Pulmonary oedema

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Pulmonary edema
Classification and external resources
ICD-10 J81.
ICD-9 514
DiseasesDB 11017
MedlinePlus 000140
eMedicine med/1955  radio/581
MeSH D011654

Pulmonary edema (American English), or oedema (British English), is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the heart to remove fluid from the lung circulation ("cardiogenic pulmonary edema") or a direct injury to the lung parenchyma ("noncardiogenic pulmonary edema").[1] Treatment depends on the cause, but focuses on maximizing respiratory function and removing the cause.

Contents

Signs and symptoms

Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety, and pale skin. A classical sign of pulmonary edema is the production of pink frothy sputum. If left untreated, it can lead to coma and even death, in general, due to its main complication of hypoxia.

If pulmonary edema has been developing gradually, symptoms of fluid overload may be elicited. These include nocturia (frequent urination at night), ankle edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), orthopnea (inability to lie down flat due to breathlessness), and paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night).

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.[1]

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, especially in the US, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) make a cardiac cause very unlikely.[1]

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[1]

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.[1]

Causes

Pulmonary edema is either due to direct damage to the tissue or a result of inadequate functioning of the heart or circulatory system.

Cardiogenic

Non-cardiogenic

This form is contiguous with ARDS (acute respiratory distress syndrome):

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)[8][9]) 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.

References

  1. ^ a b c d e Ware LB, Matthay MA. Acute pulmonary edema. N Engl J Med 2005;353:2788-96. PMID 16382065.
  2. ^ Fremont RD, Kallet RH, Matthay MA, Ware LB (June 2007). "Postobstructive pulmonary edema: a case for hydrostatic mechanisms". Chest 131 (6): 1742–6. doi:10.1378/chest.06-2934. PMID 17413051. Retrieved on 2008-09-04. 
  3. ^ Chuang YC, Wang CH, Lin YS (September 2007). "Negative pressure pulmonary edema: report of three cases and review of the literature". Eur Arch Otorhinolaryngol 264 (9): 1113–6. doi:10.1007/s00405-007-0379-9. PMID 17598119. Retrieved on 2008-09-04. 
  4. ^ Luks AM (2008). "Do we have a "best practice" for treating high altitude pulmonary edema?". High Alt. Med. Biol. 9 (2): 111–4. doi:10.1089/ham.2008.1017. PMID 18578641. Retrieved on 2008-09-04. 
  5. ^ Bates, M (2007). "High altitude pulmonary edema". Altitude Physiology Expeditions. Retrieved on 2008-09-04.
  6. ^ Hampson NB, Dunford RG (1997). "Pulmonary edema of scuba divers". Undersea Hyperb Med 24 (1): 29–33. PMID 9068153. Retrieved on 2008-09-04. 
  7. ^ Cochard G, Arvieux J, Lacour JM, Madouas G, Mongredien H, Arvieux CC (2005). "Pulmonary edema in scuba divers: recurrence and fatal outcome". Undersea Hyperb Med 32 (1): 39–44. PMID 15796313. Retrieved on 2008-09-04. 
  8. ^ Masip J, Roque M, Sánchez B, Fernández R, Subirana M, Expósito JA (December 2005). "Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis". JAMA 294 (24): 3124–30. doi:10.1001/jama.294.24.3124. PMID 16380593. 
  9. ^ Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD (April 2006). "Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis". Lancet 367 (9517): 1155–63. doi:10.1016/S0140-6736(06)68506-1. PMID 16616558. 

See also


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  • This page was last modified on 7 October 2008, at 18:58.

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