Tag Archives: Cardinal Presentations

Finally

Posted on by
Reply

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

Posted on by
Reply

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

Posted on by
Reply

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

Posted on by
1

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

Just get a walking O2 sat

Posted on by
1

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.

Golden Hour

Posted on by
Reply

Below is the LITFL summary of another look at the importance of early ABx administration in septic patients. Septic and especially severely septic patients should be taken to room 9, obtain blood cultures promptly, and initiate antibiotics as early as possible.

 

Ferrer R et al. Empiric antibiotic treatment reduces mortality in severe sepsis and septic shock from the first hour: results from a guideline-based performance improvement program. Crit Care Med 2014; 42: 1749-55. PMID: 24717459

  • This retrospective analysis of prospective surviving sepsis data of patients admitted to the ICU with severe sepsis found that delays in antibiotic administration resulted in a concomitant increase in hospital mortality. Though the results are compelling with a linear relationship between time to administration and hospital mortality discovered it is key to interpret this study with caution as the data are uncontrolled for the antibiotic administration to time metric primarily studied by this paper. Multiple potential confounders exist that might account for the observed relationship that should be studied prospectively. In the meantime it makes reasonable sense to administer antibiotics as soon as possible after the actual discovery of real sepsis.  
  • Recommended by: William Paolo