A 70 y/o man presents with new exertional dyspnea, orthopnea/PND, wide pulse pressure (~100 mm Hg), and elevated JVP. A physical finding is identified (video). Echo: preserved systolic function, no valvular disease. Thoughts? What would you do next? #PhysicalExam#cardiotwitter
Incredible discussion. Like many here I questioned the echo. Then realized Quincke's pulse = high-output state (not always AR). Sent for RHC to confirm high-output HF. Sure enough, CO was 12.5 L/min (CI 4.8 L/min/m2). Workup for cause underway. #PhysicalExam led to diagnosis.
Physical exam was pivotal in this case. Without it, most of us would have concluded that this was "just another case of diastolic heart failure" and stopped there. Without seeing Quincke's pulse, there is no question that I would have unknowingly marched down the wrong path.
At this point thiamine deficiency (beriberi) and AV shunt are highest on my differential. Patient drinks ~2 glasses of wine/day. EtOH causes thiamine deficiency via several mechanisms, so even if patients consume a normal diet and don't appear malnourished, it is still possible.
Thanks @DocRock54 for asking for follow-up. The thiamine assay won't result until 12/22. If negative, then next step will be to look for shunt. I have corresponded with the authors of the excellent review below, who offered some advice about shunt workup (see image). More soon.
UPDATE. This patient has wet beriberi. Thiamine replacement should result in total cure. Heinrich Quincke is still helping patients nearly 100 years after his death. Is that not immortality?
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1/9 A 33 y/o F with carpal tunnel syndrome presents with polyuria and polydipsia. She has a fasting serum glucose of 212 mg/dL and a hemoglobin a1c of 9.7%.
Do you have an approach to hyperglycemia?
2/9 The first step is to determine whether we are dealing with insulin-dependent hyperglycemia or insulin-independent hyperglycemia.
3/9 Insulin-dependent hyperglycemia occurs as a result of insulin deficiency; insulin-independent hyperglycemia occurs despite the presence of insulin and is primarily the result of insulin resistance.
1/10
A young man presents with hematuria and is found to have these painful skin lesions on physical exam.
2/10
In a patient with hematuria, the first question I always ask is: what is the source of that blood?
Is it glomerular or non-glomerular?
3/10
How can we tell if the bleeding is glomerular or not? We have to evaluate the urine sediment. But the eyes can’t see what the mind doesn’t know. So what are we looking for?
2/9 The etiologies of weakness can be subdivided into 4 main categories:
3/9 What are the signs of an UMN lesion?
No (or minimal) muscle atrophy, no fasciculations, increased tone, + Babinski’s, and increased reflexes, the latter of which is demonstrated below in a different patient with a L-sided stroke.
1/10
A 76 y/o man presents with swallowing difficulty.
So why are we looking at his hands?
2/10
What’s your approach to dysphagia?
The first thing we want to determine is whether dysphagia is oropharyngeal or esophageal.
3/10
The patient not have trouble initiating a swallow and there is no choking, coughing, or drooling. Food material seems to get stuck in the middle of his chest.
These features point away from oropharyngeal dysphagia and toward esophageal dysphagia.
This middle-age patient was admitted several weeks ago with cardiogenic shock of unclear etiology. He is recovering well on the ward when I meet him. This is what I see:
2/11
Here's another view of these vigorous carotid pulses (Corrigan's pulse). Classically associated with aortic regurgitation (like we saw 2 weeks ago), there are several other causes:
1. High-output state (eg, wet beriberi) like we saw last week 2. Coarctation of the aorta
3/11
I immediately think he must have aortic regurgitation. I listen, but I don't hear a diastolic murmur.
Still, I evaluate his nail beds and this is what I see: