pl. edemas pl. edemata [Gr. oidēma, swelling, tumor]
A local or generalized condition in which body tissues contain an excessive amount of tissue fluid in the interstitial spaces.
SYN: SEE: hydrops
SEE: anasarca; SEE: ascites; SEE: dropsy; SEE: hydrothorax; SEE: pericardial effusion

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EDEMA Edematous arm caused by subclavian vein stenosis
edematous (ĕ-dē′măt-ŭs), adj.

Edema may result from increased permeability of the capillary walls; increased capillary pressure caused by venous obstruction or heart failure; lymphatic obstruction; disturbances in renal function; reduction of plasma proteins; inflammatory conditions; fluid and electrolyte disturbances, esp. those causing sodium retention; malnutrition; starvation; or chemical substances such as bacterial toxins, venoms, caustics, and histamine. Diagnostic studies (thorough history, physical examination, urinalysis, serum chemistries and liver functions, thyroid function, and chest x-ray) help determine the cause and guide treatment.

Bed rest helps relieve lower extremity edema. Sitting with the feet and legs elevated may also reduce edema in the lower extremities. Dietary salt should be restricted to less than 2 g/day. Fluid intake may be restricted to about 1500 mL in 24 hr. This prescription may be relaxed when free diuresis has been attained. Diuretics relieve swelling when renal function is good and when any underlying abnormality of cardiac function, capillary pressure, or salt retention is being corrected simultaneously. Any effective diuretic may be used. Diuretics are contraindicated in preeclampsia and when serum potassium levels are very low (<3.0 mEq/dL). They may be ineffective in edema associated with advanced renal insufficiency. The diet in edema should be adequate in protein, high in calories, and rich in vitamins. Patients with significant edema should weigh themselves daily to gauge fluid loss or retention.

Edema is documented according to type (pitting, nonpitting, or brawny), extent, location, symmetry, and degree of pitting. Areas over bony prominences are palpated for edema by pressing with the fingertip for 5 sec, then releasing. Normally, the tissue should immediately rebound to its original contour; the depth of indentation is then measured and recorded. The patient is questioned about increased tightness of rings, shoes, waistlines of garments, and belts. Periorbital edema is assessed; abdominal girth and ankle circumference are measured; and the patient's weight and fluid intake and output are monitored. Fragile edematous tissues are protected from damage by careful handling and positioning and by providing and teaching about special skin care. Edematous extremities are mobilized and elevated to promote venous return, and lung sounds auscultated for evidence of increasing pulmonary congestion. Prescribed therapies, including sodium restriction, diuretics, angiotensin-converting enzyme inhibitors, protein replacement, and elastic stockings are provided, and the patient is instructed in their use.

angioneurotic edema

SEE: Angioedema.

Berlin edema

SEE: Commotio retinae.

brain edema

Swelling of the brain. Causes include increased permeability of brain capillary endothelial cells, focal strokes, swelling of brain cells associated with hypoxia or water intoxication, trauma to the skull, or interstitial edema due to obstructive hydrocephalus.
SYN: SEE: brain swelling; SEE: cerebral edema

edema bullosum vesicae

Edema affecting the bladder.

cardiac edema

Edema caused by congestive heart failure. It is most apparent in the dependent portion of the body and/or the lungs.

cerebral edema

SEE: Brain edema.

dependent edema

Edema of the lower extremities or, if the patient is lying down, of the sacrum.

diabetic macular edema

Swelling of the macula of the retina resulting from leakage of fluids from damaged blood vessels in the eye. It is a major cause of loss of vision in diabetics and is related to poor control of blood glucose.

edema of the glottis

Pathological edema in the tissues lining the vocal structures of the larynx. It may result from improper use of the voice, excessive use of tobacco or alcohol, chemical fumes, or viral, bacterial, or fungal infections. Clinically, the patient often presents with hoarseness or, in severe cases, with respiratory distress and stridor.
SEE: epiglottitis

Initially, hoarseness and, later, complete aphonia characterize this condition. Other symptoms are extreme dyspnea, at first on inspiration only, but later also on expiration; stridor; and a barking cough when the epiglottis is involved.

high-altitude pulmonary edema

ABBR: HAPE Pulmonary edema that may occur in aviators, mountain climbers, or anyone exposed to decreased atmospheric pressure.
SEE: hypoxia

inflammatory edema

Edema associated with inflammation. The cause is assumed to be damage to the capillary endothelium. It is usually nonpitting and localized, red, tender, and warm.

