Given the prevalence of pulmonary oedema in the ICU, the intensivists' obsession with fluid balance, the daily Xrays ("it's more wet than yesterday" etc), the constant battle against lung water should probably be better represented in the final exam. One might surmise that the college examiners view this as a simple problem with solutions so puerile that even a shaved ape should be able to implement them. Question 29.1 from the second paper of 2008 is the only queston which has ever directly discussed pulmonary oedema, and it was in the context of distinguishing cardiac from non-cardiac causes.
This chapter addresses the topic of pulmonary oedema with greater respect than would be expected from its historical exam appearances. Of the many digital sources, LITFL offers the most concise review of acute pulmonary oedema, written by Mike Cadogan. The time-poor candidate may limit their reading to the most exam-relevant reference for answering Question 29.1 from the second paper of 2008, which would have to be the NEJM article by Ware et al (2005). For the complete nutter, Gluecker et al (1999) have published a classic article detailing the clinical and radiological features of pulmonary oedema, with numerous pictures and long digressions on physiology.
These are numerous. Generally, people divide them into cardiogenic causes and non-cardiogenic causes.
Cardiogenic | Non-cardiogenic |
Excessive LV afterload
Excessive LV preload
Excessive left atrial afterload
Poor contractility
Ineffective contractility
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Increased capillary permeability
Neurogenic pulmonary oedema
Drug-induced pulmonary oedema
Raised pulmonary arterial pressure
Negative pressure pulmonary oedema
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There are two distinct radiological phases. The interstitial phase is the fluid filling up spaces between acini; the alveolar phase is where that fluid floods the air spaces. Both phases tend to appear at the same time in ICU patients, at least in the context of fluid overload and heart failure.
Question 29.1 from the second paper of 2008 asked how you would go about telling them apart, besides taking a careful history and performing a thorough exmaination. Realistically, history and examination will give you most of the answers. For instance, the first sentences of a telephone handover will reveal that the patient has recently had a pneumonectomy while holidaying in the Himalayas. Therefore, the real question is how to distinguish capillary leakage syndromes from cardiac causes of pulmonary oedema.
The college answer suggested TTE, BNP, PICCO and PAWP measurement.
Investigation | Cardiogenic pulmonary oedema | Non-cardiogenic pulmonary oedema |
History |
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Examination |
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ECG findings |
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Troponin |
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Brain natriuretic peptide (BNP) |
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Chest Xray |
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Echocardiography |
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Swan-Ganz catheter |
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Weirdly, the use of BNP to discriminate between different causes of pulmonary oedema has attracted some strongly pejorative comments from the LITFL audience. Its use in the context of emergency medicine was somehow viewed as wasteful and lazy, a crutch of the amateur. The real man examines the patient and takes a full history, they might say. However, BNP has been well validated in that setting (Maisel et al, 2002) and appears to be more accurate than any historical information, physical examination findings or other laboratory investigations. Karmapaliotis et al (2007) also investigated this issue in the ICU setting, where one may not have the luxury of good history or examination. At a cut-off twice as high as in the ED (≤ 200 pg/ml), BNP had a specificity of 91% for ARDS. However, it must be pointed out that these studies excluded patients with known severe systolic dysfunction. BNP is also raised in renal failure and sepsis (like troponin), and has the additional limitation of rarity and expense. The downtown hospitals of rural Nebrahoma may not have BNP kits available to every breathless patient.
Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.
Monnet, Xavier, et al. "Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/ARDS." Intensive care medicine 33.3 (2007): 448-453.
Ware, Lorraine B., and Michael A. Matthay. "Acute pulmonary edema." New England Journal of Medicine 353.26 (2005): 2788-2796.
Gluecker, Thomas, et al. "Clinical and radiologic features of pulmonary edema." Radiographics 19.6 (1999): 1507-1531.
Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.
Maisel, Alan S., et al. "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure." New England Journal of Medicine 347.3 (2002): 161-167.