1/6 A young man is admitted to the hospital with malaise and fever. You examine his hands and find these tender nodules.
This should generate a hypothesis.
(Heart sounds in this thread best heard with headphones or a decent computer speaker)
2/6 With your hypothesis in mind, you listen to the patient's heart. You anticipate what you might hear.
"The ears can't hear what the mind doesn't know."
3/6 Based on the holosystolic murmur at the apex that you anticipated you would hear, you diagnose the patient with mitral valve endocarditis. Two days later, his heart sounds change. Take a listen.
An additional diagnosis has now been made.
4/6 Two days later, you know longer hear the pericardial friction rub. In fact, his heart sounds are difficult to hear at all. He develops hypotension and pre-syncope and his neck looks like this:
This should generate a hypothesis.
5/6 You confirm your hypothesis with a bedside maneuver (video features a different patient with the same diagnosis):
6/6 You have diagnosed infective endocarditis of the mitral valve with pericardial involvement, evolving to pericardial effusion with cardiac tamponade. All with your eyes and ears.
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:
1/10
A 60 y/o woman presents with subacute, progressive, severe hyponatremia (Na 118).
Let’s walk through an approach to this common problem.
2/10
First we confirm we are dealing with hypotonic hyponatremia.
This begins to narrow our differential.
3/10
Next we want to know the status of extracellular fluid volume. Our patient has low JVP, no peripheral edema, and dry mucous membranes, narrowing our differential even further.
1/9 A 70-year-old man presents with dyspnea. What do you notice when you first meet him?
This finding should generate a hypothesis, which we will circle back to eventually.
2/9 Before we do, let’s talk about dyspnea. The two main systems responsible for dyspnea are the heart and the lungs.
3/9 The jugular venous pulse can serve as a pivot point. It can take you toward or away from the heart. With this in mind, let’s evaluate the patient’s neck. Here, he is in the upright position. (Sometimes the jugular venous pulse is better seen on the left.)
1/8 A young man comes to our clinic for evaluation of rapid weight gain. He has heard "diet and exercise" several times before he sees us.
The driver license photo was taken ~9 months prior.
We make some observations, leading us to generate a hypothesis.
2/8
Based on our hypothesis, we examine the patient further. And we make several more important observations, increasing the likelihood of our hypothesis.
3/8
We remember that skin thickness can be an important sign in this condition, from Lynn Loriaux's 2017
@NEJM review.
(Examiner's hand is shown above, patient's below.)
1/8
A young man presents with dyspnea. We start with his hands.
My hand is gloved in the second photo (for frame of reference, I can palm a basketball).
Our patient has a finding that should generate a hypothesis.
2/8
Our hypothesis takes us to the patient’s mouth.
3/8
A high-arched palate. Otherwise note as an “ogival” arch. These arches are pointed at the top and are a key feature of Gothic architecture, beginning in the 12th century.