This is a 🧡 about physical examination, and what role it (still) plays in modern clinical practice. Decided to write this after seeing a post earlier this yr by @RichardLehman1 on this issue and some people replying that examination was much less relevant in the modern era
I'd like to share 3 case examples of why I don't believe that is true. POCUS is a valuable *adjunct* to the initial clinical assessment, which includes both history & exam (H&E). The H&E should direct which tests you want & what Q you're asking

1. MR case
2. AS case
3. HF case
Case 1
Pt referred to @UHS_valveclinic with new murmur. Completely asymptomatic, very fit & active. Phys exam revealed a prominent systolic murmur, no other abN findings.

TTE images were is PLAX

@echo_stepbystep @iamritu @purviparwani @rajdoc2005 @mswami001
And again. Tried different transducer positions, deliberate foreshortening, AP5Ch view etc...still couldn't see it
However, murmur suggested there *was* an abnormality, we just hadn't demonstrated it

So...moved patient from left lateral position flat on to back, to try something different

Now, we can see an MR jet swirling around the LA!
The CW Doppler shows quite a dense signal!
Even able to zoom up & get a PISA measurement...MR radius was 6mm, EROA 0.2cm2

On balance, we reported moderate MR

The point is...we persisted & persisted to find an MR jet *because of the exam findings*

Without exam, some may have given up & said 'no obvious abnormality'
Case 2
Patient referred to @UHS_valveclinic with exertional SOB. No CP, palpitations, HF symptoms.

Exam - slow-rising carotid pulse! Harsh ESM! Absent S2!

So, we do the TTE. Again challenging images. Here is the best of multiple CW Doppler traces from AP5Ch window
Mean gradient 32mmHg. Vmax ~3.7m/s. Suggested moderate AS

But, examination findings consistent with severe AS

Of course we know we *should* perform RSE imaging in such cases, but multiple prior studies have shown this is frequently not done (e.g. time pressures)
However, we strongly suspected we had not demonstrated highest gradients we tried all other non-apical windows...and got this from modified RSE

Vmax now ~4.3-4.4m/s, mean gradient ~40mmHg...confirmed severe AS

Again, phys exam findings informed the subsequent test
Case 3 - an old one

40yr old lady presents with 2month history leg swelling. No other symptoms - no SOB, orthopnoea, PND, chest pain. Just ankle swelling

No relevant PMHx except obesity (BMI 35). No regular medication. No alcohol, non-smoker. No red flag symptoms
Exam - sinus rhythm. Positioned in bed at 45 degrees, neck was examined and JVP was definitely not elevated. No murmurs. Chest clear. No abdo masses. Marked bilateral pitting oedema to the knees
Cardiology opinion had been sought. I was a registrar (resident) & recalled a great line I had seen former mentor @heartdoc_aam use:

"In the absence of diuretic use, the normal venous pressure effectively rules out HF as a cause of ankle oedema"

So that's what I wrote here!
Few mins later, irate medical consultant comes to find me on ward, says sarcastically "I'm very impressed by your diagnostic prowess all from the JVP"

Insisted this was bound to be HF & he wanted an echocardiogram. I was a trainee, in no position to refuse

Echo was normal
Blood results-albumin 21 (~1/2 normal)

This was in days before BNP widely used. Today, the thought of not doing an echo in such a patient seems unbelievable..."surely you'd just do one, to be sure?"

The purist in me says no! Realist knows that's challenging today
Recall basic physiology. Oedema happens in HF due to transudation of fluid from intravascular compartment into interstitium due to raised hydrostatic pressure within blood vessels...which comes from elevated filling pressures in right heart.
If RV - and thus RA - pressures are so high that (considerable) fluid has moved into interstitial space, the JVP (surrogate of RAp) cannot be normal (well, that's what I was taught! 😁)
In summary

I agree certain aspects of physical examination are no longer necessary today (e.g. is there reverse splitting of S2 that might indicate LBBB or AS?)

