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[edit] Diagnosis
In general, pulmonary edema is suspected due to findings in the medical history, such as
previous cardiovascular disease, and physical examination: End-inspiratory crackles
(sounds heard at the end of a deep breath) on auscultation (listening to the breathing
through a stethoscope) are characteristic for pulmonary edema. The presence of a third
heart sound (S3) is predictive of cardiogenic pulmonary edema.[2]
In general, blood tests are performed for electrolytes (sodium, potassium) and markers of
renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-
reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT)
are typically requested. B-type natriuretic peptide (BNP) is available in many hospitals,
sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) make a cardiac
cause very unlikely.[2]
The diagnosis is confirmed on X-ray of the lungs, which shows increased fluid in the
alveolar walls. Kerley B lines, increased vascular filling, pleural effusions, upper lobe
diversion (increased blood flow to the higher parts of the lung) may be indicative of
cardiogenic pulmonary edema, whereas patchy alveolar infiltrates with air bronchograms
are more indicative of noncardiogenic edema[2]
Low oxygen saturation and disturbed arterial blood gas readings may strengthen the
diagnosis and provide grounds for various forms of treatment. If urgent echocardiography
is available, this may strengthen the diagnosis, as well as identify valvular heart disease.
In rare occasions, insertion of a Swan-Ganz catheter may be required to distinguish
between the two main forms of pulmonary edema.[2]
[edit] Causes
Pulmonary edema is either due to direct damage to the tissue or a result of inadequate
functioning of the heart or circulatory system.
[edit] Cardiogenic
[edit] Non-cardiogenic
May occur after upper airway obstruction, intravenous fluid overload, neurogenic causes
(seizures, head trauma, strangulation, electrocution). Can also be seen with ARDS (acute
respiratory distress syndrome):
[edit] Alveolar
[edit] Other/unknown
[edit] Therapy
Focus is initially on maintaining adequate oxygenation. This may happen with high-flow
oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or
variable positive airway pressure (VPAP)[11][12]) or mechanical ventilation in extreme
cases.
When circulatory causes have led to pulmonary edema, treatment with intravenous
nitrates (glyceryl trinitrate), and loop diuretics, such as furosemide or bumetanide, is the
mainstay of therapy. These improve both preload and afterload, and aid in improving
cardiac function.