1/8 A young woman presents with progressive dyspnea. You walk into the room and this is what you see.
What finding is present?
2/8 Central cyanosis indicates the presence of hypoxemia. SPO2 by pulse oximetry is 80%. ABG on room air shows PaO2 of 40 mm Hg and PaCO2 of 30 mm Hg.
We reference our framework for hypoxemia to begin the process of narrowing our differential diagnosis.
3/8 The first thing we want to know is the A-a gradient.
A (from the alveolar gas equation) = 112 mm Hg
a (from the ABG) = 40 mm Hg
A-a = 112 - 40 = 72 mm Hg.
Elevated.
4/8 Next we revisit the physical examination for more clues. There is profound peripheral cyanosis. But what else do you notice?
If you don't specifically look for this finding you might never notice it. "The eyes can't see what the mind doesn't know."
5/8 Clubbing indicates that we are likely dealing with an anatomic shunt.
6/8 The patient's precordial movement shown here is suggestive of an intracardiac shunt. @PeteSullivanPDx teaches that the chest can move in this way when blood travels from a higher pressure chamber to a lower pressure chamber. In this case, from the right to the left.
7/8 Our diagnosis is confirmed with an echo with agitated saline contrast. Bubbles appear in the LV within 3 beats.
Bubbles are normally filtered by the lungs. They only appear in the L side of the heart if there is an intracardiac (few beats) or intrapulmonary shunt (>5 beats).
8/8 We diagnosed an intracardiac shunt with our eyes, a Q-tip, and a few specific hypothesis-driven tests.
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: