Pulmonary edema

Pulmonary edema
Classification and external resources

Acute pulmonary edema
ICD-10 J81.
ICD-9 514 518.4
DiseasesDB 11017
MedlinePlus 000140
eMedicine med/1955 radio/581
MeSH D011654

Pulmonary edema (American English), or oedema (British English; both words from the Greek οἴδημα), is fluid accumulation in the lungs.[1] 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").[2] 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 classic 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 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]

Causes

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

When directly or indirectly caused by increased pulmonary blood pressure, pulmonary edema may appear when this pressure increases from the normal 15 mmHg[3] to above 25 mmHg.[4]

Cardiogenic

Non-cardiogenic

May occur after upper airway obstruction, intravenous fluid overload, neurogenic causes (seizures, head trauma, strangulation, electrocution). Can also be seen with ARDS (adult respiratory distress syndrome):

Alveolar

Other/unknown

Management

Focus is initially on maintaining adequate oxygenation. The patient is given high-flow oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or variable positive airway pressure (VPAP)[11][12]) or mechanical ventilation and PEEP in very severe 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.

Viagra (Sildenafil) is used as a preventative treatment for altitude-induced pulmonary edema[13][14], although the mechanism of action is not known. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason.[15]

References

  1. pulmonary edema at Dorland's Medical Dictionary
  2. 2.0 2.1 2.2 2.3 2.4 Ware LB, Matthay MA. Acute pulmonary edema. N Engl J Med 2005;353:2788-96. PMID 16382065.
  3. What Is Pulmonary Hypertension? From Diseases and Conditions Index (DCI). National Heart, Lung, and Blood Institute. Last updated September 2008. Retrieved on 6 April, 2009.
  4. Chapter 41, page 210 in: Cardiology secrets By Olivia Vynn Adair Edition: 2, illustrated Published by Elsevier Health Sciences, 2001 ISBN 1560534206, 9781560534204
  5. Hampson NB, Dunford RG (1997). "Pulmonary edema of scuba divers". Undersea Hyperb Med 24 (1): 29–33. PMID 9068153. http://archive.rubicon-foundation.org/2388. Retrieved 2008-09-04. 
  6. 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. http://archive.rubicon-foundation.org/4032. Retrieved 2008-09-04. 
  7. 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. PMC 2783608. http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=17413051. Retrieved 2008-09-04. 
  8. 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. 
  9. 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. 
  10. Bates, M (2007). "High altitude pulmonary edema". Altitude Physiology Expeditions. http://www.altitude.org/altitude_sickness.php#HAPE. Retrieved 2008-09-04. 
  11. 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. http://jama.ama-assn.org/cgi/content/full/294/24/3124. 
  12. 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. 
  13. Richalet JP, Gratadour P, Robach P, et al. (2005). "Sildenafil inhibits altitude-induced hypoxemia and pulmonary hypertension". Am. J. Respir. Crit. Care Med. 171 (3): 275–81. doi:10.1164/rccm.200406-804OC. PMID 15516532. 
  14. Perimenis P (2005). "Sildenafil for the treatment of altitude-induced hypoxaemia". Expert Opin Pharmacother 6 (5): 835–7. doi:10.1517/14656566.6.5.835. PMID 15934909. 
  15. Fagenholz PJ, Gutman JA, Murray AF, Harris NS (2007). "Treatment of high altitude pulmonary edema at 4240 m in Nepal". High Alt. Med. Biol. 8 (2): 139–46. doi:10.1089/ham.2007.3055. PMID 17584008. 

See also

External links