What is edema

Edema is a build up of fluid in the body which causes the affected tissue to become swollen. The swelling can occur in one particular part of the body or may be more general, depending on the cause. Edema usually occurs in the feet, ankles and legs, but it can involve your entire body.

Common causes of edema include:

• Eating too much salt
• Sunburn
• Heart failure
• Kidney disease
• Liver problems from cirrhosis
• Chronic lung disease
• Thyroid disease
• Pregnancy
• Problems with lymph nodes, especially after mastectomy
• Some medicines, such as corticosteroids, medicine for high blood pressure (hypertension), nonsteroidal anti-inflammatory drugs (NSAIDS), such as ibuprofen or naproxen or hormone replacement medications
• Standing or walking a lot when the weather is warm
• Low levels of protein in the blood, caused by poor nutrition
• The contraceptive pill

Immobility and standing for long periods are the 2 most common causes of edema in the legs.

Other possible causes of edema include:

• a blood clot
• severe varicose veins
• a leg injury or leg surgery
• burns to the skin
• acute mountain sickness
• cancer, especially kidney, liver, or ovarian cancers
• some types of chemotherapy, including cisplatin (Platinol) and docetaxel (Docefrez, Taxotere)

To keep swelling down, your doctor may recommend keeping your legs raised when sitting, wearing support stockings, limiting how much salt you eat, or taking a medicine called a diuretic – also called a water pill. When edema is a sign of an underlying disease, the disease itself requires separate treatment.

Edema causes

It’s normal to have some swelling in your legs at the end of the day, particularly if you’ve been sitting or standing for long periods.

Edema occurs when tiny blood vessels in your body (capillaries) leak fluid. The fluid builds up in surrounding tissues, leading to swelling.

Edema is often a symptom of an underlying health condition.

Mild cases of edema may result from:

• Sitting or staying in one position for too long
• Eating too much salty food
• Having premenstrual signs and symptoms
• Being pregnant

Edema can also be a side effect of some medications, including:

• Some heart and blood pressure medications
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Steroid drugs
• Estrogens
• Certain diabetes medications called thiazolidinediones
• Some antidepressants
• Some hormone replacement therapies

In some cases, however, edema may be a sign of a more serious underlying medical condition. Several diseases and conditions may cause edema, including:

• Congestive heart failure. If you have congestive heart failure, one or both of your heart’s lower chambers lose their ability to pump blood effectively. As a result, blood can back up in your legs, ankles and feet, causing edema. Congestive heart failure can also cause swelling in your abdomen. Sometimes, this condition can cause fluid to accumulate in your lungs (pulmonary edema), which can lead to shortness of breath.
• Cirrhosis. Fluid may accumulate in your abdominal cavity (ascites) and in your legs as a result of liver damage (cirrhosis).
• Kidney disease. When you have kidney disease, extra fluid and sodium in your circulation may cause edema. The edema associated with kidney disease usually occurs in your legs and around your eyes.
• Kidney damage. Damage to the tiny, filtering blood vessels in your kidneys can result in nephrotic syndrome. In nephrotic syndrome, declining levels of protein (albumin) in your blood can lead to fluid accumulation and edema.
• Weakness or damage to veins in your legs. If you have chronic venous insufficiency, the one-way valves in your leg veins are weakened or damaged, which allows blood to pool in your leg veins and causes swelling. Sudden onset of swelling in one leg accompanied by pain in your calf muscle can be due to a blood clot (deep vein thrombosis, or DVT) in one of your leg veins. If this occurs, seek medical help immediately.
• Inadequate lymphatic system. Your body’s lymphatic system helps clear excess fluid from tissues. If this system is damaged — for example, by cancer surgery — the lymph nodes and lymph vessels draining an area may not work correctly, and edema can occur.
• Severe, long-term protein deficiency. An extreme lack (deficiency), of protein in your diet over a long period of time can lead to fluid accumulation and edema.

A problem in one part of your arm or leg can cause fluid retention further down your arm or leg, if you have:

• a problem with your lymphatic system, which drains fluid from tissues
• a vein condition, such as deep vein thrombosis
• the build-up of fat, usually in the legs
• a burn or other type of injury.

Risk factors for developing edema

If you are pregnant, your body retains more sodium and water than usual due to the fluid needed by the fetus and placenta. This can increase your risk of developing edema.

Your risk of edema may be increased if you take certain medications, including:

• High blood pressure medications
• Nonsteroidal anti-inflammatory drugs
• Steroid drugs
• Estrogens
• Certain diabetes medications called thiazolidinediones

A chronic illness — such as congestive heart failure or liver or kidney disease — can increase your risk of edema. Also, surgery can sometimes obstruct a lymph node, leading to swelling in an arm or leg, usually on just one side.

Edema complications

If left untreated, edema can cause:

• Increasingly painful swelling
• Difficulty walking
• Stiffness
• Stretched skin, which can become itchy and uncomfortable
• Increased risk of infection in the swollen area
• Scarring between layers of tissue
• Decreased blood circulation
• Decreased elasticity of arteries, veins, joints and muscles
• Increased risk of skin ulcers

Edema symptoms

The accumulation of fluid under the skin causes swelling or puffiness of the tissue directly under your skin, often in the lower legs and ankles (known as peripheral edema).

As well as swelling or puffiness of the skin, edema can also cause:

• skin discoloration
• areas of skin that temporarily hold the imprint of your finger when pressed (known as pitting edema)
• aching, tender limbs
• stiff joints
• weight gain
• increased abdominal size
• stretched or shiny skin

Edema diagnosis

To understand what might be causing your edema, your doctor will first perform a physical exam and ask you questions about your medical history. This information is often enough to determine the underlying cause of your edema. In some cases, X-rays, ultrasound exams, magnetic resonance imaging, blood tests or urine analysis may be necessary.

Edema treatment

Mild edema is often temporary and clears up by itself. For example, if you’ve been standing up for too long on a hot day, your ankles may swell up until you get the chance to put your feet up and rest.

More-severe edema may be treated with drugs that help your body expel excess fluid in the form of urine (diuretics). One of the most common diuretics is furosemide (Lasix). However, your doctor will determine whether these types of medications are a good option for you based on your personal medical history.

Severe edema treatment:

• losing weight (if you’re overweight)
• taking regular exercise, such as walking, swimming or cycling
• raising your legs three to four times a day to improve your circulation
• avoiding standing for long periods of time

If an underlying condition is causing the fluid imbalance, it should clear up after the condition has been diagnosed and treated.

Long-term management typically focuses on treating the underlying cause of the swelling. If edema occurs as a result of medication use, your doctor may adjust your prescription or check for an alternative medication that doesn’t cause edema.

Edema home remedies

The following may help decrease edema and keep it from coming back. Before trying these self-care techniques, talk to your doctor about which ones are right for you.

• Movement. Moving and using the muscles in the part of your body affected by edema, especially your legs, may help pump the excess fluid back toward your heart. Ask your doctor about exercises you can do that may reduce swelling.
• Elevation. Hold the swollen part of your body above the level of your heart several times a day. In some cases, elevating the affected body part while you sleep may be helpful.
• Massage. Stroking the affected area toward your heart using firm, but not painful, pressure may help move the excess fluid out of that area.
• Compression. If one of your limbs is affected by edema, your doctor may recommend you wear compression stockings, sleeves or gloves, usually worn after your swelling has gone down, to prevent further swelling from occurring. These garments keep pressure on your limbs to prevent fluid from collecting in the tissue.
• Protection. Keep the affected area clean, moisturized and free from injury. Dry, cracked skin is more prone to scrapes, cuts and infection. Always wear protection on your feet if that’s where the swelling typically occurs.
• Reduce salt intake. Follow your doctor’s suggestions about limiting how much salt you consume. Salt can increase fluid retention and worsen edema.

Pulmonary edema

Pulmonary edema is a condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe.

In most cases, heart problems cause pulmonary edema. But fluid can accumulate for other reasons, including pneumonia, exposure to certain toxins and medications, trauma to the chest wall, and exercising or living at high elevations.

Pulmonary edema that develops suddenly (acute pulmonary edema) is a medical emergency requiring immediate care. Although pulmonary edema can sometimes prove fatal, the outlook improves when you receive prompt treatment for pulmonary edema along with treatment for the underlying problem. Treatment for pulmonary edema varies depending on the cause but generally includes supplemental oxygen and medications.

Figure 1. Lungs alveoli

Figure 2. Pulmonary Alveoli (microscopic view)

Pulmonary edema symptoms

Depending on the cause, pulmonary edema symptoms may appear suddenly or develop over time.

Flash (sudden) pulmonary edema symptoms

• Extreme shortness of breath or difficulty breathing (dyspnea) that worsens when lying down
• A feeling of suffocating or drowning
• Wheezing or gasping for breath
• Anxiety, restlessness or a sense of apprehension
• A cough that produces frothy sputum that may be tinged with blood
• Chest pain if pulmonary edema is caused by heart disease
• A rapid, irregular heartbeat (palpitations)

If you develop any of these signs or symptoms, call your local emergency number for an ambulance and medical assistance right away. Pulmonary edema can be fatal if not treated.

Long-term (chronic) pulmonary edema symptoms

• Having more shortness of breath than normal when you’re physically active.
• Difficulty breathing with exertion.
• Difficulty breathing when you’re lying flat.
• Wheezing.
• Awakening at night with a breathless feeling that may be relieved by sitting up.
• Rapid 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. The weight gain is from buildup of fluid in your body, especially in your legs.
• Swelling in your lower extremities.
• Fatigue.

