Name:
A 57-Year-Old with Dyspnea and Lower Extremity Edema
Description:
A 57-Year-Old with Dyspnea and Lower Extremity Edema
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Duration:
T00H07M14S
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
[upbeat intro music]
DR. HANDY: Hi, welcome to Harrison's Podclass where we discuss important concepts in internal medicine. I'm Cathy Handy.
DR. WIENER: And I'm Charlie Wiener and we're coming to you from the Johns Hopkins School of Medicine. Welcome to episode 51: A 57-Year-Old with Dyspnea and Lower Extremity Edema. Okay, Cathy, here's the question. A 57-year-old man with a known history of congestive heart failure presents to the emergency department with increasing dyspnea and lower extremity edema over the past few weeks. On exam, he has an elevated jugular venous pressure and bilateral lower extremity pitting edema.
DR. WIENER: He also has dullness to percussion, decreased tactile fremitus and decreased breath sounds at his right base. A chest radiograph reveals a moderate size right pleural effusion, a small left pleural effusion and pulmonary vascular congestion. He's afebrile and denies any chest discomfort. His breathing improves with an intravenous dose of furosemide.
DR. HANDY: All right, that's good. If the question was about management, I was going to suggest IV furosemide as the treatment for decompensated heart failure.
DR. WIENER: Well, that's not the question, there is more. So a right sided thoracentesis is performed and pleural fluid analysis reveals a pH of 7.42, an LDH of 280, a pleural fluid protein of four milligrams per deciliter and 400 white blood cells all of them mononuclear. Serum protein at the same time as his thoracentesis is 7.5 milligrams per deciliter and his serum LDH is 600.
DR. HANDY: Interesting, I'm not sure actually I would have done a thoracentesis in this person immediately. Certainly if his breathing wasn't getting any better you could do one for therapeutic purposes. I guess it's reasonable on this case for diagnostic purposes because you mentioned that it's asymmetric but if it were bilateral, I don't think I would've done it because the most common cause of pleural effusions are left ventricular failure and we know by his history that he has heart failure.
DR. WIENER: Okay, well, given that it was done, how do you interpret the results? And did we learn anything new from the test?
DR. HANDY: Well, let's take a step back and talk about the pathophysiology to distinguish transudative versus exudative pleural effusions mechanistically. Transudates are typically benign and are caused by systemic factors that promote fluid transudation into the pleural space. Usual causes are an elevated pulmonary capillary pressure such as in heart failure or a reduced serum oncotic pressure such as in cirrhosis. In contrast, exudates are the result of local factors such as inflammation or malignancy that allow protein-rich fluid to build up in the pleural space.
DR. HANDY: The most common causes of exudates are pneumonia, cancers or pulmonary emboli.
DR. WIENER: And how do we use the labs to distinguish transudates from exudates?
DR. HANDY: In 1972, Richard Light, a former Oslo resident at Johns Hopkins Hospital and colleagues published a clinical trial that defines criteria to distinguish transudative pleural effusions from exudative pleural effusions. These criteria which have stood the test of time, say that a pleural effusion is exudative if any of the following three criteria are met. So the three criteria which are called Light's criteria now: a pleural fluid LDH to serum LDH ratio that's greater than 0.6, plural fluid protein to serum protein ratio that's greater than 0.5, or pleural fluid LDH that's greater than two thirds the upper limit of normal for the serum LDH.
DR. WIENER: So how would you interpret the results in this case?
DR. HANDY: In this case, since the pleural fluid protein is 4.8 and the serum protein is 7.5, this effusion would be classified as an exudate because the ratio is greater than half or 0.5. It doesn't meet the other criteria with LDH.
DR. WIENER: But meeting one criteria is enough?
DR. HANDY: Exactly.
DR. WIENER: Okay, so the question now asks based on these results, you would recommend the following, option A is continued management for congestive heart failure, the effusion is likely a transudate that has been misclassified as an exudate; option B says, intravenous antibiotics for possible pneumonia and apparent pneumonic effusion; option C is a large bore chest tube placement on the right side with the installation of doxycycline to prevent fluid reaccumulation; option D is a thoracentesis on the left side to make sure that the left side is not also exudative; or E, thoracoscopy and pleural biopsy to exclude malignancy or tuberculosis as the cause of the exudative effusion is on the right side.
DR. HANDY: Right, this is a good question, I think the answer is A and this is a good point to bring up. So I already mentioned that he has heart failure and I think that that's the cause of the fluid builds up in him. So I think that this is truly a transudative effusion that's been misclassified. In this case, some people might think to also measure for BNP, or brain natriuretic peptides but that's not well established so it's reasonable to do in the blood but would not add it on to pleural studies.
DR. WIENER: So why do you think this effusion has been misclassified and how do you reconcile that with Light's criteria?
DR. HANDY: While Light's criteria almost never misclassifies an exudative effusion as a transudate, about 25% of transudates may be misclassified as an exudate, like what happened in this scenario. So this patient's presentation including improvement from furosemide suggests that his effusions are from congestive heart failure. The administration of diuretics might increase the likelihood of a transudative effusion from heart failure being misclassified as an exudate.
DR. HANDY: The serum protein to fluid protein gradient, greater than three milligrams per deciliter in this case argues that this effusion most likely is a transudate. And the difference between the serum and pleural fluid protein would typically be less in an exudative process. Also the pleural fluid white blood cell count being less than a 1,000 also argues that this is not due to an inflammatory process.
DR. HANDY: One could make the argument that the effusion did not need to be sampled in the first place if the patient was clinically improving with management of heart failure with the IV furosemide. There's no need for more aggressive diagnostic or therapeutic procedures for a heart failure-related pleural effusion if the patient is improving clinically.
DR. WIENER: What did you think about the other options?
DR. HANDY: So I don't think that this is an infection or a malignancy and the history and physical that you mentioned does not support that. So all the other answers address the diagnosis or management of either infection or malignancy so I would rule those out.
DR. WIENER: So the teaching point here is that Light's criteria will almost never misclassify an exudate as a transudate but there are circumstances where a clinical transudate may be classified by the criteria as an exudate. Understanding the pathophysiology of pleural effusions and the limitations of lab testing will help manage the patient appropriately.
DR. HANDY: And to learn more, you can check out the chapter on diagnostic procedures in respiratory disease and also the chapter on disorders of the pleura. [outro music] [Mr. Shanahan] This is James Shanahan, publisher at McGraw Hill. Harrison's Podclass is brought to you by McGraw Hill's Access Medicine. The online medical resource that delivers the latest trusted content from the best minds in medicine.
DR. HANDY: Go to accessmedicine.com to learn more.