Monday, December 29, 2014

Femoral pulse during CPR - Arterial or Venous?

There are many uncertainties about how each of us will die.

Based on my experience in the ED, however, many of us will spend our last minutes on Earth with a stranger's hand shoved into our groin.

Your own hand? Fine.
I'm talking about the checking the femoral pulse during CPR, of course. It's a well-enshrined part of our resuscitation practices, but what it is it actually telling us?

The Theory
The idea, of course, is that effective CPR will produce an arterial pulse, albeit weak, that will generate a cardiac output about 20% of normal. Palpating a femoral pulse during compressions supposedly verifies that the CPR is being effectively delivered.

Evidence that the femoral pulse is venousHowever, there is some uncertainty about what a palpable femoral pulse actually represents. Hilty used ultrasound in a study of central line placement during cardiac arrest, and noted that 9/20 patients appeared to have femoral venous pulsations, rather than arterial.
Note that this was in the dark ages of ED ultrasound (1997), back before Christian Doppler was born. 

Based on this finding, as well as on a case report of two kids getting open-chest cardiac compressions, many people now believe that the femoral pulse during CPR is just the venous back-flow. A video posted by an emergency physician in Qatar supports this view, where he demonstrates interrogation of the femoral vessels with power doppler during CPR:

The femoral vein shows much brighter signal than the artery, suggesting that the venous flow far exceed the arterial. Of course, since this is power doppler, we don't know the direction of the flow.

Evidence that the femoral pulse is arterial?
Cardiac arrest, asystole when EMS arrived in the ED, the LUCAS dutifully chugging along.  

Probe placed in the right groin, angled cephalad slightly. First, with color doppler:


The femoral artery seems to show a fairly well-defined arterial pulse, while the femoral vein has a turbulent, almost "yin-yang-like" character, that does not suggest effective flow. So based on this clip, it seems like the femoral pulse indeed reflects arterial impulses, not venous.

(BTW, here's a clip of the same view, while the LUCAS was taking a break. Just so you know that there was no spontaneous cardiac activity mucking up the doppler.)


So, what does the femoral pulse tell us about CPR quality?
Not much, probably.
The scanty and conflicting "evidence" (i.e. collection of anecdotes) reviewed here doesn't make it clear if pulsations in the groin are coming from the artery, the vein, or perhaps even both. This looks like a promising avenue for an emergency ultrasound study!

In the meantime, assessing the quality of CPR is likely best done with end-tidal CO2, although a recent Ultrasound Podcast episode suggested using focused echo  to optimize compressions. 

Monday, December 15, 2014

Septic hip in Kids, part 2: This time it's personal...

I wrote about the "textbook" approach to differentiating the septic hip from plain ol' synovitis in a previous post Septic hip in kids: 5 myths of ED evaluation. Today, I want to review a real case of mine, and highlight both the weakness of the older methods, and the advantages of the newer perspective.

The Case

A 4 year-old male complained of pain in his hip, bad enough that he couldn't put his weight on it. It had started 1 day ago, but had worsened despite acetaminophen. There was no significant recent trauma. He has seemed ill yesterday, though, and while the parents had not taken a temperature, he had "felt hot," and had some mild chills. His temperature in the ED was 100.2.

His right hip was held in slight flexion and external rotation, and he could not bear weight. Labs were obtained, and showed a WBC of 12.2, and (after hours of waiting) and ESR of 28. The CRP doesn't get run at night.

Were the Kocher criteria helpful? (Spoiler: No!)

Kocher-type criteria are applied to help decide on the need to perform an ultrasound, and then decide on the need for aspirating a hip effusion if it is found on US. How did our patient do?
  • Non-weight-bearing - 1 point
  • Temp < 38.5 - 0 points
  • WBC > 12 - 1 point
  • ESR < 40 - 0 point
  • CRP - not available
So, 2 points, which means that he has a probability of having septic arthritis of...
Sultan 2010
... somewhere around 11 - 60%. But notice that if the WBC had been just trivially lower, say 11.8 instead of 12.2, we would have only had 1 point, and the risk would have dropped to 3- 36%.

Heck, say we also had given him a strong analgesic, and he was then able to walk a little. He would have then had 0 predictors, and so only had a risk of somewhere between < 0.2% and ... 17%???

Clearly, these criteria are not helpful at "ruling-out" the possibility of septic arthritis, so I decided to decide by looking at the hip.

Was Ultrasound helpful? (Spoiler: Yes!)

Quick guide to placing the probe :
From Tsung and Blaivas

First I checked the "good" hip, the left side:


I then checked the "bad" hip, the right:


Looked like there was a difference!

Generally, any effusion greater than 5 mm, or 2 mm greater than the contralateral side, is considered positive. This looks pretty unambiguous, and the radiologogist agreed, and told me that a formal ultrasound was not needed in this case.

Clinical course:

The hip was aspirated by IR in the ED (Those guys are total champs at this, but I'm doing this next time! Very straight-forward.), and the patient admitted. The cell count cam back quite high, around 100,000 white cells/ml, which would have placed this patient as a "true positive" case of septic arthritis in almost any study.

However, by the time this result came back, the patient was tearing around the pediatric floor, completely asymptomatic. The culture never grew out an organism, and he was discharged as a transient synovitis.

Bottom Line:

This was the first time I had a patient where I was truly concerned about septic arthritis of a pediatric hip. The use of US clarified the diagnosis early in the visit, and pointed to a greater role in future case. As I highlighted in my prior post, use of point-of-care US in the ED has the potential to "flip" the older diagnostic and therapeutic pathway - use it!

Saturday, December 13, 2014

Pulmonary Embolus: See the echo, and believe the ECG!

Too many people are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. In particular, two beliefs stick in my craw:

“The most common sign of PE on the ECG is tachycardia”
This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%). Likewise, the average heart rate in Kosuge’s 2007 study was only 94!

“PE = S1Q3T3
S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge has found that only 20-22% of PE patients had an S1Q3T3, while the TWI in leads III and V1 was far more sensitive.

The Case
An 80-something year old male was brought to the ED by EMS, feeling weak. 

He said that this had been going on for about a week, and was getting worse. Only when directly queried did he admit to orthostasis, and in fact had syncoped while shopping the day prior. He denied any chest pain, but endorsed some mild dyspnea.

He had a history of CAD, PCI, and a remote history of a PE. His memory and the records were vague on this last point, and he was not on anticoagulation.

His vitals and exam were unremarkable. Since this could have been ACS, or even mild CHF, a troponin and BNP were ordered.

The ECGs
An ECG was immediately obtained:
The baseline wanders, but there is a clear S1Q3T3. Furthermore, there is T wave
inversion (TWI) in the anterior leads, from V1 to V5,. These findings suggest RV strain

Kosuge showed in 2007 that, in patients with anterior TWI and symptoms suggestive of either ACS or PE, TWI in both leads III and V1 strongly favored PE over ACS.1 

A recent update from Kosuge confirms and extends those results, demonstrating that TWI in both leads III and V1 and/or peak TWI in leads V1 or V2 was extremely sensitive and specific for PE (versus ACS due to LAD occlusion).2

So, the ECG proves it, right? Unfortunately, when the emergencu physician reviewed the ECG from 5 months prior...

An arguable S1Q3T3, and TWI in III and V1-V4.
… and from 7 years prior...

'Bout the same.
... it seemed like the ECG findings were, perhaps, simply chronic. Well, when in doubt, break out the ultrasound!

The Echos
Parasternal long-axis

There is a dilated and hypokinetic RV, while the anterior wall contracts nicely.

Parasternal short axis

Septal bowing, or D-shaped septum (“Movahed’s sign?”)

Apical 4-chamber

Markedly dilated, hypokinetic RV free wall, with preserved apical contractility
(a.k.a. McConnell’s sign)

Triscuspid valve – color Doppler

Moderate regurgitation,  max velocity 5 m/s by CW Doppler, indicating very high pulmonary artery pressure

Clinical course
Given the patient’s CKD, and the stable hemodynamic status, unfractionated heparin was started, and the patient was admitted. A V/Q scan the following day confirmed an acute PE, apparently with significant chronic emboli as well! Anticoagulation was bridged to oral therapy, and the patient was discharged back home.

Bottom line:
The ECG can be very helpful is suggesting PE. Many physicians are nihilistic about studying the ECG for signs of PE, and believe that the ECG is too non-specific to play a role. 

In particular, two elements of the conventional wisdom are often uttered without considering the evidence:

“The most common sign of PE on the ECG is tachycardia”
This is not necessarily true. For example, Ferrari found that TWI in V1-V4 was far more common in PE (68% of patients) than was sinus tachycardia (only 36%).3 Likewise, the average heart rate in Kosuge’s study was only 94!

“No S1Q3T3 = no signs of PE”
S1Q3T3 can be very specific for PE, and is helpful to note. But it isn’t the only thing to look for on the ECG, and the poor sensitivity of this sign could mean missing a PE. Kosuge found that only 20-22% of PE patients had a PE,1,2 while the TWI in leads III and V1 was far more sensitive.

Perhaps the ECG isn’t completely sensitive for picking up every tiny sub-segmental embol-ette.  Remember, though, that the ECG isn’t that sensitive for picking up every little troponin leak either! But the ECG is darn good for picking up the STEMI patient that needs emergent therapy, and the analogy with PE is likely true as well – the ECG will suggest the diagnosis in patients who are at high risk from large PEs.

1.         Kosuge M, Kimura K, Ishikawa T, et al. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves. Am J Cardiol. 2007;99(6):817-821. doi:10.1016/j.amjcard.2006.10.043.
2.         Kosuge M, Ebina T, Hibi K, et al. Differences in negative T waves between acute pulmonary embolism and acute coronary syndrome. Circ J Off J Jpn Circ Soc. 2014;78(2):483-489.
3.         Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M. The ecg in pulmonary embolism : Predictive value of negative t waves in precordial leads—80 case reports. Chest. 1997;111(3):537-543. doi:10.1378/chest.111.3.537.