High-altitude pulmonary edema symptoms

• Shortness of breath after exertion, which progresses to shortness of breath at rest
• Cough
• Difficulty walking uphill, which progresses to difficulty walking on flat surfaces
• Fever
• A cough that produces frothy sputum that may be tinged with blood
• A rapid, irregular heartbeat (palpitations)
• Chest discomfort
• Headaches, which may be the first symptom

Pulmonary edema complications

If pulmonary edema continues, it can raise pressure in the pulmonary artery (pulmonary hypertension), and eventually the right ventricle in your heart becomes weak and begins to fail. The right ventricle has a much thinner wall of muscle than does the left side of your heart because it is under less pressure to pump blood into the lungs. The increased pressure backs up into the right atrium and then into various parts of your body, where it can cause:

• Lower extremity and abdominal swelling
• Buildup of fluid in the membranes that surround your lungs (pleural effusion)
• Congestion and swelling of the liver

When not treated, acute pulmonary edema can be fatal. In some instances, it may be fatal even if you receive treatment.

Pulmonary edema causes

Your lungs contain numerous small, elastic air sacs called alveoli. With each breath, these air sacs take in oxygen and release carbon dioxide. Normally, the exchange of gases takes place without problems.

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

Heart-related (cardiogenic) pulmonary edema

Cardiogenic pulmonary edema is a type of pulmonary edema caused by increased pressures in the heart.

This condition usually occurs when the diseased or overworked left ventricle isn’t able to pump out enough of the blood it receives from your lungs (congestive heart failure). As a result, pressure increases inside the left atrium and then in the veins and capillaries in your lungs, causing fluid to be pushed through the capillary walls into the air sacs.

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 muscle 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. Or it isn’t a clot that brings on the problems, but rather it is a gradual narrowing of the coronary arteries resulting in a weakness of the left ventricular muscle. Although the rest of your heart tries to compensate for this loss, either it’s unable to do so effectively or it’s weakened by the extra workload. When the pumping action of your heart is weakened, blood gradually backs up into your lungs, forcing fluid in your blood to pass through the capillary walls into the air sacs. This is chronic congestive heart failure.
• Cardiomyopathy. When your heart muscle is damaged by causes other than blood flow problems, the condition is called cardiomyopathy. Because cardiomyopathy weakens the ventricles — your heart’s main pump — your heart may not be able to respond to conditions that require it to work harder, such as a surge in blood pressure, a faster heartbeat with exertion, or using too much salt that causes water retention or infections. When the left ventricle can’t keep up with the demands that are placed on it, fluid backs up into your lungs.
• Heart valve problems. In mitral valve disease or aortic valve disease, the valves that regulate blood flow in the left side of your heart either don’t open wide enough (stenosis) or don’t close completely (insufficiency). This allows blood to flow backward through the valve (regurgitation). 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 left ventricle also dilates to allow more blood flow, but this makes the left ventricle’s pumping action less efficient. Because it’s working so much harder, the left ventricular muscle eventually thickens, which puts greater stress on the coronary arteries, further weakening the left ventricular muscle. 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 can lead to damage to the heart muscle and worsening of coronary artery disease.

Other conditions may lead to cardiogenic pulmonary edema, such as high blood pressure due to narrowed kidney arteries (renal artery stenosis) and fluid buildup due to kidney disease or heart problems.

Non-heart-related (noncardiogenic) pulmonary edema

Pulmonary edema that isn’t caused by increased pressures in your heart is called noncardiogenic pulmonary edema.

In this condition, fluid may leak from the capillaries in your lungs’ air sacs because the capillaries themselves become more permeable or leaky, even without the buildup of back pressure from your heart. Some factors that can cause noncardiogenic pulmonary edema include:

• Acute respiratory distress syndrome (ARDS). This serious disorder occurs when your lungs suddenly fill with fluid and inflammatory white blood cells. Many conditions can cause ARDS, including severe injuries (trauma), systemic infection (sepsis), pneumonia and severe bleeding.
• 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 generally occurs at elevations above 8,000 feet (about 2,400 meters) can also affect hikers or skiers who start exercising at higher altitudes without first becoming acclimated, which can take from a few days to a few weeks. But even people who have hiked or skied at high altitudes in the past aren’t immune.Although the exact cause isn’t completely understood, HAPE seems to develop as a result of increased pressure from constriction of the pulmonary capillaries. Without appropriate care, high-altitude pulmonary edema can be fatal, but this risk can be minimized.
• Nervous system conditions. A type of pulmonary edema called neurogenic pulmonary edema can occur after some nervous system conditions or procedures — such as after a head injury, seizure or subarachnoid hemorrhage or after brain surgery.
• Adverse drug reaction. Many drugs — ranging from illegal drugs such as heroin and cocaine to aspirin — are known to cause noncardiogenic pulmonary edema.
• Pulmonary embolism. Pulmonary embolism, a condition that occurs when blood clots travel from blood vessels in your legs to your lungs, can lead to pulmonary edema.
• Viral infections. Pulmonary edema can be caused by viral infections such as the hantavirus and dengue virus.
• Lung injury. Pulmonary edema can occur after surgery to remove blood clots from your lungs, but it occurs only in the part of the lung from which the clots were removed. It can also occur after a collapsed lung has been re-expanded or rarely after volumes of fluid have been removed from the lung. Noncardiogenic pulmonary edema also occurs in the lung directly below blunt trauma to the chest wall with the most common cause being auto accidents.
• Exposure to certain toxins. These include toxins you inhale as well as those that may circulate within your own body, for example, if you inhale (aspirate) some of your stomach contents when you vomit. Inhaling toxins such as ammonia and chlorine, which can occur with train accidents, causes intense irritation of the small airways and alveoli, resulting in fluid accumulation.
• Smoke inhalation. Smoke from a fire contains chemicals that damage the membrane between the air sacs and the capillaries, allowing fluid to enter your lungs.
• Near drowning. Inhaling water causes noncardiogenic pulmonary edema that is reversible with immediate attention.

Pulmonary edema prevention

Pulmonary edema is not always 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. High blood pressure (hypertension) can lead to serious conditions such as stroke, cardiovascular disease and kidney failure. In many cases, you can lower your blood pressure or maintain a healthy level by getting regular exercise; maintaining a healthy weight; eating a diet rich in fresh fruits, vegetables and low-fat dairy products; and limiting salt and alcohol.
• 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 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. Lifestyle changes may include limiting fats (especially saturated fats); eating more fiber, fish, and fresh fruits and vegetables; exercising regularly; stopping smoking; and drinking in moderation.
• Don’t smoke. If you smoke and can’t quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit. Smoking can increase your risk of cardiovascular disease. Also avoid secondhand smoke.
• Eat a heart-healthy diet. Eat a healthy diet that’s low in salt, sugars and solid fats and rich in fruits, vegetables and whole grains.
• Limit salt. It’s especially important to use less salt (sodium) if you have heart disease or high blood pressure. In some people with severely damaged left ventricular function, excess salt may be enough to trigger congestive heart failure. If you’re having a hard time cutting back on salt, it may help 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, about 30 minutes a day, helps you control blood pressure and cholesterol levels and maintain a healthy weight. If you’re not used to exercise, start out slowly and build up gradually. Be sure to get your doctor’s OK before starting an exercise program.
• Maintain a healthy weight. Being even slightly overweight increases your risk of cardiovascular disease. On the other hand, even losing small amounts of weight can lower your blood pressure and cholesterol and reduce your risk of diabetes.
  Manage stress. To reduce your risk of heart problems, try to reduce your stress levels. Find healthy ways to minimize or deal with stressful events in your life.

Preventing high-altitude pulmonary edema

If you travel or climb at high altitudes, acclimate yourself slowly. Although recommendations vary, most experts advise ascending no more than 1,000 to 1,200 feet (about 305 to 366 meters) a day once you reach 8,200 feet (about 2,500 meters). Rest an extra day every 600 to 1,200 feet (about 183 to 366 meters) when you’re at a high elevation (8,200 feet, or about 2,500 meters).

Some climbers take prescription medications such as acetazolamide (Diamox Sequels) or nifedipine (Procardia) to help prevent symptoms of high-altitude pulmonary edema. To prevent high-altitude pulmonary edema, start taking the medication at least one day before ascent. Continue taking the medication for about five days after you’ve arrived at your high-altitude destination.

Pulmonary edema diagnosis

Because pulmonary edema requires prompt treatment, you’ll initially be diagnosed on the basis of your symptoms and a physical exam, electrocardiogram and chest X-ray.

Once your condition is more stable, your doctor will ask about your medical history, especially whether you have ever had cardiovascular or lung disease.

Tests that may be done to diagnose pulmonary edema or to determine why you developed fluid in your lungs include:

• Chest X-ray. A chest X-ray will likely be the first test you have done to confirm the diagnosis of pulmonary edema and exclude other possible causes of your shortness of breath.
• Pulse oximetry. In pulse oximetry, a sensor attached to your finger or ear uses light to determine how much oxygen is in your blood.
• Blood tests. You may 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). Your blood may also be checked for levels of a substance called B-type natriuretic peptide (BNP). Increased levels of B-type natriuretic peptide (BNP) may indicate that your pulmonary edema is caused by a heart condition. Other blood tests may be done — including tests of your kidney function, thyroid function and blood count — as well as tests to exclude a heart attack as the cause of your pulmonary edema.
• Electrocardiogram (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.
• Echocardiogram. An echocardiogram is a noninvasive test that uses a wand-shaped device called a transducer to generate high-frequency sound waves that are reflected from the tissues of your 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 heart valve problems, abnormal motions of the ventricular walls, fluid around the heart (pericardial effusion) and congenital heart defects. It can also show areas of diminished blood flow in your heart and if your heart pumps blood effectively when it beats. It can also estimate if there’s increased pressure in the right side of the heart and increased pressure in the pulmonary arteries.
• Transesophageal echocardiography (TEE). In a traditional cardiac ultrasound exam, the transducer remains outside your body on the chest wall. But in TEE, a doctor inserts a soft, flexible tube (catheter) with a transducer attached to the tip through your mouth and guides it into your esophagus — the passage leading to your stomach. The esophagus lies immediately behind your heart, which allows your doctor to see a closer and more accurate picture of your heart and central pulmonary arteries.
• Pulmonary artery 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 doctor inserts a small, balloon-tipped catheter through a vein in your leg or arm and guides it into a pulmonary artery. The catheter has two openings connected to pressure transducers. The balloon is inflated and then deflated, giving pressure readings.
• Cardiac catheterization. If tests such as an ECG or echocardiography don’t uncover the cause of your pulmonary edema, or you also have chest pain, your doctor may suggest cardiac catheterization and coronary angiogram. During cardiac catheterization, a doctor inserts a long, thin catheter in an artery or vein in your groin, neck or arm and threads it through your blood vessels to your heart using X-ray imaging. Doctors then inject dye into the blood vessels of your heart to make them visible under X-ray imaging (coronary angiogram). During this procedure, doctors can perform treatments such as opening a blocked artery, which may quickly improve the pumping action of your left ventricle. Cardiac catheterization can also be used to measure the pressure in your heart chambers, assess your heart valves and look for causes of pulmonary edema.

Pulmonary edema treatment

Giving oxygen is the first step in the treatment for 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. Your doctor will monitor your oxygen level closely. Sometimes it may be necessary to assist your breathing with a machine such as a mechanical ventilator.

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

• Preload reducers. Preload reducing medications decrease the pressure caused by fluid going into your heart and lungs. Doctors commonly prescribe nitroglycerin and diuretics such as furosemide (Lasix) to treat pulmonary edema. Diuretics may make you urinate so much initially that you may temporarily need a urinary catheter while you’re in the hospital. The drug nifedipine (Procardia) may sometimes be prescribed.
• Morphine (Avinza, MS Contin). This narcotic may be used to relieve shortness of breath and anxiety. But some doctors believe that the risks of morphine may outweigh the benefits and are more apt to use other more-effective drugs.
• Afterload reducers. These medications, such as nitroprusside (Nitropress), dilate your blood vessels and take a pressure load off your heart’s left ventricle.
• Blood pressure medications. If you have high blood pressure when you develop pulmonary edema, you’ll be given medications to control it. Alternatively, if your blood pressure is too low, you’re likely to be given medications to raise it.

If your pulmonary edema is caused by another condition such as a nervous system condition, your doctor will treat the condition that is causing it and the pulmonary edema.

Treating high-altitude pulmonary edema

If you’re climbing or traveling at high altitudes and experience mild symptoms of high-altitude pulmonary edema, descending 2,000 to 3,000 feet (about 600 to 900 meters) as quickly as you can, within reason, should relieve your symptoms. You should also reduce physical activity and keep warm, as physical activity and cold can make your condition worse.

Oxygen is usually the first treatment and can often relieve your symptoms. If supplemental oxygen isn’t available, you may use portable hyperbaric chambers, which imitate a descent for several hours until you can descend to a lower elevation.

In addition to oxygen and descending to a lower elevation, the medication nifedipine (Procardia) may help reduce pressure in the pulmonary arteries and improve your condition.

When symptoms are more severe, you’ll likely need help in your descent. A helicopter rescue may be necessary for the most serious cases because high-altitude pulmonary edema can be life-threatening.

Some climbers take prescription medications such as acetazolamide (Diamox Sequels) or nifedipine to help treat or prevent symptoms of high-altitude pulmonary edema. To prevent high-altitude pulmonary edema, medication is started at least one day before ascent.

Pulmonary edema home remedies

Depending on your condition, your doctor may recommend lifestyle changes, including:

• Controlling your high blood pressure. If you have high blood pressure, take your medications as prescribed and check your blood pressure regularly. Record the results. Ask your doctor for guidelines regarding your optimal blood pressure.
• Controlling other medical conditions. Control any underlying medical conditions, such as controlling your glucose levels if you have diabetes.
• Avoiding the cause of your condition. If your condition is due to drugs, allergens or high altitudes, avoid these to minimize further damage to your lungs.
• Quitting smoking. If you smoke, quit smoking.
• Eating a healthy diet. Your doctor may recommend that you follow a low-salt diet. Ask for a referral to a dietitian if you need help evaluating the salt content in foods. Also eat a healthy diet of fruits, vegetables and whole grains.
• Maintaining a healthy weight and exercising. Maintain a healthy weight and exercise regularly.

Cerebral edema

Altitude illness refers to a group of syndromes that result from hypoxia. Acute mountain sickness and high-altitude cerebral edema are manifestations of the brain pathophysiology, while high-altitude pulmonary edema (HAPE) is that of the lung. Everyone traveling to altitude is at risk, regardless of age, level of physical fitness, prior medical history, or previous altitude experience.

The high-altitude environment generally refers to elevations over 1500 m (4800 ft). Moderate altitude, 2000-3500 m (6400-11,200 ft), includes the elevation of many US ski resorts. Although arterial oxygen saturation is well maintained at these altitudes, low PO2 results in mild tissue hypoxia, and altitude illness is common.

Very high altitude refers to elevations of 3500-5600 m (11,200-18,000 ft). Arterial oxygen saturation is not maintained in this range, and extreme hypoxemia can occur during sleep, with exercise, or with illness. High-altitude cerebral edema and high-altitude pulmonary edema are most common at these altitudes.
Extreme altitude is over 5600 m. At these elevations, successful long-term acclimatization is not possible; in fact, deterioration ensues. Individuals must progressively acclimatize to intermediate altitudes to reach extreme altitude.

Hypoxia is the primary physiological insult on ascent to high altitude. The fraction of oxygen in the atmosphere remains constant (0.21) at all altitudes, but the partial pressure of oxygen decreases along with barometric pressure on ascent to altitude. The inspired partial pressure of oxygen (PiO2) is lower still because of water vapor pressure in the airways. At the altitude of International Airport at La Paz, Bolivia (4062 m; 13,327 ft), PiO2 is 98.18 mm Hg, which is equivalent to breathing 12.8% oxygen at sea level. See the Figure 3 below.

The response to hypoxia depends on both the magnitude and the rate of onset of hypoxia. The process of adjusting to hypoxia, termed acclimatization, is a series of compensatory changes in multiple organ systems over differing time courses from minutes to weeks. While the fundamental process occurs within the metabolic machinery of the cell, acute physiologic responses are essential in allowing the cells time to adjust.

The most important immediate response of the body to hypoxia is an increase in minute ventilation, called the hypoxic ventilatory response and is triggered by oxygen sensing cells in the carotid bodies. Increased ventilation produces a higher alveolar PO2. Concurrently, a lowered alveolar PCO2 produces a respiratory alkalosis, acting as a brake on the respiratory center of the brain and subsequently limiting further increases in ventilation. Renal compensation, through excretion of bicarbonate ions, gradually brings the blood pH back toward normal and allows further increase in ventilation. This process, termed ventilatory acclimatization, requires approximately 4 days at a given altitude and is greatly enhanced by acetazolamide. Patients with inadequate carotid body response (genetic or acquired, eg, after surgery or radiation) or pulmonary or renal disease may have an insufficient hypoxic ventilatory response and thus not adapt well to high altitude.

In addition to ventilatory changes, circulatory changes occur that increase the delivery of oxygen to the tissues. Ascent to high altitude initially results in increased sympathetic activity, leading to increased resting heart rate, cardiac output, and mildly increased blood pressure. Within minutes of exposure, the pulmonary circulation reacts to hypoxia with vasoconstriction. This may improve ventilation/perfusion matching and gas exchange, but the resulting pulmonary hypertension can lead to a number of pathological syndromes at high altitude, including high-altitude pulmonary edema and altitude-related right heart failure.

Figure 3. Partial pressure of inspired oxygen versus altitude

The incidence of acute mountain sickness varies depending on the rate of ascent and the maximum altitude reached. In moderate altitude (2000-3500 m) ski resorts, the incidence ranges from 10-40%. Rapid ascent to approximately 4000 m has been associated with incidences of 60-70%.

Travelers flying to a high altitude destination such as Lhasa, Tibet (3810 m; 12,500 ft) or La Paz, Bolivia (4062 m; 13,327 ft) can expect an acute mountain sickness incidence of 25-35%. In those who hike above 4000 m (and so ascend at a moderate pace), 25-50% will suffer from acute mountain sickness. High altitude cerebral edema is estimated to occur in about 1% or less of persons traveling above 4000 m and in 1-3% of those with acute mountain sickness.

No significant difference based on gender exists. The incidence of acute mountain sickness is not markedly affected by menstrual cycle phase and does not differ in pregnant women versus nonpregnant women.

Age has a small effect in adults; younger adults are slightly more susceptible. Children have similar occurrence rates of altitude cerebral syndromes to those of adults.

Cerebral blood flow increases immediately on ascent to high altitude, returning toward normal over about a week. The magnitude of the increase varies but averages 24% at 3810 m and more at higher altitude. Presently, it is believed that this flow increase is partially responsible for the headache of acute mountain sickness ¹.

Hemoglobin concentration increases after ascent to high altitude, thereby improving the oxygen-carrying capacity of the blood. Initially, it increases as a result of hemoconcentration from a reduction in plasma volume secondary to altitude diuresis and fluid shifts. Subsequently, over days to weeks of hypoxia exposure, erythropoietin stimulates increased red blood cell production. In addition, the marked alkalosis of extreme altitude causes a leftward shift of the oxyhemoglobin dissociation curve, facilitating loading of the hemoglobin with oxygen within the pulmonary capillary bed.

Sleep architecture is altered at high altitude, with frequent arousals, and nearly universal subjective reports of disturbed sleep. This generally improves after several nights at a constant altitude, though periodic breathing (Cheyne-Stokes respiration) remains common above 2700 m. The use acetazolamide has been demonstrated to reduce the symptoms of high altitude sleep disturbance.

The exact pathophysiology of acute mountain sickness/high altitude cerebral edema is unknown. The current hypothesis is that hypoxia elicits neurohumoral and hemodynamic responses in the brain that ultimately result in capillary leakage from microvascular beds and edema. Whether mild acute mountain sickness or headache alone is actually due to brain edema remains an open question.

Studies using ultrasonographic assessment of optic nerve sheath diameter, which has been shown to correlate with intracranial pressure, has demonstrated increased optic nerve sheath diameter swelling in both acute mountain sickness and high altitude pulmonary edema cases.

Magnetic resonance imaging (MRI) studies demonstrate that the brain swells on ascent to altitude in both those with and those without acute mountain sickness, presumably from vasodilation. True edema, however, was only detected in severe acute mountain sickness and high altitude cerebral edema. Factors that might contribute to a hydrostatic brain edema are multiple and include cerebral vasodilation, elevated cerebral capillary pressure, impaired cerebral autoregulation, as well as alterations in the permeability of the blood-brain barrier through cytokine activation.

Susceptibility to acute mountain sickness demonstrates great individual variability because of genetic differences. Individual susceptibility is reproducible; a past history of acute mountain sickness is the best predictor.

The natural history of acute mountain sickness varies with altitude, ascent rate, and other factors. In general, the illness is self-limiting and symptoms improve slowly, with complete resolution in 1-3 days without treatment. However, with continued ascent, acute mountain sickness is very likely to worsen and is more likely to progress to high altitude cerebral edema.

High altitude cerebral edema may progress to stupor and coma over hours to days if untreated. Once coma has developed, death is more likely despite aggressive treatment; death is due to brain herniation. The usual course is rapid, complete recovery if descent is immediate and treatment is started promptly. Slower recovery results when treatment is delayed. In rare cases, patients with either severe or prolonged high altitude cerebral edema may have persistent neurologic deficits. Ataxia commonly persists for days to weeks and is often the last finding to resolve.

The golden rules of altitude illness are as follows:

• If you feel unwell at altitude, it is altitude illness unless proven otherwise.
• If you have symptoms of altitude illness, go no higher.
• If your symptoms are worsening, fail to improve with treatment, or if high altitude cerebral edema or high altitude pulmonary edema are present, descend immediately.

High altitude cerebral edema causes

Rapid ascent to altitudes greater than 2500 m can cause acute mountain sickness.

The risk of high altitude cerebral edema or acute mountain sickness increases with altitude.

Special attention should be paid to the elevation at which the person sleeps. Daytime climbs to higher elevations, with return to a lower sleeping altitude are preferred.

Continued ascent despite symptoms of acute mountain sickness is a major risk factor for developing high altitude cerebral edema. At altitudes over 5000 m, ascents of as little as 200 m for individuals with moderate acute mountain sickness have precipitated high altitude cerebral edema.

High altitude cerebral edema frequently is seen secondary to high altitude pulmonary edema, presumably because of rapidly worsening hypoxia, which is equivalent to continued ascent.

High altitude cerebral edema prevention

Recommendations on staged ascents, by and large, are adequate for the average person, but some persons still become ill despite a slow, staged ascent. Persons traveling to high altitude should allow adequate time for acclimatization and pay careful attention to symptoms. Helpful guidelines to avoid altitude illness include the following:

• Avoid abrupt ascent to sleeping elevations over 3000 m (10,000 ft).
• Spend 1-2 nights at an intermediate elevation (2500-3000 m) before further ascent.
• Above 3000 m, sleeping elevations should not increase by more than 300-400 m per night.
• When topography or village locations dictate more rapid ascent, or after every 1000 m gained, spend a second night at the same elevation.
• Day hikes to higher elevations, with return to lower sleeping elevations help to improve acclimatization.
• Drink plenty of water or electrolyte solution. Both sensible and insensible fluid losses are exaggerated at altitude. The average consumption of fluid should be increased to approximately 3-4 liters per day.
• Avoid overexertion.
• Avoid alcohol consumption in the first 2 days at a new, higher elevation; in addition to concerns about respiratory depression and exaggerated sleep hypoxemia, an acute mountain sickness headache the next morning is all too easily dismissed as a hangover.

Many travelers wonder how long acclimatization lasts after a sojourn to high altitude. Some value in preventing acute mountain sickness may persist for a week or more.

Acetazolamide effectively prevents acute mountain sickness; it accelerates acclimatization by inducing a bicarbonate diuresis, stimulating ventilation, and improving sleep-breathing patterns. It does not mask symptoms of acute mountain sickness. Acetazolamide prophylaxis is indicated for persons with an unavoidable rapid ascent, such as flying in to a high city (eg, Lhasa, Tibet; La Paz, Bolivia), or with a history of recurrent acute mountain sickness. Since it is also useful for treatment, acetazolamide should be in the high altitude traveler’s medical kit, along with written instructions. A recent survey concluded that most trekkers carrying acetazolamide did not know how to use it properly.

Dexamethasone also effectively prevents acute mountain sickness but does not improve acclimatization. Because of the concern of rebound symptoms and the adverse effect profile, this medication cannot be routinely recommended for prophylaxis.

Ibuprofen may be taken prophylactically to reduce the likelihood of acute mountain sickness. Taking 600 mg 3 times per day has been shown to decrease acute mountain sickness symptoms ².

In the past, ginkgo biloba had been suggested for acute mountain sickness prophylaxis. Importantly, a number of recent well-designed studies have found it to be ineffective at preventing acute mountain sickness. The studies that also included acetazolamide found that acetazolamide alone was effective and that combining ginkgo and acetazolamide did not provide any increased effectiveness. Ginkgo cannot be recommended for acute mountain sickness ³.

High altitude cerebral edema symptoms

Acute mountain sickness is a syndrome of nonspecific symptoms with a broad spectrum of severity. acute mountain sickness occurs in nonacclimatized personsin the first 48 h after ascent to altitudes above 2500 m, especially after rapid ascent (1 d or less). Symptoms usually begin a few hours after arrival at the new altitude but may arise as much as a day later, often after the first night’s sleep. Headache is the principal symptom, typically frontal and throbbing.

Gastrointestinal symptoms (anorexia, nausea, or vomiting), and constitutional symptoms (weakness, lightheadedness, dizziness, or lassitude) are common. acute mountain sickness is similar to an alcohol hangover, or to a nonspecific viral infection, but without fever or myalgias.

Symptoms of high altitude cerebral edema, particularly ataxia, commonly persist for days to weeks after descent. In rare cases, patients may have long-term neurologic deficits after severe or prolonged high altitude cerebral edema.

Fluid retention is characteristic of acute mountain sickness, and persons with acute mountain sickness often report reduced urination, in contrast to the spontaneous diuresis observed with successful acclimatization. As acute mountain sickness progresses, the headache worsens, and vomiting, oliguria, and increased lassitude develop. Ataxia and altered level of consciousness herald the onset of clinical high altitude cerebral edema.

Using the Lake Louise consensus criteria, the diagnosis of acute mountain sickness requires headache plus at least one of the following symptoms:

• gastrointestinal (anorexia, nausea, vomiting),
• constitutional (lightheadedness,
• dizziness,
• weakness, fatigue), or
• insomnia.

Most conditions similar to acute mountain sickness can be excluded by history and physical examination. Onset of symptoms more than 3 days after ascent, lack of headache, or failure to improve with descent, oxygen, or dexamethasone suggests another diagnosis. Dehydration is commonly confused with acute mountain sickness, as it can cause headache, weakness, nausea, and decreased urine output.

The most common history in high altitude cerebral edema is a person continuing ascent despite symptoms of acute mountain sickness; however, rarely, it may develop in the absence of acute mountain sickness after a very rapid ascent or at extreme altitude in an apparently acclimatized person. Also, high altitude cerebral edema commonly occurs in conjunction with high altitude pulmonary edema.

In a patient with symptoms of acute mountain sickness who develops gait ataxia (i.e, unable to walk heel-to-toe in a straight line) or mental status changes, high altitude cerebral edema is the diagnosis until proven otherwise. Immediate treatment and descent is indicated. Regardless of acute mountain sickness symptoms, a combination of ataxia and mental status changes suggests high altitude cerebral edema. Aside from the aforementioned gait ataxia and mental status change, the neurologic examination findings are otherwise normal. In rare cases, focal neurologic signs (eg, cranial nerve III palsy, cranial nerve VI palsy) appear in end-stage high altitude cerebral edema, although they are more suggestive of other causes of focal deficits at altitude (e.g, stroke, transient ischemic attack [TIA], migraine, brain neoplasm).

High altitude cerebral edema treatment

Prehospital Care

Management of acute mountain sickness follows 3 axioms: (1) no further ascent until symptoms resolve, (2) descend to a lower altitude if no improvement occurs with medical therapy, and (3) at the first sign of high altitude cerebral edema, descend immediately. Predicting the eventual severity from the initial clinical presentation is not possible, and patients must be watched closely for progression of illness. A small percentage (< 10%) of persons with acute mountain sickness will go on to develop high altitude cerebral edema, especially with continued ascent in the presence of acute mountain sickness symptoms.
Descent to an altitude below that where symptoms started is always effective treatment but may not be practical or possible given the topography, weather, the patient’s ultimate trekking or climbing goals, or group resources. Accordingly, a descent of 500-1000 m is usually sufficient.

Acetazolamide accelerates acclimatization and thus quickens resolution of the illness, but this may still require 12-24 hours; it is of limited value in high altitude cerebral edema because of its relatively slow action. Acetazolamide can be taken episodically without fear of rebound symptoms when it is discontinued. Dexamethasone swiftly reverses symptoms (2-4 h) but does not improve acclimatization. It is the drug of choice for treating high altitude cerebral edema and should be given early. Both agents may be used to treat acute mountain sickness if the victim does not descend. Oxygen is extremely effective, but availability is often limited.

Portable hyperbaric chambers made of coated fabric (eg, Gamow bag, CERTEC, PAC) are now widely available among adventure travel groups on expeditions and in high-altitude clinics. These are all lightweight, coated fabric bags about 2 m long and 0.7 m in diameter. The patient is placed completely within the bag, which is sealed shut and inflated with a manually operated pump, pressurizing the inside to 105-220 mmHg above ambient atmospheric pressure. Depending on the elevation of use, a physiologic (simulated) descent of up to 2000 m may be achieved within minutes. Continuous pumping is necessary to flush CO2 out of the system, unless a chemical scrubber system is used. Patients are typically treated in 1-hour increments and then are reevaluated.

Importantly, in high altitude cerebral edema cases, these chambers should only be used as a means of acute/temporizing care (eg, to improve a patient’s ability to more safely participate in their evacuation in technical terrain). They should never be considered as a replacement for actual descent.

Coca leaf tea is widely recommended in South America, on the Internet, and in the popular press as a cure for altitude illness; however, no studies support this claim. Coca leaf tea may act as a mild stimulant and improve well-being at altitude, which may be its primary effect. Garlic, likewise, has been advocated for prophylaxis and treatment of altitude illness. Animal studies show efficacy in preventing hypoxic pulmonary hypertension, but studies in humans are lacking and its use cannot be recommended at this time. Additional medications not shown to have any benefit include calcium channel blockers, naproxen, phenytoin, and antacids. Alcohol and other respiratory depressants, such as benzodiazepines, should be avoided in someone with acute mountain sickness due to the risk of exaggerated hypoxemia.

Emergency Department Care

All of the symptoms of acute mountain sickness improve dramatically with descent, and, by the time a patient reaches the emergency department, further treatment is rarely indicated.

Oxygen 4 L/min or to keep SaO2 above 90% should be used in patients who continue to be acutely ill with either severe acute mountain sickness or high altitude cerebral edema after descent.

Dexamethasone should be continued in symptomatic patients with high altitude cerebral edema.

Inpatient care

Hospitalization is not indicated for acute mountain sickness. Hospitalization is usually indicated for patients with high altitude cerebral edema, depending on severity. Patients with focal neurologic deficits or persistent mental status changes should be admitted. After descent, care is supportive.

Residual headache or nausea in patients with acute mountain sickness should be treated symptomatically. Continue dexamethasone for 1-2 days after descent in patients with uncomplicated high altitude cerebral edema or until the mental status clears in patients with severe high altitude cerebral edema who require hospitalization.

Ataxia due to high altitude cerebral edema commonly persists for days to weeks after descent, but persistent mental status changes or the presence of focal neurologic deficits should prompt a complete neurologic evaluation. Brain tumors that suddenly become symptomatic at altitude, Guillain-Barré syndrome, herpes encephalitis, and cortical blindness have all been misdiagnosed as high altitude cerebral edema.

Macular edema

Macular edema is the build-up of fluid in the macula, an area in the center of the retina. The retina is the light-sensitive tissue at the back of the eye and the macula is the part of the retina responsible for sharp, straight-ahead vision. Fluid buildup causes the macula to swell and thicken, which distorts vision.

Macular edema causes

Macular edema occurs when there is abnormal leakage and accumulation of fluid in the macula from damaged blood vessels in the nearby retina. A common cause of macular edema is diabetic retinopathy, a disease that can happen to people with diabetes. Macular edema can also occur after eye surgery, in association with age-related macular degeneration, or as a consequence of inflammatory diseases that affect the eye. Any disease that damages blood vessels in the retina can cause macular edema.

Figure 4. Macula

Macular edema symptoms

The primary symptom of macular edema is blurry or wavy vision near or in the center of your field of vision. Colors might also appear washed out or faded. Most people with macular edema will have symptoms that range from slightly blurry vision to noticeable vision loss. If only one eye is affected, you may not notice your vision is blurry until the condition is well-advanced.

Macular edema causes

Diabetic macular edema

Diabetic macular edema is caused by a complication of diabetes called diabetic retinopathy. Diabetic retinopathy is the most common diabetic eye disease and the leading cause of irreversible blindness in working age Americans. Diabetic retinopathy usually affects both eyes.

Diabetic retinopathy is caused by ongoing damage to the small blood vessels of the retina. The leakage of fluid into the retina may lead to swelling of the surrounding tissue, including the macula.

Diabetic macular edema is the most common cause of vision loss in people with diabetic retinopathy. Poor blood sugar control and additional medical conditions, such as high blood pressure, increase the risk of blindness for people with diabetic macular edema. Diabetic macular edema can occur at any stage of diabetic retinopathy, although it is more likely to occur later as the disease goes on.

Experts estimate that approximately 7.7 million Americans have diabetic retinopathy and of those, about 750,000 also have diabetic macular edema. A recent study suggests that non-Hispanic African Americans are three times more likely to develop diabetic macular edema than non-Hispanic whites, most likely due to the higher incidence of diabetes in the African American population.

Eye surgery

Macular edema may develop after any type of surgery that is performed inside the eye, including surgery for cataract, glaucoma, or retinal disease. A small number of people who have cataract surgery (experts estimate only 1-3 percent) may develop macular edema within a few weeks after surgery. If one eye is affected, there is a 50 percent chance that the other eye will also be affected. Macular edema after eye surgery is usually mild, short-lasting, and responds well to eye drops that treat inflammation.

Age-related macular degeneration

Age-related macular degeneration (AMD) is a disease characterized by deterioration or breakdown of the macula, which is responsible for sharp, central vision. In neovascular age-related macular degeneration, also called “wet” age-related macular degeneration, blood vessels begin to grow up from the choroid (the bed of blood vessels below the retina) and into the retina. These new and abnormal blood vessels leak fluid into the macula and cause macular edema.

Blockage of retinal blood vessels

When retinal veins are blocked (retinal vein occlusion), blood does not drain properly and it leaks into the retina. If it leaks into the macula, this produces macular edema. Leakage is worsened by the severity of the blockage, how many veins are involved, and the pressure inside them. Retinal vein occlusion is most often associated with age-related atherosclerosis, diabetes, high blood pressure, and eye conditions such as glaucoma or inflammation.

Inflammatory diseases that affect the retina

Uveitis describes a group of inflammatory diseases that cause swelling in the eye and destroy eye tissues. The term “uveitis” is used because the diseases most often affect a part of the eye called the uvea. However, uveitis is not limited to the uvea. Uveitis can affect the cornea, iris, lens, vitreous, retina, optic nerve, and the white of the eye (sclera).

Inflammatory diseases and disorders of the immune system may also affect the eye and cause swelling and breakdown of tissue in the macula. These disorders include cytomegalovirus infection, retinal necrosis, sarcoidosis, Behçet’s syndrome, toxoplasmosis, Eales’ disease, and Vogt-Koyanagi-Harada syndrome.

Macular edema diagnosis

To diagnose macular edema, your eye care professional will conduct a thorough eye exam and look for abnormalities in the retina. The following tests may be done to determine the location and extent of the disease:

• Visual acuity test. A visual acuity test is a common way to identify vision loss and can help to diagnose vision loss as a result of macular edema. This test uses a standardized chart or card with rows of letters that decrease in size from top to bottom. Covering one eye, you will be asked to read out loud the smallest line of letters that you can see. When done, you will test the other eye.
• Dilated eye exam. A dilated eye exam is used to more thoroughly examine the retina. It gives additional information about the condition of the macula and helps detect the presence of blood vessel leakage or cysts. Drops are placed in your eyes to widen, or dilate, your pupils. Your eye care professional then examines your retina for signs of damage or disease.
• Fluorescein angiogram. If earlier tests indicate you could have macular edema, your eye care professional may perform a fluorescein angiogram. In this test, a special dye is injected into your arm and a camera takes photos of the retina as the dye travels through the blood vessels. This test helps your ophthalmologist identify the amount of damage to the macula.
• Optical coherence tomography. This is a test that uses a special light and a camera for detailed views of the cell layers inside the retina. It detects the thickness of the retina and so it’s useful in determining the amount of swelling in the macula. Your eye care professional may also use optical coherence tomography after your treatment to track how well you are healing.
• The Amsler Grid. The Amsler Grid provides an easy way to test whether or not your central vision has changed. It can recognize even small changes in your vision. If you need reading glasses, wear them when you look at the Amsler grid. The grid should be at the same distance from your eyes as your usual reading material – about 14 inches. Test both eyes, one at a time, to see if any parts of the grid look distorted, missing, or dark. Mark the areas of the chart that you’re not seeing properly and bring it with you to your next eye exam.

Figure 5. Amsler grid

Macular edema treatment

Treatment for macular edema is determined by the type of macular edema you have. The most effective treatment strategies first aim at the underlying cause of macular edema, such as diabetes or high blood pressure, and then directly treat the damage in the retina.

Treatments for diabetic macular edema and macular edema caused by other conditions are often the same. However, some cases of macular edema may need additional treatments to address associated conditions.

In the recent past, the standard treatment for macular edema was focal laser photocoagulation, which uses the heat from a laser to seal leaking blood vessels in the retina. However, recent clinical trials, have led doctors to move away from laser therapy to drug treatments injected directly into the eye.

Anti-VEGF injections

The current standard of care for macular edema is intravitreal injection. During this painless procedure, numbing drops are applied to the eye, and a short thin needle is used to inject medication into the vitreous gel (the fluid in the center of the eye). The drugs used in this treatment –Avastin, Eylea, and Lucentis – block the activity of a substance called vascular endothelial growth factor (VEGF). VEGF promotes blood vessel growth. In a healthy eye, this is not a problem. But in some conditions, the retina becomes starved for blood and vascular endothelial growth factor (VEGF) becomes overactive. This causes the growth of fragile blood vessels which can rupture and leak blood into the retina and macula, causing macular edema. Anti-VEGF treatment blocks the activity of vascular endothelial growth factor (VEGF) and slows the progress of macular edema.

