Pulmonary edema, Lung Fluid, Lung Edema

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Pulmonary edema, Lung Fluid, Lung Edema

Postby patoco » Fri Jun 22, 2007 9:28 am

Pulmonary Edema

Introduction

Your lungs contain millions of small, elastic air sacs called alveoli. With each breath, the air sacs take in oxygen and release carbon dioxide, a waste product of metabolism. Normally, the exchange of oxygen and carbon dioxide takes place without problems. But sometimes increased pressure in the blood vessels in your lungs forces fluid into the air sacs, filling them with fluid and preventing them from absorbing oxygen — a condition called pulmonary edema.

In most cases, heart problems are the cause of pulmonary edema. But fluid can accumulate in your lungs for other reasons, including lung problems such as pneumonia, exposure to certain toxins and medications, and exercising or living at high elevations.

Acute pulmonary edema is a medical emergency and requires immediate care. Although pulmonary edema can sometimes prove fatal, the outlook is often good when you receive prompt treatment for pulmonary edema along with therapy for the underlying problem.

Signs and symptoms

Depending on the cause, the symptoms of pulmonary edema may appear suddenly or develop slowly over weeks or months.

Signs and symptoms that come on suddenly are usually severe and may include:

Extreme shortness of breath or difficulty breathing
A feeling of suffocating or drowning
Wheezing or gasping for breath
Anxiety and restlessness
A cough that produces frothy sputum that may be tinged with blood
Excessive sweating
Pale skin
Chest pain when pulmonary edema is caused by coronary artery disease
Signs and symptoms that develop more gradually include:

Difficulty breathing when you're lying flat as opposed to sitting up
Awakening at night with a breathless feeling

Having more shortness of breath than normal when you're physically active

Significant weight gain when pulmonary edema develops as a result of congestive heart failure, a condition in which your heart pumps too little blood to meet your body's needs

If you develop any of these signs or symptoms, call 911 or emergency medical assistance right away. Pulmonary edema can be fatal if not treated.

Causes

Your lungs are two spongy, elastic organs inside your rib cage that stretch and contract as you breathe. Although your lungs can hold up to 4 quarts of air, you generally inhale only a fraction of that with each breath.

Two major airways (bronchi) carry air into your lungs. These airways subdivide into smaller airways (bronchioles) that finally end in clusters of tiny air sacs. Each lung has about 300 million air sacs, which inflate like miniature balloons every time you inhale.

Wrapped around each air sac are capillaries that connect the arteries and veins in your lungs. The capillaries are so narrow that red blood cells have to pass through them in single file. Each red blood cell absorbs oxygen, while the plasma — the fluid containing the red blood cells — releases carbon dioxide.

But in certain circumstances the alveoli fill with fluid instead of air, preventing oxygen from being absorbed into your bloodstream. A number of factors can cause fluid to accumulate in your lungs, but most have to do with your heart (cardiac pulmonary edema). Understanding the relationship between your heart and lungs can help explain why.

How your heart works

Your heart is composed of two upper and two lower chambers. The upper chambers (the right and left atria) receive incoming blood. The lower chambers, the more muscular right and left ventricles, pump blood out of your heart. The heart valves — which keep blood flowing in the correct direction — are gates at the chamber openings.

Normally, deoxygenated blood from your body enters the right atrium and flows into the right ventricle, where it's pumped through large blood vessels (pulmonary arteries) to your lungs. There, the blood releases carbon dioxide and picks up oxygen. The oxygen-rich blood then returns to the left atrium through the pulmonary veins, flows through the mitral valve into the left ventricle, and finally leaves your heart through another large artery, the aorta. The aortic valve at the base of the aorta keeps the blood from flowing backward into your heart. From the aorta, the blood travels to the rest of your body.

What goes wrong

Cardiac pulmonary edema — also known as congestive heart failure — occurs when the left ventricle isn't able to pump out enough of the blood it receives from your lungs. As a result, pressure increases inside the left atrium and then in the pulmonary veins and capillaries, causing fluid to be pushed through the capillary walls into the air sacs.

Congestive heart failure can also occur when the right ventricle is unable to overcome increased pressure in the pulmonary artery, which usually results from left heart failure, chronic lung disease, or high blood pressure in the pulmonary artery (pulmonary hypertension).

Medical conditions that can cause the left ventricle to become weak and eventually fail include:

Coronary artery disease. Over time, the arteries that supply blood to your heart can become narrow from fatty deposits (plaques). A heart attack occurs when a blood clot forms in one of these narrowed arteries, blocking blood flow and damaging the portion of your heart muscle supplied by that artery. The result is that the damaged heart muscle can no longer pump as well as it should. Although the rest of the heart tries to compensate for this loss, it's either unable to do so effectively or it's weakened by the extra workload. Normally, the ventricles pump about 50 percent to 60 percent of the blood they contain with each contraction. But when the pumping action of the heart is weakened, this figure may fall as low as 15 percent. In that case, blood backs up into the lungs, forcing fluid in the blood to pass through the capillary walls into the air sacs.

Cardiomyopathy. When your heart muscle is damaged by causes other than blood flow problems, the condition is called cardiomyopathy. Often, cardiomyopathy has no known cause, although it sometimes runs in families. Less common causes include infections (myocarditis), alcohol abuse and the toxic effects of drugs such as cocaine and some types of chemotherapy. Because cardiomyopathy weakens the left ventricle — the heart's main pump — it may not be able to respond to conditions that require it to work harder, such as a surge in blood pressure or infections. When the left ventricle can't keep up with the demands placed on it, fluid backs up into the lungs.

Heart valve problems. In mitral valve disease or aortic valve disease, the valves that regulate blood flow either don't open wide enough (stenosis) or don't close completely (insufficiency). This allows blood to flow backward through the valve. When the valves are narrowed, blood can't flow freely into your heart and pressure in the left ventricle builds up, causing the left ventricle to work harder and harder with each contraction.

The increased pressure extends into the left atrium and then to the pulmonary veins, causing fluid to accumulate in your lungs. On the other hand, if the mitral valve leaks, some blood is backwashed toward your lung each time your heart pumps. If the leakage develops suddenly, you may develop sudden and severe pulmonary edema.

High blood pressure (hypertension). Untreated or uncontrolled high blood pressure causes a thickening of the left ventricular muscle, and accelerates coronary artery disease.

If pulmonary edema persists, it can raise pressure in the pulmonary artery and eventually the right ventricle begins to fail. The right ventricle has a much thinner wall of muscle than does the left side. The increased pressure backs up into the right atrium and then into various parts of the body, where it can cause leg swelling (edema), abdominal swelling (ascites) or a buildup of fluid in the pleural space (pleural effusion).

Noncardiac pulmonary edema

Not all pulmonary edema is the result of heart disease. Fluid may also leak from the capillaries in the lungs' air sacs because the capillaries themselves become more permeable or leaky, even without the buildup of back pressure from the heart. In that case, the condition is known as noncardiac pulmonary edema because the heart isn't the cause of the problem. Some factors that can cause increased capillary permeability leading to noncardiac pulmonary edema are:

Lung infections. When pulmonary edema results from lung infections, such as pneumonia, the edema occurs only in the part of the lung that's inflamed.

Exposure to certain toxins. These include toxins you inhale — such as chlorine, ammonia or nitrogen dioxide — as well as those that may circulate within your own body. For example, women giving birth may develop pulmonary edema when amniotic fluid reaches the lungs through the veins of the uterus (amniotic fluid embolism).
Severe allergic reactions (anaphylaxis). You can have serious allergic reactions to some medications as well as to certain foods and insect venom.

Smoke inhalation. Children and older adults are especially vulnerable to lung damage caused by breathing smoke from structural fires. Smoke contains chemicals that damage the membrane between the air sacs and the capillaries, allowing fluid to enter the lungs.

Drug overdose. More than 20 drugs — ranging from narcotics such as heroin to diabetes medications and aspirin — are known to cause noncardiac pulmonary edema. Aspirin-induced pulmonary edema can occur in people who take increasingly large doses of aspirin to relieve pain or other symptoms. For reasons that aren't clear, smokers who use aspirin are at greater risk.

Acute respiratory distress syndrome (ARDS). This serious disorder occurs when your lungs suddenly fill with fluid and inflammatory blood cells. Many conditions can cause ARDS, including severe injuries (trauma), systemic infection (sepsis), pneumonia or shock. ARDS sometimes develops after extensive surgery. Symptoms usually appear within 24 to 72 hours after the original illness or trauma.

High altitudes. Mountain climbers and people who live in or travel to high-altitude locations run the risk of developing high altitude pulmonary edema (HAPE). This condition — which typically occurs at elevations above 8,000 feet — can also affect hikers or skiers who start exercising at higher altitudes without first becoming acclimated. But even people who have hiked or skied at high altitudes in the past aren't immune. Although the exact mechanism isn't completely understood, HAPE seems to develop as a result of increased pressure from constriction of the pulmonary capillaries. Symptoms include headaches, insomnia, fluid retention, cough and shortness of breath. Without appropriate care, HAPE can be fatal.

When to seek medical advice

Acute pulmonary edema is life-threatening. Get emergency assistance if you have any of the following acute signs and symptoms:

Trouble breathing or a feeling of suffocating (dyspnea)
A bubbly, wheezing or gasping sound when you breathe
Pink, frothy sputum when you cough
Profuse sweating
Lightheadedness
A blue or gray tone to your skin
A severe drop in blood pressure
Acute pulmonary edema is likely to be incapacitating, so don't attempt to drive yourself to the hospital. Instead, dial 911 or emergency medical care and wait for help.

Screening and diagnosis

Because pulmonary edema requires prompt treatment, you'll initially be diagnosed on the basis of your symptoms and a physical exam. You may also have blood drawn — usually from an artery in your wrist — so that it can be checked for the amount of oxygen and carbon dioxide it contains (arterial blood gas concentrations).

Once your condition is more stable, your doctor will ask about your medical history, especially whether you have ever had cardiovascular or lung disease. You will also likely have a chest X-ray, which can help support a diagnosis of pulmonary edema. And you may have further tests to determine why you developed fluid in your lungs. These tests may include:

Electrocardiography (ECG). This noninvasive test can reveal a wide range of information about your heart. During an ECG, patches attached to your skin receive electrical impulses from your heart. These are recorded in the form of waves on graph paper or a monitor. The wave patterns show your heart rate and rhythm, and whether areas of your heart show diminished blood flow.

Echocardiography (diagnostic cardiac ultrasound exam). Another noninvasive test, echocardiography uses a wand-shaped device called a transducer to generate high-frequency sound waves that are reflected from the tissues of the heart. The sound waves are then sent to a machine that uses them to compose images of your heart on a monitor.

The test can help diagnose a number of heart problems, including valve problems, abnormal motions of the ventricular walls, fluid around the heart (pericardial effusion) and congenital heart defects. It also accurately measures the amount of blood your left ventricle ejects with each heartbeat (ejection fraction, or EF). The ventricles don't empty all their blood with each beat, but in most cases the EF should be greater than 50 percent. When the left ventricle begins to fail, this number falls. Although a low EF often indicates a cardiac cause for pulmonary edema, it's possible to have cardiac pulmonary edema with a normal EF.

Transesophageal echocardiography (TEE). In a traditional cardiac ultrasound exam, the transducer remains outside your body on the chest wall. But in TEE, a soft, flexible tube with a special transducer tip is inserted through your mouth and into your esophagus — the passage leading to your stomach. This provides a clearer view of your heart and central pulmonary arteries than does traditional echocardiography. You'll be given a sedative to make you more comfortable and prevent gagging. You may have a sore throat for a few days after the procedure, and there's a slight risk of perforation or bleeding from the esophagus.

Cardiac catheterization. If other tests don't reveal the reason for your pulmonary edema, your doctor may suggest a procedure to measure the pressure in your lung capillaries (wedge pressure). During this test, a small, balloon-tipped catheter is inserted through a vein in your leg or arm into a pulmonary artery. The catheter has two openings connected to pressure transducers. The balloon is inflated and then deflated, giving pressure readings.

Complications

When not treated, acute pulmonary edema can be fatal. In some instances it may be fatal even if you receive treatment. The outcome depends in part on the condition of your heart and lungs before you developed edema and on the amount of fluid in your lungs. Drug-induced pulmonary edema is a frequent cause of death in people who abuse narcotics.

Treatment

Administering oxygen is the first step in treating any kind of pulmonary edema. You usually receive oxygen through a face mask or nasal cannula — a flexible plastic tube with two openings that deliver oxygen to each nostril. This should ease some of your symptoms. Sometimes it may be necessary to assist your breathing with a machine.

Depending on your condition and the reason for your pulmonary edema, you may also receive one or more of the following medications:

Furosemide (Lasix). This diuretic works quickly to expel excess fluid from your body in cases of cardiac pulmonary edema.

Morphine (Astramorph, Roxanol). This narcotic, for years a mainstay in treating cardiac pulmonary edema, may be used to relieve shortness of breath and associated anxiety. But some doctors now believe that the risks of morphine may outweigh the benefits and are more apt to use other, more effective, drugs.

Afterloaders. These are drugs that dilate the peripheral vessels and take a pressure load off the left ventricle.

Aspirin. Your doctor may recommend starting aspirin therapy if you're not already taking it. Aspirin helps thin the blood so that it moves through your small blood vessels more easily.

Blood pressure medications. If you have high blood pressure when you develop pulmonary edema, you'll be given medications to control it. On the other hand, if your blood pressure is too low, you're likely to be given drugs to raise it.

Treating high-altitude pulmonary edema (HAPE)

If you're climbing or traveling at high altitudes and experience mild symptoms of HAPE, descending a few thousand feet should relieve your symptoms. Oxygen also is helpful. When symptoms are more severe, you'll likely need help in your descent. A helicopter rescue may be necessary for the most serious cases.

Sometimes, however, immediate rescue isn't possible. With this in mind, researchers have devised several experimental therapies. In one, the distressed climber is placed in an airtight bag known as a hyperbaric bag, which is then pumped with air, simulating the air pressure at a lower altitude. A night's sleep in the bag seems to relieve symptoms — at least temporarily.

Some climbers take the prescription medication acetazolamide (Diamox) to prevent symptoms of HAPE. Diamox can occasionally have side effects — including tingling or burning in the hands, feet and mouth, confusion, diarrhea, nausea, and thirst — and must be started three days before your ascent.

Prevention

Pulmonary edema often isn't preventable, but these measures can help reduce your risk:

Preventing cardiovascular disease

Cardiovascular disease is the leading cause of pulmonary edema. You can reduce your risk of many kinds of heart problems by following these suggestions:

Control your blood pressure. More than 50 million Americans have high blood pressure (hypertension), which can lead to serious conditions such as stroke, cardiovascular disease and kidney failure. Most adults should have their blood pressure checked at least once every two years. This is a noninvasive and painless procedure using an inflatable cuff that wraps around your upper arm. The test takes just a few minutes. Under new, stricter national blood pressure guidelines issued in May 2003, a resting blood pressure reading below 120/80 millimeters of mercury (mm Hg) is considered normal. If your resting blood pressure is consistently 140/90 mm Hg or higher, you have high blood pressure. A reading in between these levels places you in the prehypertensive category. In many cases, you can lower your blood pressure or maintain a healthy level by getting regular exercise, eating a diet rich in fresh fruits, vegetables and low-fat dairy products, and limiting alcohol and coffee.

Watch your blood cholesterol. Cholesterol is one of several types of fats essential to good health. But too much cholesterol can be too much of a good thing. Higher than normal cholesterol levels (hypercholesterolemia) can cause fatty deposits to form in your arteries, impeding blood flow and increasing your risk of vascular disease. But lifestyle changes can often keep your cholesterol levels low. This includes limiting fats to no more than 30 percent of your diet, eating more fiber, fish, and fresh fruits and vegetables, exercising regularly, stopping smoking, and drinking in moderation.

Don't smoke. If you smoke, the single most important thing you can do for your heart and lung health is to stop. Continuing to smoke increases your risk of a second heart attack or heart-related death and also increases your risk of lung cancer and other lung problems such as emphysema. What's more, you're at risk even if you don't smoke but live or work with someone who does. Exposure to secondhand smoke has been shown to be a contributing factor to coronary artery disease. If you can't stop smoking by yourself, ask your doctor to prescribe a treatment plan to help you quit.

Eat a heart-healthy diet. Fish is one of the cornerstones of a heart-healthy diet — it contains omega-3 fatty acids, which help improve blood cholesterol levels and prevent blood clots. It's also important to eat plenty of fruits and vegetables, which contain antioxidants, vitamins and minerals that help prevent everyday wear and tear on your coronary arteries. Limit your intake of all types of fats to no more than 30 percent of your daily calories, and animal (saturated) and trans fats (hydrogenated oils) to 10 percent or less.

Limit salt. It's especially important to limit your salt intake if you have heart disease. In some people with impaired left ventricular function, excess salt — even in a single meal or a bag of chips —may be enough to trigger congestive heart failure. If you're having a hard time cutting back on salt, it may be helpful to talk to a dietitian. He or she can help point out low sodium foods as well as offer tips for making a low salt diet interesting and good-tasting.

Exercise regularly. Exercise is vital for a healthy heart. Regular aerobic exercise helps maintain a healthy weight, controls blood pressure and cholesterol levels, helps prevent diabetes and maintains muscle tone. Aim for at least 30 minutes of exercise on most days. If you're not used to exercise, start out slowly and build up gradually.

Maintain a healthy weight. Being even slightly overweight increases your risk of cardiovascular disease. On the other hand, losing only 5 to 10 pounds can lower your blood pressure and reduce your risk of diabetes.
Get enough folic acid (folate). An essential B vitamin, folate may reduce blood levels of homocysteine, an amino acid that builds and maintains tissues. Too much homocysteine can promote the formation of plaque in your arteries. To get 400 micrograms of folate a day, eat green, leafy vegetables, citrus fruits, legumes, peanuts and cereal grains. If you're not sure how much folate you're getting from your diet, talk to your doctor about a folic acid supplement, or choose a multivitamin supplement that contains at least 400 micrograms of folic acid.

Manage stress. To reduce your risk of heart problems, try to reduce your stress levels. Rethink workaholic habits and find healthy ways to minimize or deal with stressful events in your life.

Preventing HAPE

If you travel or climb at high altitudes, acclimate yourself slowly. Although recommendations vary, most experts advise ascending no more than 1,000 or 2,000 feet a day once you reach 8,000 feet. In addition, it's important to drink plenty of water to stay hydrated. The higher you ascend the more rapidly you breathe, which means you lose larger amounts of water in the air you exhale from your lungs. Finally, although being physically fit won't necessarily prevent HAPE, people in good condition tend to be less stressed at high altitudes.

Self-care

The following suggestions may speed your recovery from cardiac pulmonary edema and help prevent a recurrence:

Get at least seven hours of sleep a night. Take a nap during the day if you feel tired.

Listen to medical advice. Follow your doctor's advice about controlling any underlying health problems, including advice about diet and exercise.

Try to get at least 30 minutes of exercise on most days. If your exercise plan seems too hard or too easy, talk to your doctor or a rehabilitation therapist.

Weigh yourself in the morning before breakfast. Call your doctor if you've gained 2 to 3 pounds in a single day.

Avoid drinking alcohol. Your lungs and heart work harder when you drink alcohol.

If you've experienced noncardiac pulmonary edema — including some forms of ARDS — take care to minimize any further damage to your lungs, and as far as possible avoid the cause of your condition, such as drugs, allergens or high altitudes.

http://www.mayoclinic.com/health/pulmon ... DSECTION=1

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Pleural effusion

Alternative names

Fluid in the chest; Pleural fluid
Definition Return to top

A pleural effusion is an accumulation of fluid between the layers of the membrane that lines the lungs and chest cavity.

Causes, incidence, and risk factors

Your body produces pleural fluid in small amounts to lubricate the surfaces of the pleura, the thin membrane that lines the chest cavity and surrounds the lungs. A pleural effusion is an abnormal collection of this fluid.

Two different types of effusions can develop:

Transudative pleural effusions are often caused by abnormal lung pressure. Congestive heart failure is the most common cause.
Exudative effusions form as a result of inflammation (irritation and swelling) of the pleura. This is often caused by lung disease. Examples include lung cancer, pneumonia, tuberculosis and other lung infections, drug reactions, asbestosis, and sarcoidosis.

Symptoms

Shortness of breath
Chest pain, usually a sharp pain that is worse with cough or deep breaths
Cough
Hiccups
Rapid breathing
There may be no symptoms.

Signs and tests

During a physical examination, the doctor will listen to the sound of your breathing with a stethoscope and may tap on your chest to listen for dullness.

The following tests may help to confirm a diagnosis:

Chest x-ray
Thoracic CT
Ultrasound of the chest
Thoracentesis
Pleural fluid analysis

The cause and type of pleural effusion is usually determined by thoracentesis (a sample of fluid is removed with a needle inserted between the ribs).

Treatment

Treatment may be directed at removing the fluid, preventing its re-accumulation, or addressing the underlying cause of the fluid buildup.

Therapeutic thoracentesis may be done if the fluid collection is large and causing pressure, shortness of breath, or other breathing problems, such as low oxygen levels. Treatment of the underlying cause of the effusion then becomes the goal.

For example, pleural effusions caused by congestive heart failure are treated with diuretics and other medications that treat heart failure. Pleural effusions caused by infection are treated with antibiotics specific to the causative organism. In patients with cancer or infections, the effusion is often treated by using a chest tube to drain the fluid. Chemotherapy, radiation therapy, or instilling medication within the chest that prevents re-accumulation of fluid after drainage may be used in some cases.

Expectations (prognosis)

The expected outcome depends upon the underlying disease.

Complications

A lung surrounded by a fluid collection for a long time may collapse.
Pleural fluid that becomes infected may turn into an abscess, called an empyema, which requires prolonged drainage with a chest tube placed into the fluid collection.

Pneumothorax (air within the chest cavity) can be a complication of the thoracentesis procedure.
In rare cases, surgery is needed to remove the abscess.

Calling your health care provider

Call your health care provider if symptoms suggestive of pleural effusion develop.

Call your provider or go to the emergency room if shortness of breath or difficulty breathing occurs immediately after thoracentesis.

Update Date: 8/7/2006

Updated by: David A. Kaufman, M.D., Assistant Professor, Division of Pulmonary, Critical Care & Sleep Medicine, Mount Sinai School of Medicine, New York, NY. Review provided by VeriMed Healthcare Network.

http://www.nlm.nih.gov/medlineplus/ency ... 000086.htm

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Thoracentesis

Alternative names

Pleural fluid aspiration; Pleural tap

Definition

Thoracentesis is a procedure to remove fluid from the space between the lining of the outside of the lungs (pleura) and the wall of the chest. Normally, very little fluid is present in this space. An accumulation of excess fluid between the layers of the pleura is called a pleural effusion.

How the test is performed

A small area of skin on your chest or back is washed with a sterilizing solution. Some numbing medicine (local anesthetic) is injected in this area. A needle is then placed through the skin of the chest wall into the space around the lungs called the pleural space. Fluid is withdrawn and collected and may be sent to a laboratory for analysis (pleural fluid analysis).

How to prepare for the test

No special preparation is needed before the procedure. A chest x-ray is may be performed before and after the test.

Do not cough, breathe deeply, or move during the test to avoid injury to the lung.

How the test will feel

You will on a bed or sit on the edge of a chair or bed with your head and arms resting on a table. The skin around the procedure site is disinfected and the area is draped. A local anesthetic is injected into the skin. The thoracentesis needle is inserted above the rib into the pleural space.

There will be a stinging sensation when the local anesthetic is injected, and you may feel a sensation of pressure when the needle is inserted into the pleural space.

Inform your health care provider if you develop shortness of breath or chest pain.

Why the test is performed

The test is performed to determine the cause of the fluid accumulation or to relieve the symptoms associated with the fluid accumulation.

Normal Values

Normally the pleural cavity contains only a very small amount of fluid.

What abnormal results mean

The analysis of the fluid will indicate possible causes of pleural effusion such as infection, cancer, heart failure, cirrhosis, and kidney disease. If infection is suspected, a culture of the fluid is often done to determine whether microorganisms are present and if so, to identify them.