However, physical exam without question retains an important role
I worry that with rise of virtual consultations, our clinical assessments will be incomplete. Virtual clinic means history only then tests, no examination

This isn't meant to be a 🧡 about #POCUS, but again I'll say I think it's a great adjunct, especially in acute setting
But hope I'm not a luddite for suggesting examination is still a very important part of clinical examination!

A key change these days is medicolegal culture, fear of being sued, important Q : "Is clinical accumen enough today?"

Are lots of tests done 'just in case'? Yes!!
Discussion welcome! 😁

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More from @dr_benoy_n_shah

22 May
1/ I know some of us have already had a brief discussion about this, but this is the most astonishing presentation I have seen in a long time.

We should discuss!

I must stress, I have *not* seen the actual presentation, I've seen the slides & write up on TCTMD only
2/ This study is derived from the TVT registry, looking at TAVIs with the Sapien 3/Ultra between 2015-2020

Of 159661 TAVIs, 37660 were in low risk patients (STS score <3%) & 3243 had bicuspid AV. They've propensity score matched to compare TAVI in BAV vs trileaflet AV valves
3/ Almost all the BAV pts made it into the propensity score-matched group (3168/3243 = 97.7%)

Mean age 69yrs
Mean STS score 1.7%
Mean LVEF 57%
Read 14 tweets
13 Mar

Pt in early 50s, unwell for 2 weeks. Grows Staphylococcus aureus in blood cultures within 48hrs. No obvious source. No murmurs on exam.

TTE requested - image quality not great, but here's a PLAX view of the AV.
Here's a still photo.
Red arrow indicates the strand we saw on the AV.
Seemed a bit long to be a Lambls, but could be; I've seen these described as a filament or fibrin strand too.
Importantly, no aortic regurgitation
Read 18 tweets
21 Dec 20

Last case of 2020!

@BrHeartValveSoc @TheBJCA @global_wic @BSEcho @ASE360

This is a tough one! This will separate the men from the boys, the women from the girls...are you Luke Skywalker or are you already the Obi-Wan Kenobi of valve disease?!
Mid 70s patient, known ischaemic cardiomyopathy & aortic stenosis.
⬆️⬆️ dyspnoea.
Clinical signs suggest severe AS.
BP 90/50mmHg, HR 60bpm.
This is the resting ECG (hint - showing this for a reason - πŸ˜‰)
Here is PLAX view of the AV...πŸ‘‡πŸ½
Read 25 tweets
26 Oct 20

Old case from 2010...but you know what they say...old is gold! 😁

Female, mid 70s, inter-hospital transfer for urgent angiography due to chest tightness with ischaemic ECG. CP came on 12hrs after distressing news of sudden family death. ECG πŸ‘‡πŸ½ Image
Exam - loud systolic murmur, so urgent TTE requested before angio. Here is PLAX. Apologies no ECG, cables on portable Vivid-i were broken!

@angularboxoid @JonathanWHinton @hannahcvimaging @cardiodan @hannahzr @TharushaGunawa4 @MayooranShan @DrMarkMills @dorsetcardio @brwcole
PLAX Zoom...
Read 28 tweets
10 Oct 20
#EACTS2020 Update!

What a busy day! Great session related to TAVI and discussion of low risk patients and insights from the πŸ‡ΊπŸ‡Έ TVT database containing results from over 330,000 patients! Read more below... warning, long but interesting (hopefully!) thread...
First presentation included 2yr outcomes from PARTNER 3 trial from Dr Vinod Thourani πŸ‘‡
We were reminded of the 1year results presented last year at ACC

Significant difference in composite 1o EP at 1yr, endpoint was death / stroke / rehospitalization

At 2 yrs, similar results for this composite EP
Read 27 tweets
10 Oct 20
#EACTS2020 Update


Well, had to choose this! Not often there's a RCT in heart valve disease!

Study: Perceval sutureless valve vs a stented tissue aortic valve, both by full sternotomy and mini sternotomy approaches

@EACTS @BrHeartValveSoc
47 sites across 3 continents recruiting from 2016-2018

578 underwent isolated AVR

Mean age 75yrs
Authors report quicker surgery and better outcomes for the Perceval valve *in combination with* mini-sternotomy approach
Read 9 tweets

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