.2% (95% CI 62.7 to 90.5) and a specificity of 39.3% (95% CI 29.5 to 50.0) for pulmonary embolism. The combination of both variables yielded a sensitivity of 100.0% (95% CI 87.0 to 100.0) and a specificity of 11.0% (95% CI 6.6 to 21.0).

CONCLUSION:

In summary, our study found that an ambulatory heart rate change of >10 BPM or a ≥2% absolute decrease in ambulatory oxygen saturation from baseline during a standardized 3-minute walk test are highly correlated with pulmonary embolism. Although the findings appear promising, neither of these variables can currently be recommended as a screening tool for pulmonary embolism until larger prospective studies examine their performance either alone or with pre-existing rules.

A large red herring

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The patient is a 20s y/o AAF, multip, last normal period 3 weeks ago (definite date), who presented to another facility with spotting and occasional moderate bleeding for about a week with 4 days of crampy pelvic pain, worse on the left than the right.  There, she was diagnosed with trichomonas and treated empirically for gonorrhea and chlamydia.  She had a positive pregnancy test and reportedly had transabdominal and transvaginal ultrasounds.  She stated they told her she definitely had a pregnancy in her left tube.  She was given instructions to see her regular doctor in 48 hours for a repeat evaluation and discharged.

It is at this point that the big red flashing lights in my head go off and I think to myself “Wait, WHAT?  Someone DISCHARGED a confirmed ectopic?  No way.  Maybe they said it was a possibility and she misinterpreted.”  Whatever the sequence of events, all that mattered was that I get the records and do an ultrasound myself.

Her records came in from the other ED after a couple of attempts (as per usual).  A few things that I learned from her records:
1. she was indeed told that she had an ectopic and that she should see her regular doctor or OB in 48 hours.
2. she did get treated for STDs.
3. sure, she had an ultrasound, but there wasn’t any interpretation available unless I called and had them hold the phone up to the speaker (didn’t have time to do this).
4. my dislike for paper charts is warranted when I can’t read what someone says about my patient.

Initial vitals normal with a HR 100, BP 118/78
She was tender in the LLQ and suprapubic areas without peritoneal signs.  Cervix was closed, she had a small to moderate amount of dark blood in the vaginal vault, and had uterine and left adnexal tenderness on bimanual exam.

I started fluids, gave her some meds for her nausea, and put in all the usual orders.

Labs:
-WBC 13.8 (88% Neut)
-Hb 9.6
-CMP unremarkable
-U/A positive for blood/protein/ketones but micro negative
-Quant 12000+
-Swabs + for trich

And then came the ultrasound:

transverse view, abdominal probe

transverse view, abdominal probe

longitudinal view, abdominal probe

longitudinal view, abdominal probe

A few things about this caused even more red light flashing: first, how could a gestational sac be THAT SIZE in someone whose last period was 3 weeks ago?  Second, what was that OTHER thing behind the uterus on the left?  Third, if the sac was really that big, why was there no pole?

The transvaginal exam was more or less to confirm my suspicions that this was not normal.  I knew that my plan was now to call the specialists with the fancy machine and adnexal expertise.  I couldn’t actually get a GOOD view in two planes (sorry, Dr. O’Brien!) due to patient discomfort, but this one was good enough.

longitudinal view, transvaginal probe

longitudinal view, transvaginal probe

I hadn’t seen any free fluid in her pelvis on either exam.  However, when OB came down, they found some.  They confirmed my suspicions and admitted the patient to go to the OR.

In my brief lit search just prior to posting, I found that this pseudosac finding is not extremely common (the average reported frequency is about 10% of cases).  I feel like this patient’s story would have raised enough red flags to make me uncomfortable sending her home without OB involvement even without the ultrasound, but the date/quant discrepancy coupled with a sac that was definitely not consistent (even though it WAS in the uterus) clinched the diagnosis for me.

Everything including the lipid sink

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80+ yo gentleman with PMH of COPD, CHF, CAD, CKD, initially hospitalized for urosepsis and NSTEMI with a worsening AKI, and baseline CKD. Tuned him up and sent him to the floor where he accidentally received an overdose of his carvedilol. Got the call that the patient was hypotensive to 70s systolic, bradycardic to 30s.

Immediately pacer pads were placed to ward off evil spirits
-Started with 1L crystalloid bolus –> no response and with risk factors and pmhx, didn’t want to fluid overload
-Tried atropine (3-4 doses) –> no response
-Tried glucagon 50mcg/kg loading dose followed by 3mg/hr infusion –> still no luck and exhausted all the glucagon in the pharmacy
Running out of options here. I remember reading an article in Annals about using lipid infusions in beta blocker overdoses and figured it was worth a shot.

Started 20% Intralipid bolus through central line at 1.5ml/kg followed by 0.25ml/kg/min for 30min. Maybe it was the lipid infusion or just the combined effects of everything but by 6am, pt’s BP and HR had improved to normal limits and he began talking again.
It was a nice result but one I couldn’t celebrate that much – within a week, patient decided to go to palliative care and that was the last I heard of him.