The anti-VEGF drugs all work in similar ways to block vessel formation and prevent leakage in the retina. A recent clinical trial that directly compared the effectiveness of the three drugs for diabetic macular edema found that the drugs performed similarly for patients with mild vision problems. However, Eylea performed better for those with more serious vision loss (20/50 or worse). Your eye care professional will discuss which drug treatment is the best option for you.

Anti-inflammatory treatments

Corticosteroid (steroid) treatments, which reduce inflammation, are the primary treatment for macular edema caused by inflammatory eye diseases. These anti-inflammatory drugs are usually administered via eye drops, pills, or injections of sustained-release corticosteroids into or around the eye. Clinicians now have the option of three FDA-approved sustained-release corticosteroid implants for more serious or longer-lasting conditions:

• Ozurdex is an implant that delivers an extended release dose of dexamethasone. It is approved for diabetic macular edema, macular edema following retinal vein occlusion, and [non-infectious] uveitis.
• Retisert is an implant that delivers an extended release dose of fluocinolone acetonide. It is approved for the treatment of uveitis, as well as diabetic macular edema that doesn’t respond to corticosteroids.
• Iluvien is an implant that releases small doses of fluocinolone acetonide over the course of several years. The U.S. Food and Drug Administration has approved it for treating diabetic macular edema.

Nonsteroidal anti-inflammatory drugs (NSAIDs), in the form of eye drops, are sometimes used either before or after cataract surgery to prevent the development of macular edema. Because they are chemically different from corticosteroids, NSAIDs may be used when the eye doesn’t respond to steroid treatment or to avoid the side-effects of steroid use in the eye.

Vitrectomy

Some cases of macular edema are caused when the vitreous (the gel that fills the area between the lens and the retina) pulls on the macula. Surgery to remove the vitreous gel, called a vitrectomy, relieves the pulling on the macula. Vitrectomy also may be required to remove blood that has collected in the vitreous or to correct vision when other treatments for macular edema are unsuccessful. Most vitrectomy surgeries are performed as outpatient surgery.

Corneal edema

The cornea makes up the front wall of the eye. It is normally clear. It helps focus the light entering the eye. Normally, the cells lining the inside of the cornea (endothelial cells) help maintain a healthy balance of fluids within the cornea and prevent the cornea from swelling. Corneal edema or swelling of the cornea is usually a complication following cataract surgery, but it can also be caused by glaucoma. The incidence of unobvious descemet’s membrane detachment in a seemingly uncomplicated cataract surgery is approximately 47% ⁴, however, those of clinical significance vary between 0.044% and 0.5% in phacoemulsification ⁵. Corneal edema can lead to glare, cloudy blurred vision and eye discomfort. The risk factors predisposing a patient to develop an intraoperative descemet membrane detachment are shallow anterior chamber, suboptimal quality of the operating instruments, hard nuclear cataracts, misdirected stream of fluid, or viscoelastic that gains entry into the space between the stroma and descemet membrane ⁶.

What is glaucoma?

Glaucoma is a disease that damages your eye’s optic nerve. It usually happens when fluid builds up in the front part of your eye. That extra fluid increases the pressure in your eye, damaging the optic nerve. Glaucoma is a leading cause of blindness for people over 60 years old. But blindness from glaucoma can often be prevented with early treatment.

Your eye constantly makes aqueous humor. As new aqueous flows into your eye, the same amount should drain out. The fluid drains out through an area called the drainage angle. This process keeps pressure in the eye (called intraocular pressure or IOP) stable. But if the drainage angle is not working properly, fluid builds up. Pressure inside the eye rises, damaging the optic nerve.

The optic nerve is made of more than a million tiny nerve fibers. It is like an electric cable made up of many small wires. As these nerve fibers die, you will develop blind spots in your vision. You may not notice these blind spots until most of your optic nerve fibers have died. If all of the fibers die, you will become blind.

Some people have a higher than normal risk of getting glaucoma. This includes people who:

• are over age 40
• have family members with glaucoma
• are of African or Hispanic heritage
• have high eye pressure
• are farsighted or nearsighted
• have had an eye injury
• have corneas that are thin in the center
• have thinning of the optic nerve
• have diabetes, migraines, poor blood circulation or other health problems affecting the whole body

Talk with an ophthalmologist about your risk for getting glaucoma. People with more than one of these risk factors have an even higher risk of glaucoma.

Types of glaucoma

There are two major types of glaucoma.

Primary open-angle glaucoma

This is the most common type of glaucoma. It happens gradually, where the eye does not drain fluid as well as it should (like a clogged drain). As a result, eye pressure builds and starts to damage the optic nerve. This type of glaucoma is painless and causes no vision changes at first.

Some people can have optic nerves that are sensitive to normal eye pressure. This means their risk of getting glaucoma is higher than normal. Regular eye exams are important to find early signs of damage to their optic nerve.

Angle-closure glaucoma (also called “closed-angle glaucoma” or “narrow-angle glaucoma”)

This type happens when someone’s iris is very close to the drainage angle in their eye. The iris can end up blocking the drainage angle. You can think of it like a piece of paper sliding over a sink drain. When the drainage angle gets completely blocked, eye pressure rises very quickly. This is called an acute attack. It is a true eye emergency, and you should call your ophthalmologist right away or you might go blind.

Here are the signs of an acute angle-closure glaucoma attack:

• Your vision is suddenly blurry
• You have severe eye pain
• You have a headache
• You feel sick to your stomach (nausea)
• You throw up (vomit)
• You see rainbow-colored rings or halos around lights

Many people with angle-closure glaucoma develop it slowly. This is called chronic angle-closure glaucoma. There are no symptoms at first, so they don’t know they have it until the damage is severe or they have an attack.

Angle-closure glaucoma can cause blindness if not treated right away.

Glaucoma symptoms

Open-angle glaucoma

With open-angle glaucoma, there are no warning signs or obvious symptoms in the early stages. As the disease progresses, blind spots develop in your peripheral (side) vision.

Most people with open-angle glaucoma do not notice any change in their vision until the damage is quite severe. This is why glaucoma is called the “silent thief of sight.” Having regular eye exams can help your ophthalmologist find this disease before you lose vision. Your ophthalmologist can tell you how often you should be examined.

Angle-closure glaucoma

People at risk for angle-closure glaucoma usually show no symptoms before an attack. Some early symptoms of an attack may include blurred vision, halos, mild headaches or eye pain. People with these symptoms should be checked by their ophthalmologist as soon as possible. An attack of angle-closure glaucoma includes the following:

• severe pain in the eye or forehead
• redness of the eye
• decreased vision or blurred vision
• seeing rainbows or halos
• headache
• nausea
• vomiting

Normal tension glaucoma

People with “normal tension glaucoma” have eye pressure that is within normal ranges, but show signs of glaucoma, such as blind spots in their field of vision and optic nerve damage.

Glaucoma suspects

Some people have no signs of damage but have higher than normal eye pressure (called ocular hypertension). These patients are considered “glaucoma suspects” and have a higher risk of eventually developing glaucoma. They should be carefully monitored by an ophthalmologist.

Corneal edema symptoms

The patients usually present with diminution of vision in the immediate postoperative period with a lack of expected gain in quality of vision. This may be associated with raised intraocular pressure and hence symptoms pertaining to the same may be present. In addition, pain, photophobia (sensitivity to light), watering, congestion may be present to variable degree due to corneal edema and associated inflammation.

A long-standing corneal edema may be associated in the initial stages with bullae and the rupture of the same may lead to severe photophobia and pain.

Glaucoma diagnosis

The only sure way to diagnose glaucoma is with a complete eye exam. A glaucoma screening that only checks eye pressure is not enough to find glaucoma.

During a glaucoma exam, your ophthalmologist will:

• measure your eye pressure
• inspect your eye’s drainage angle
• examine your optic nerve for damage
• test your peripheral (side) vision
• take a picture or computer measurement of your optic nerve
• measure the thickness of your cornea

Glaucoma treatment

Glaucoma damage is permanent—it cannot be reversed. But medicine and surgery help to stop further damage. To treat glaucoma, your ophthalmologist may use one or more of the following treatments.

Medication

Glaucoma is usually controlled with eyedrop medicine. Used every day, these eye drops lower eye pressure. Some do this by reducing the amount of aqueous fluid the eye makes. Others reduce pressure by helping fluid flow better through the drainage angle.

Glaucoma medications can help you keep your vision, but they may also produce side effects. Some eye drops may cause:

• a stinging or itching sensation
• red eyes or red skin around the eyes
• changes in your pulse and heartbeat
• changes in your energy level
• changes in breathing (especially if you have asthma or breathing problems)
• dry mouth
• blurred vision
• eyelash growth
• changes in your eye color, the skin around your eyes or eyelid appearance.

All medications can have side effects. Some drugs can cause problems when taken with other medications. It is important to give your doctor a list of every medicine you take regularly. Be sure to talk with your ophthalmologist if you think you may have side effects from glaucoma medicine.

Never change or stop taking your glaucoma medications without talking to your ophthalmologist. If you are about to run out of your medication, ask your ophthalmologist if you should have your prescription refilled.

Laser surgery

There are two main types of laser surgery to treat glaucoma. They help aqueous drain from the eye. These procedures are usually done in the ophthalmologist’s office or an outpatient surgery center.

• Trabeculoplasty. This surgery is for people who have open-angle glaucoma. The eye surgeon uses a laser to make the drainage angle work better. That way fluid flows out properly and eye pressure is reduced.
• Iridotomy. This is for people who have angle-closure glaucoma. The ophthalmologist uses a laser to create a tiny hole in the iris. This hole helps fluid flow to the drainage angle.