Additional conditions under which the test may be performed include the following:

Pneumonia
Hemothorax
Pulmonary veno-occlusive disease
Pancreatitis
Pulmonary embolism
Thyroid disease
Collagen vascular disease
Asbestos-related pleural effusion
Drug reactions

What the risks are

Pneumothorax (collapse of the lung)
Fluid re-accumulation
Pulmonary edema
Bleeding
Infection
Respiratory distress

Special considerations

A chest x-ray is often done after the procedure to detect possible complications.

Update Date: 8/7/2006

Updated by: David A. Kaufman, M.D., Assistant Professor, Division of Pulmonary, Critical Care & Sleep Medicine, Mount Sinai School of Medicine, New York, NY. Review provided by VeriMed Healthcare Network.

http://www.nlm.nih.gov/medlineplus/ency ... 003420.htm

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Pleurodesis treatment

I am due to have pleurodesis treatment. I would like to know what this is and how it is done?

It is quite common for fluid to collect when cancer affects the lungs, causing breathlessness. Fluid can gather between the sheets of tissue covering of the outside of the lung and lining the chest cavity. These sheets of tissue are called the pleura. You can see the pleura in the diagram below.

The fluid stops the lung from fully expanding when you breathe. So as it builds up, the collected fluid will cause shortness of breath.

You can have treatment to stop this fluid from building up and help relieve the symptoms. This treatment is called pleurodesis. It seals the space between pleura with sterile talc. The idea is to put in something that will irritate the pleura. This makes them stick together. Then there is no space in which the fluid can collect. This can be done as an outpatient treatment. But this may depend on how well you are. You may have to stay in hospital overnight if there is a lot of fluid to drain off as this can take some time and the nurses will want to keep an eye on you.

This treatment does not treat the cancer. But it is very useful for relieving difficult symptoms such as breathlessness. It should be easier to breathe after this treatment. If it doesn't work completely the first time, then you can have it done again.

If you have had fluid drained from your pleural effusion before, you will know what to expect, as the procedure is very similar. First, your doctor will have to give you a small injection of local anaesthetic. When this has worked, the doctor will put a wide needle (cannula) into your chest, usually through your side. The tip of the needle goes into the space where the fluid is collecting. This is attached to a drainage tube called a chest drain and a collecting bottle or bag. Your doctor will put a stitch (called a purse string suture) around the tube to hold it in place.

If there is fluid on your chest, your doctor will want to drain it off first. As long as the drainage bottle or bag is kept lower than your chest, this will happen automatically. If there is a lot of fluid, draining it can take a while. It has to be slow, because draining off a large amount of fluid too quickly can make your blood pressure drop suddenly and you may feel faint.

Once the fluid has stopped draining, the doctor injects the talc into the pleural space through the drain. The drain is clamped and left for an hour. During that time, you will be asked to lie in different positions on your bed – on one side and then the other, for example. This is to help the drug or talc circulate between the pleura. After that, your doctor may want the drain to be attached to some suction. This helps the pleura to stick together. As the aim of putting in the talc is to irritate and inflame the pleura, it is not surprising that this part of the process can be a bit uncomfortable. For most people this is mild and doesn't last long. But do tell your doctor if it is a problem for you.

After all this, your doctor or nurse will take the drain out and pull the stitch tight to close the small opening in your chest wall. The stitch stays in for about a week.

http://www.cancerhelp.org.uk/help/default.asp?page=5291

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Effectiveness of CT for Clinical Stratification of Occupational Lung Edema.

Ind Health. 2007 Jan

Masaki Y, Sugiyama K, Tanaka H, Uwabe Y, Takayama M,
Sakai M, Hayashi T, Otsuka M, Suzuki S.

Division of Environmental Medicine, National Defense Medical College Research Institute.

Key words: Spray, Smoke, Polytetarafluoroethylene, Zinc chloride, CT scan, Military, Occupational, Lung

We treated two occupational lung diseases in different situations during military training. The purpose of this study is to investigate the availability of CT scanning for the evaluation of inhalation pulmonary edema. Two soldiers suffered severe lung edema after using a spray for the daily maintenance of their firearms. Four soldiers suffered severe dyspnea after undertaking drills in a narrow zone where numerous smoke bombs had been used. We evaluated these patients from several aspects. CT scans of the chest of spray-induced patients revealed bilateral infiltration predominantly in the upper lung fields.

The patients received steroid pulse treatment and gradually recovered. CT scans of the chest of smoke-induced patients revealed bilateral ground-glass attenuation with peripheral lung sparing. The patients gradually recovered with steroid therapy. In accordance with previous studies, CT scans of the chest in our patients demonstrated that the periphery of the lungs remained normal, except in cases of serious injury.

When differential diagnosis is required, we consider that CT scans of the chest are particularly useful; CT findings are useful in determining the severity of lung injury as well as the diagnosis of inhalation pulmonary edema.

http://www.jstage.jst.go.jp/article/ind ... 8/_article

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Cardiopulmonary Function After Recovery From Swimming-induced Pulmonary Edema.

