A friend has been diagnosed with pulmonary oedema and given 6 months to live, is this true?

Question

What treatment is available for him?

Answer 1

Pulmonary edema is a description of his medical condition, describing fluid and edema in the lungs.
Many diseases can lead to pulmonary edema and depending on the cause and severity of the disease will be a better predictor of his chances of living/dying.
Congestive heart failure, hypertensive emergency, vasculitic diseases are just a few of the many medical conditions that may cause pulmonary edema.
Unable to make an educated response without knowing more information.

Answer 2

Wow, guess you got a lot of info. from the first two answers there!
I would also factor in age, other physical conditions, etc.
I wish you both well as you go through this together.
A well informed person who cares is always such a blessing to a person with an illness.
Sayin' a prayer for you both.

Answer 3

If a responsible physician estimates 6 months to live, then the main cause of the edema is too advanced for effective treatment.

http://en.wikipedia.org/wiki/Pulmonary_edema

Answer 4

Pulmonary edema 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 or due to a direct injury to the lung parenchyma . Treatment depends on the cause, but focuses on maximizing respiratory function and removing the cause.Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to coma and even death, generally due to its main complication of hypoxia.
If pulmonary edema has been developing gradually, symptoms of fluid overload may be elicited. These include frequent urination at night, ankle edema (swelling of the legs, generally of the "pitting" variety, where the skin is slow to return to normal when pressed upon), inability to lie down flat due to breathlessness and paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night).
Pulmonary edema is generally suspected due to findings in the medical history, such as previous cardiovascular disease, and physical examination: end-inspiratory crackles on auscultation are characteristic for pulmonary edema. The presence of a third heart sound is predictive of cardiogenic pulmonary edema.
Blood tests are generally 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.
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, while patchy alveolar infiltrates with air bronchograms are more indicative of noncardiogenic edema
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.
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) or mechanical ventilation in extreme cases.
When circulatory causes have led to pulmonary edema, treatment with intravenous nitrates 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.
There are no causal therapies for direct tissue damage; removal of the causes is the most important measure

Answer 5

http://www.nlm.nih.gov/medlineplus/ency/article/000140.htm