Operating room surgery

Some glaucoma surgery is done in an operating room. It creates a new drainage channel for the aqueous humor to leave the eye.

• Trabeculectomy. This is where your eye surgeon creates a tiny flap in the sclera (white of your eye). He or she will also create a bubble (like a pocket) in the conjunctiva called a filtration bleb. It is usually hidden under the upper eyelid and cannot be seen. Aqueous humor will be able to drain out of the eye through the flap and into the bleb. In the bleb, the fluid is absorbed by tissue around your eye, lowering eye pressure.
• Glaucoma drainage devices. Your ophthalmologist may implant a tiny drainage tube in your eye. It sends the fluid to a collection area (called a reservoir). Your eye surgeon creates this reservoir beneath the conjunctiva (the thin membrane that covers the inside of your eyelids and white part of your eye). The fluid is then absorbed into nearby blood vessels.

Corneal edema treatment

Treatment of corneal edema, is based on the underlying cause of the condition. Most commonly, the endothelial cells responsible for pumping fluid out of the cornea are damaged. In glaucoma, the intraocular pressure needs to be reduced. In inflammatory conditions, the inflammation needs to be treated. Hypertonic saline drops or ointment can temporarily help reduce swelling of the cornea. In patients where the edema builds up overnight, some doctors recommend using a hair dryer to blow air on the eyes to increase evaporation of tears, and thus reduce the swelling of the cornea.

Descemet’s stripping automated endothelial keratoplasty, or DSAEK, is currently the standard surgical treatment for patients who have visually significant corneal edema not responsive to medical therapy.

Medical management

Medical management includes the use of hypertonic agents, such as sodium chloride 5% eye drops or 6% ointment. These drugs create a hypertonic tear film that draws water out of the edematous cornea. In author’s experience, ointment formulation is more effective than the solution form. Applying ointment at night may significantly reduce the early morning symptoms. Hypertonic agents may lead to irritation in some cases, and they may not be that effective in reducing the stromal edema. Hypertonic saline can lead to resolution of corneal edema in almost one-third of patients, especially in early cases, but the treatment may have to be continued for 3 months ⁷.

Bandaged contact lenses, especially extended-wear hydrophilic contact lenses are useful in reducing pain associated with epithelial bullae ⁷. A thin, high water content lens is suitable in these cases as the oxygen permeability is better in these lenses. It must be remembered that it does not lead to any reduction in epithelial or stromal edema. They act by creating an effective precorneal protective layer that shields the swollen epithelium from the lid movement and prevents the rupture of bullae ⁸.

Hydrophilic extended-wear contact lenses along with hypertonic saline drops can be used to create a hypertonic reservoir. This reservoir continuously bathes the cornea, providing corneal deturgescence for a relatively longer period. Bandaged contact lenses is especially useful in cases where the patient is symptomatic owing to rupture of bullae ⁷. Considering the potential risk of infection, prolonged use of bandaged contact lenses is discouraged, and a broad-spectrum antibiotic must be used along with these lenses ⁷.

One important thing to remember is that associated abnormalities such as raised intraocular pressure or inflammation should be looked for and managed simultaneously.

Raised intraocular pressure can be managed with topical antiglaucoma medications or surgical options such as trabeculectomy with mitomycin C or a glaucoma drainage implant in cases not controlled with topical therapy. Lowering the intraocular pressure not only improves the corneal edema but also prevents further damage to endothelium. Although any class of anti-glaucoma can be useful two groups of drugs, carbonic anhydrase inhibitors and Prostaglandin analogues must be avoided ⁹. Inhibition of corneal endothelial carbonic anhydrase pumps can lead to decreased fluid flow from stroma to aqueous, resulting in precipitation of corneal edema. Prostaglandin analogues, theoretically, can flare up the intraocular inflammation ⁹.

Associated inflammation must be treated with topical steroids. It is better to avoid using steroids at a higher frequency since associated problems like raise in intraocular pressure may further delay clearing of corneal edema ¹⁰.

Surgical management

The presence of descemet’s membrane detachment in the immediate postoperative phase requires surgical intervention in the form of intracameral air or gas injection ⁴. Most of the other surgical options such as anterior stromal puncture, amniotic membrane, conjunctival flap, phototherapeutic keratectomy, corneal collagen cross-linking, endothelial keratoplasty and penetrating keratoplasty are reserved for delayed onset or persistent corneal edema due to irreversible corneal endothelial damage ¹¹.

Spontaneous reattachment is commonly seen in planar and nonscrolled descemet membrane detachment within days after surgery ¹². It has been reported by Mackool and Holtz ¹³ that intervention is often required in cases of extensive, central, nonplanar descemet’s membrane detachment with scrolled or torn edges. Assia et al. ¹⁴ suggested that nonplanar and nonscrolled descemet’s membrane detachments could reattach even if the separation between the descemet’s membrane and stroma was >1 mm.

Descemetopexy

Sparks ¹⁵ first described this procedure in three eyes with extensive descemet membrane detachments. Several studies have reported successful anatomical and visual outcomes with this procedure ¹⁶. Three major tamponade agents used are air, 15%–20% SF6 and 12%–14% C3F8. Due to the fast absorption of air, SF6 and C3F8 are the preferred agents ¹⁷.

The major complication reported is pupillary block (7.7%), which can be prevented and managed with the use of cycloplegics, prophylactic laser iridotomy, oral and topical antiglaucoma drugs, or a partial fill of anterior chamber with air or gas ¹⁸.

Another concern with the use of long-acting gases is the corneal endothelial toxicity, which has been reported, in animal studies ¹⁹.

Figure 6. Structure of the cornea (human eye)

Figure 7. Corneal edema

Peripheral edema

Lymphoedema is a long-term (chronic) condition that causes swelling in the body’s tissues. It can affect any part of the body, but usually develops in the arms or legs.

It develops when the lymphatic system doesn’t work properly. The lymphatic system is a network of channels and glands throughout the body that helps fight infection and remove excess fluid.

It’s important that lymphoedema is identified and treated as soon as possible. If it isn’t treated, it can get worse.

Lymphoedema is thought to affect more than 200,000 people in the US. Primary lymphoedema is rare and is thought to affect around 1 in every 6,000 people. Secondary lymphoedema is much more common.

Secondary lymphoedema affects around 2 in 10 women with breast cancer, and 5 in 10 women with vulval cancer. About 3 in every 10 men with penile cancer get lymphoedema.

People who have treatment for melanoma in the lymph nodes in the groin can also get lymphoedema. Research has shown around 20-50% of people are affected.

Your treatment team will let you know if you’re at risk of getting lymphoedema from your cancer or cancer treatment. Any planned treatment you have will try to avoid causing damage to your lymph nodes.

Lymphoedema symptoms

The main symptom of lymphoedema is swelling in all or part of a limb or another part of the body. It can be difficult to fit into clothes, and jewellery and watches can feel tight.

At first, the swelling may come and go. It may get worse during the day and go down overnight. Without treatment, it will usually become more severe and persistent.

Other symptoms in an affected body part can include:

• an aching, heavy feeling
• difficulty with movement
• repeated skin infections
• hard, tight skin
• folds developing in the skin
• wart-like growths developing on the skin
• fluid leaking through the skin

Lymphoedema complications

Cellulitis is the most common complication of lymphoedema. It can also have a significant psychological impact.

Cellulitis

If you have lymphoedema, the build-up of fluid in your tissues makes you more vulnerable to infection.

Cellulitis is a bacterial infection of the deep layer of skin (dermis) that often affects people with lymphoedema. Cellulitis can also sometimes cause lymphoedema.

Symptoms of cellulitis can include:

• redness and a feeling of heat in the skin
• pain and increased swelling in the affected area
• a high temperature (fever)
• chills

Antibiotics taken by mouth (orally) can usually be used to treat cellulitis, although severe cases may need to be treated in hospital with antibiotics given directly into a vein (intravenously).

Psychological impact

Living with a long-term condition that affects your appearance can cause a great deal of distress and lead to periods of depression.

You may be depressed if you’ve been feeling down for the past few months and no longer find pleasure in things you usually enjoy.

If this is the case, talk to your doctor or a member of your lymphoedema treatment team. Effective treatments are available for depression.

Talking to other people with lymphoedema can be reassuring and decrease feelings of isolation, stress and anxiety.

Lymphoedema causes

Lymphoedema is caused by a problem with the lymphatic system, a network of vessels and glands spread throughout the body. The main functions of the lymphatic system are helping fight infection and draining excess fluid from tissues.

There are two main types of lymphoedema:

1. Primary lymphoedema – caused by faulty genes that affect the development of the lymphatic system; it can develop at any age, but usually starts during infancy, adolescence, or early adulthood
2. Secondary lymphoedema – caused by damage to the lymphatic system or problems with the movement and drainage of fluid in the lymphatic system; it can be the result of an infection, injury, cancer treatment, inflammation of the limb, or a lack of limb movement

Primary lymphoedema

Primary lymphoedema is caused by alterations (mutations) in genes responsible for the development of the lymphatic system.

The “faulty” genes cause the parts of the lymphatic system responsible for draining fluid to not develop properly or not work as they should.

Primary lymphoedema often runs in families, although not every child born to someone with the condition will develop it themselves.

Secondary lymphoedema

Secondary lymphoedema develops in people who previously had a normal lymphatic system that then becomes damaged.

It can have a number of different causes. Some of the most common causes are explained below.

Surgery for cancer

Treatment for cancer can involve surgery to remove sections of the lymphatic system.

The surgeon will try to limit damage to your lymphatic system, although this isn’t always possible. There’s a particular risk of lymphoedema occurring after treatment for any cancer where lymph glands are removed.