Journal of Sports Medicine

July 16, 2006

Ludwig BB,
Mahon RT,
Schwartzman EL.

*National Naval Medical Center, Division of Pulmonary and Critical Care, Bethesda, MD daggerNaval Medical Research Center, Undersea Medicine Department, Silver Spring, MD double daggerNaval Medical Center Portsmouth, Division of Cardiology, Portsmouth, VA.

OBJECTIVE:

This study aimed to compare cardiopulmonary function in patients with a history of swimming-induced pulmonary edema (SIPE) with controls by measuring pulmonary function tests, oxygen consumption with exercise, and the pulmonary arterial pressure response to hypoxemia. DESIGN: Case control study.

SETTING:

Tertiary Military Medical Center.

PATIENTS:

US Navy Special Warfare members who had previously suffered SIPE.

INTERVENTIONS:

Measurement of pulmonary function tests, cardiopulmonary exercise test, pulmonary artery pressure by echocardiography at rest on room air and with hypoxia.

MAIN OUTCOME MEASUREMENTS:

Pulmonary function testing, carbon monoxide diffusing capacity, maximal oxygen consumption, and pulmonary arterial pressure response to hypoxemia.

RESULTS:

Subjects who previously had SIPE did not demonstrate differences in pulmonary function tests, carbon monoxide diffusing capacity, maximal oxygen consumption, or pulmonary arterial pressure response to hypoxemia.

CONCLUSIONS:

Subjects with a history of SIPE do not have abnormal pulmonary function tests, abnormal exercise capacity, or abnormal pulmonary arterial pressure response to hypoxemia when tested in dry conditions.

http://www.cjsportmed.com/pt/re/cjsm/ab ... 44!8091!-1

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Activation of the stress protein response prevents the development of pulmonary edema by inhibiting VEGF cell signaling

2006 Jun 22 - Research Abstract

Activation of the stress protein response prevents the development of pulmonary edema by inhibiting VEGF cell signaling in a model of lung ischemia-reperfusion injury in rats.

Godzich M, Hodnett M, Frank JA, Su G, Pespeni M, Angel A, Howard MB, Matthay MA, Pittet JF.

*Laboratory of Surgical Research, Departments of Anesthesia, Surgery, andMedicine and Cardiovascular Research Institute, University of California, San Francisco, California, USA.

Lung endothelial damage is a characteristic morphological feature of ischemia-reperfusion (I/R) injury, although the molecular steps involved in the loss of endothelial integrity are still poorly understood. We tested the hypothesis that the activation of vascular endothelial growth factor (VEGF) cell signaling would be responsible for the increase in lung vascular permeability seen early after the onset of I/R in rats.

Furthermore, we hypothesized that the I/R-induced pulmonary edema would be significantly attenuated in rats by the activation of the stress protein response. Pretreatment with Ad Flk-1, an adenovirus encoding for the soluble VEGF receptor type II, prevented I/R-mediated increase in lung vascular permeability in rats.

Furthermore, the I/R-induced lung injury was significantly decreased by prior activation of the stress protein response with geldanamycin or pyrrolidine dithiocarbamate. In vitro studies demonstrated that VEGF caused an increase in protein permeability across primary cultures of bovine macro- and microvascular lung endothelial cell monolayers that were associated with a phosphorylation of VE- and E-cadherin and the formation of actin stress fibers.

Activation of the stress protein response prevented the VEGF-mediated changes in protein permeability across these cell monolayers and reduced the phosphorylation of VE-and E-cadherins, as well as the formation of actin stress fibers in these cells. .--Godzich, M., Hodnett, M., Frank, J. A., Su, G., Pespeni, M., Angel, A., Howard, M. B., Matthay, M. A., Pitte, J. F.

Activation of the stress protein response prevents the development of pulmonary edema by inhibiting VEGF cell signaling in a model of lung ischemia-reperfusion injury in rats.

http://www.fasebj.org/cgi/content/full/20/9/1519

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Levels of fibrinogen compared to crp in plasma as new marker in diagnosis of pulmonary edema of non septic origin

Harefuah. 2006 Dec;145(12):870-4, 943-4

Internal Medicine F, Western Galilee Hospital-Nahariya. Raymond.Farah@naharia.health.gov.il

INTRODUCTION:

Community-acquired pneumonia, that requires hospitalization, is a severe illness with high mortality rates, especially in cases of delay of appropriate treatment. At times, the correct diagnosis of the disease is difficult due to equivocal clinical picture or chest film, accompanying diseases that could mask or simulate the pneumonia. The aims of our study were: 1. follow-up levels of fibrinogen throughout hospitalization in the group of patients admitted to the hospital due to pneumonia and pulmonary edema of non-infectious origin; 2. an estimation opportunity using them as possible new markers for diagnosis of pneumonia and for following response to treatment.