Some of the more common cancers where this happens are:

• breast cancer
• melanoma skin cancer
• gynaecological cancers – such as cervical cancer and vulval cancer
• genitourinary cancers – such as prostate cancer or penile cancer

Radiotherapy

Radiotherapy uses controlled doses of high-energy radiation to destroy cancerous tissue, but it can also damage healthy tissue.

If radiotherapy is needed to destroy cancerous cells in your lymphatic system, there’s a risk that the lymphatic system could become permanently damaged and unable to drain fluid properly.

Infections

An infection, such as cellulitis, can sometimes cause lymphoedema. Severe cellulitis can damage the tissue around the lymphatic system, causing it to become scarred.

Filariasis is another infectious cause of lymphoedema. Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms.

The adult worms only live in the human lymphatic system and block lymph drainage. It’s a common cause of lymphoedema worldwide, but it isn’t generally a risk in the US.

Inflammation

Medical conditions that cause tissue to become red and swollen can also permanently damage the lymphatic system.

Conditions that can cause lymphoedema include:

• rheumatoid arthritis – causes pain and swelling in the joints
• eczema – causes the skin to become itchy, reddened, dry and cracked

Venous diseases

Diseases that affect the flow of blood through the veins can cause lymphoedema in some people.

The abnormal or damaged veins can cause fluid to overflow from the veins into the tissue spaces. This overwhelms and eventually exhausts the parts of the lymphatic system responsible for draining this fluid.

Some venous diseases that can lead to lymphoedema include:

• deep vein thrombosis (DVT) – a blood clot in one of the deep veins in the body
• swollen and enlarged veins (varicose veins) – where poor drainage of blood in the veins causes higher vein pressure and more fluid overflowing into the surrounding tissues

Obesity

Obesity is another possible cause of secondary lymphoedema. People who are obese, particularly those who are severely obese, have an increased risk of developing swollen body parts.

It’s not clear exactly why this is, but it’s been suggested that the extra fatty tissue affects the lymphatic channels in some way, reducing the flow of fluid through them.

In these cases, weight loss is an important part of treatment and even just starting to lose weight can make a big difference to the swelling.

Trauma and injury

In a small number of cases, lymphoedema can be caused by an accidental injury to the lymphatic system.

For example, it can sometimes occur after a road traffic accident where there’s extensive bruising or soft tissue loss.

Immobility

Movement and exercise help lymph drainage because muscle activity surrounding the lymphatic vessels massages fluid into and along them.

Reduced movement can therefore lead to lymphoedema because the fluid in the lymphatic system doesn’t get moved along.

For example, people who have limited mobility for a long period of time as a result of an illness, nerve damage or arthritis may be at risk of lymphoedema.

Lymphoedema prevention

It’s not possible to completely prevent lymphoedema, but the following advice may help reduce your chances of developing it.

If you already have lymphoedema, this advice may stop it getting worse.

Skin care

The part of your body affected by lymphoedema is more vulnerable to infection of the build-up of fluid within the tissues.

Any cuts in your skin can allow bacteria to enter your body and may quickly develop into an infection.

Skin infections can also damage your lymphatic system and cause lymphoedema to develop.

You can reduce your chances of developing skin infections by:

• not having injections or blood pressure readings in the affected area whenever possible
• treating cuts and scratches immediately with an antiseptic cream
• using insect repellents to prevent insect bites
• moisturising the skin daily to keep it supple – your doctor can prescribe a suitable cream
• avoiding very hot baths and showers – the heat from saunas, steam rooms and sun beds may increase the swelling
• using broadspectrum sunscreen cream with a high sun protection factor (SPF) to prevent sunburn
• wearing gloves for gardening and household tasks to avoid cuts if your upper limbs are affected
• using anti-fungal powder to prevent fungal infections in your skin or feet if your lower limbs are affected
• cutting your nails with nail clippers
• seeing a chiropodist for foot and nail care – make sure you tell them you have lymphoedema
• wearing shoes that fit correctly and provide support on the top of your feet if your lower limbs are affected
• using an electric razor if you need to shave to reduce the risk of cutting yourself
• not wearing tight-fitting clothes or jewellery

Contact your doctor as soon as possible if you develop symptoms of a possible skin infection, such as redness and a feeling of heat in the skin.

Healthy lifestyle

Adopting a healthy lifestyle may help reduce your risk of developing lymphoedema, and may also help control the condition if you already have it.

This includes:

• eating a healthy, balanced diet
• maintaining a healthy weight – use the healthy weight calculator to work out whether you’re a healthy weight for your height
• exercising regularly

Lymphoedema diagnosis

If you’re being treated for cancer and are at risk of developing lymphoedema, you’ll be monitored for the condition afterwards. Otherwise, see your GP if you experience symptoms of swelling.

In many cases, it’s possible to diagnose lymphoedema by:

• asking about your symptoms and medical history
• examining the affected limb and measuring the distance around it to see if it’s enlarged

Your doctor may refer you to a specialist lymphoedema treatment centre for further assessment.

Further tests

In most cases, further tests aren’t necessary, but they may occasionally be used to assess and monitor your condition.

Measuring limb volume

In some cases, tests to calculate the volume of an affected limb may be carried out.

These may include:

• using a tape measure – to measure the circumference of the limb at certain intervals to calculate its volume
• water displacement – where the affected limb is placed in a tank of water and the amount of water that’s displaced is measured to calculate the volume of the limb
• perometry – where infrared light is used to measure the outline of an affected limb and calculate its volume

Bioimpedance testing

During a bioimpedance test, small metallic discs called electrodes are placed on different parts of your body.

The electrodes release a small, painless electric charge that’s measured using a handheld device. Changes in the strength of the current can indicate the presence of fluid in your tissue.

Imaging tests

Imaging tests may also be used to help diagnose and monitor lymphoedema.

These include:

• a lymphoscintigram – where you’re injected with a radioactive dye that can be tracked using a special scanner; this shows how the dye moves through your lymphatic system and can check for any blockages
• a magnetic resonance imaging (MRI) scan – a strong magnetic field and radio waves are used to produce detailed images of the inside of your body
• an ultrasound scan – high-frequency sound waves are used to create an image of the inside of your body
• a computerised tomography (CT) scan – X-rays and a computer create detailed images of the lymph nodes

These scans can be used to create a clearer picture of the affected tissue.

Lymphoedema treatment

The recommended treatment for lymphoedema is decongestive lymphatic therapy.

Decongestive lymphatic therapy isn’t a cure for lymphoedema, but it can help control the symptoms. Although it takes time and effort, the treatment can be used to bring lymphoedema under control.

Decongestive lymphatic therapy

There are four components to decongestive lymphatic therapy:

• compression bandages – to complement exercise by moving fluid out of the affected limb and minimise further build-up
• skin care – to keep the skin in good condition and reduce the chances of infection
• exercises – to use muscles in the affected limb to improve lymph drainage
• specialised massage techniques – known as manual lymphatic drainage; this stimulates the flow of fluid in the lymphatic system and reduces swelling

Decongestive lymphatic therapy is an intensive phase of therapy, during which you may receive daily treatment for several weeks to help reduce the volume of the affected body part.

This is followed by a second phase called the maintenance phase. You’ll be encouraged to take over your care using simple self-massage techniques, wearing compression garments, and continuing to exercise.

This treatment phase aims to maintain the reduced size of the affected body part.

You’ll have reviews every few months to check how your treatment is progressing.

Compression bandages and garments

Unlike blood circulation, the lymphatic system has no central pump, such as the heart, to move fluid to the lymph glands.

Instead, it uses the massaging effect of surrounding muscles to move the fluid. This is why exercise is important.

Compression bandages or garments, such as sleeves, gloves, stockings or tights, fitted over affected limbs act as a counterforce to muscles.

This stimulates more effective lymph drainage. The combination of exercise and compression encourages the fluid to move out of the affected limb.

Compression garments may also be applied after a massage session to prevent fluid accumulating in the limb again.

Velcro wraps may be used instead of bandages or compression garments. These are easier to apply yourself.

You’ll be taught how to correctly apply compression garments or Velcro wraps so you can continue using them during the maintenance period.

Figure 8. Compression bandages and garments

Skin care

It’s important to take good care of your skin to reduce your risk of developing an infection, such as cellulitis.

Movement and exercises

Your lymphoedema care team will help devise an exercise and movement plan designed to strengthen and stimulate the muscles involved in lymph drainage.

They’ll also help you lose weight if you’re overweight. Your exercise plan will be tailored to your requirements and ability.

Your plan may involve specific limb exercises, as well as gentle activities that involve the whole body, such as swimming, cycling and walking.

Massage

To begin with, you may receive specialised massages called manual lymphatic drainage – usually carried out by a specialist therapist – to move fluid from the swollen areas into working lymph nodes, where it can be drained.

Your lymphoedema therapist will also teach you a range of simpler massage techniques that you or your carer can use during the maintenance phase of treatment to help keep the swelling down. These self-massage techniques are known as simple lymphatic drainage.

Surgery

In a small number of cases, surgery may be used to treat lymphoedema. There are three main types of surgery that may be useful for the condition:

• removal of sections of excess skin and underlying tissue (debulking)
• removal of fat from the affected limb (liposuction)
• restoration of the flow of fluid around the affected section of the lymphatic system – for example, by connecting the lymphatic system to nearby blood vessels (lymphaticovenular anastomosis)

These treatments may help reduce the size of areas of the body affected by lymphoedema, but some are still being evaluated – particularly lymphaticovenular anastomosis – and aren’t in widespread use.

Liposuction

The accumulation of fat is a significant feature of lymphoedema swelling. Liposuction is where a thin tube is inserted through small cuts (incisions) in the skin to suck fat out of tissue.

It can be used to remove excess fat from an affected limb to help reduce its size.

After surgery, you’ll have to wear a compression garment on the affected limb day and night for at least a year to help keep the swelling down.

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