METHODS:

Three groups of patients were studied: a group of 15 patients admitted due to pneumonia, a group of 15 patients admitted due to pulmonary edema, and a control group 15 healthy subjects. The blood samples for white blood cells count, erythrocyte sedimentation rates, levels of fibrinogen, C-reactive protein, albumin, were taken for each patient on admission, 48 and 72 hours following admission and on discharge day. The received dates were compared using Student t-test.

RESULTS:

The levels of fibrinogen were higher on admission, in the patients with pneumonia, maximally after 48 and 72 hours (P<0.001) p="0.0044),"> 0.027 for both groups in discharge day). The comparison of fibrinogen levels between groups of patients with pneumonia and pulmonary edema reveal statistically significant results at time of admission, after 48 and 72 hours but not on discharge day.

CONCLUSION:

Fibrinogens can be used as reliable markers for primary diagnosing of pneumonia or differential diagnosis from pulmonary edema, on admission and until 72 hours but not for patient follow-up throughout hospitalization period. Additional studies are needed for discovering other new markers for patient follow-up throughout hospitalization period.

http://www.ncbi.nlm.nih.gov/sites/entre ... uery_hl=18

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Pulmonary edema after transfusion: how to differentiate transfusion-associated circulatory overload from transfusion-related acute lung injury.

Gajic O, Gropper MA, Hubmayr RD.

Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. gajic.ognjen@mayo.edu

OBJECTIVE:

Pulmonary edema is an under-recognized and potentially serious complication of blood transfusion. Distinct mechanisms include adverse immune reactions and circulatory overload. The former is associated with increased pulmonary vascular permeability and is commonly referred to as transfusion-related acute lung injury (TRALI). The latter causes hydrostatic pulmonary edema and is commonly referred to as transfusion-associated circulatory overload (TACO). In this review article we searched the National Library of Medicine PubMed database as well as references of retrieved articles and summarized the methods for differentiating between hydrostatic and permeability pulmonary edema.

RESULTS:

The clinical and radiologic manifestations of TACO and TRALI are similar. Although echocardiography and B-type natriuretic peptide measurements may aid in the differential diagnosis between hydrostatic and permeability pulmonary edema, invasive techniques such as right heart catheterization and the sampling of alveolar fluid protein are sometimes necessary. The diagnostic differentiation is especially difficult in critically ill patients will multiple comorbidities so that the cause of edema may only be determined post hoc based on the clinical course and response to therapy. Guided by available evidence, we present an algorithm for establishing the pretest probability of TRALI as opposed to TACO. The decision to test donor and recipient blood for immunocompatibility may be made on this basis.

CONCLUSIONS:

The distinction between hydrostatic (TACO) and permeability (TRALI) pulmonary edema after transfusion is difficult, in part because the two conditions may coexist. Knowledge of strengths and limitations of different diagnostic techniques is necessary before initiation of complex TRALI workup.

http://www.ccmjournal.com/pt/re/ccm/abs ... 44!8091!-1

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High altitude pulmonary edema in a patient with previous pneumonectomy.

J Formos Med Assoc. 2007 Apr

Chou YT, Wang CL, Kao KC, Wu YK, Tsai YH.
Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Chiayi, Taiwan.

Key Words: altitude sickness, pneumonectomy, pulmonary edema, risk factors

High altitude pulmonary edema (HAPE) is a life-threatening illness that can occur in individuals ascending to altitudes exceeding 2400 m. The risk factors are rapid ascent, physical exertion and a previous history of HAPE. This work presents a case study of a 74-year-old man who underwent left side pneumonectomy 40 years ago and subsequently experienced several instances of HAPE. The well-known risk factors for HAPE were excluded in this patient. We suspect that the post-pneumonectomy condition may be a risk factor for HAPE based on this case.

http://health.elsevier.com/journals/pub ... ournals=12

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Transpulmonary dilution-derived extravascular lung water as a measure of lung edema.

Curr Opin Crit Care. 2007 Jun

Khan S, Trof RJ, Groeneveld AJ.
Department of Intensive Care, VU University Medical Center, Amsterdam, The Netherlands.

PURPOSE OF REVIEW: This review highlights current insights concerning the (measurement of) extravascular lung water as an index of pulmonary edema, by transpulmonary dilution techniques. The focus is on the applicability of the technique at the bedside in monitoring critically ill patients.

RECENT FINDINGS: Several (animal) studies have been performed to validate the technique by postmortem gravimetry in different conditions. Moreover, recent clinical data emphasize the utility of the thermodilution-derived extravascular lung water, its contribution to the clinical manifestations of acute lung injury/acute respiratory distress syndrome, its response to treatment aimed at edema prevention or resolution, and as a prognostic parameter.

SUMMARY: The thermodilution-derived extravascular lung water is a useful adjunct to assess lung vascular injury, cardiogenic edema and overhydration and to guide treatment in critically ill patients. The effects on morbidity and mortality of this approach need to be studied further.

http://www.co-criticalcare.com/pt/re/co ... 44!8091!-1

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