laryngeal edema

Edema of the larynx, usually resulting from an allergic reaction and causing airway obstruction unless treated. Therapy consists of intravenous or intratracheal epinephrine, emergency tracheostomy, or both.

malignant edema

Rapid destruction of tissue by cutaneous or subcutaneous infections, such as anthrax or by clostridial species.

negative pressure pulmonary edema

Pulmonary edema occurring in a patient with upper airway obstruction and negative intrapleural pressures, e.g., in a child with epiglottitis.

edema neonatorum

Edema in newborn, esp. premature, infants. This condition is usually transitory, involving the hands, face, feet, and genitalia; it rarely becomes generalized.

pitting edema

Evidence of fluid in soft tissues, esp. those of dependent body parts like the lower extremities. When pressed firmly with a finger, tissues that are swollen with extravascular fluid retain the shape of the depression produced by the finger.

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PITTING EDEMA Demonstration of pitting edema

post-traumatic edema

SEE: Traumatic edema.

pretibial edema

Edema of the lower leg anterior to the shin (the tibia).

pulmonary edema

A potentially life-threatening edema in the interstitium and alveoli of the lungs. The collected fluid may block the exchange of oxygen and carbon dioxide and produce respiratory failure.

Fluid may seep out of the alveolar capillaries if these blood vessels are damaged and become excessively permeable to liquids (noncardiogenic pulmonary edema) or if hydrostatic pressures within blood vessels exceed the strength of the normal alveolar capillary wall (cardiogenic pulmonary edema). Cardiogenic pulmonary edema can result from any condition that compromises left ventricular function, causing elevations in pulmonary venous, and capillary hydrostatic pressures (congestive heart failure), including myocardial infarction, ischemia, or myocardial stunning; severe valvular heart disease; arrhythmias; excessive intravenous fluid administration; and diastolic dysfunction.

Noncardiogenic pulmonary edema usually results from blood vessel injury, as happens in the adult respiratory distress syndrome (sepsis, shock, aspiration pneumonia, airway obstruction). Occasionally, protein-rich fluid floods the lungs from drug exposure (such as heroin overdose), hypoalbuminemia, high-altitude exposure (mountain sickness), fresh water aspiration in near drowning, hemorrhage in or around the brain, or other conditions. Pulmonary edema can occur as a chronic or acute condition.

Chronic symptoms of heart failure include dyspnea or exertion, nocturnal dyspnea, orthopnea, and cough. When pulmonary edema develops rapidly, patients experience a rapid onset of shortness of breath and suffocation and often demonstrate labored, noisy breathing; cough producing frothy, bloody sputum; gasping; anxiety; palpitations; and altered mental status caused by inadequate oxygenation. Signs of the condition include a rapid respiratory rate, heaving of the chest and abdomen, intercostal muscle retractions, diffuse crackles on lung examination, and, often, cold, clammy skin with diaphoresis and cyanosis. Tachycardia, jugular vein distention, and a diastolic (S3) gallop occur. As cardiac output decreases, the pulse becomes thready, and blood pressure falls. Pulmonary artery catheterization helps identify left-sided failure (elevated pulmonary wedge pressures), and arterial blood gases show hypoxia. Profound respiratory alkalosis occurs when patients hyperventilate when trying to increase their oxygenation; acidosis may occur with respiratory fatigue and failure. To improve the movement of air into and out of the chest, the patient will often sit upright to breathe and resist lying down.

Patients who are short of breath and who have pulmonary rales, low oxygen saturation rates, and/or a history of heart disease should have a chest x-ray taken urgently, to see if they may have characteristic findings of pulmonary edema on radiography. These findings include an enlarged heart shadow, central congestion, and pulmonary effusions. The diagnosis of acute pulmonary edema can be aided by evidence of an elevated beta natriuretic peptide (BNP), or the results of echocardiography, although these tests are usually not required to establish the diagnosis. In patients who do not have a history of heart disease or acute cardiac decompensation, noncardiogenic pulmonary edema may present as dyspnea, rales, and impaired oxygenation without cardiomegaly or a reduction in cardiac ejection fraction.

In the patient with known heart failure, adherence to one's medical regimen and dietary restrictions can prevent episodic pulmonary edema.

Oxygen (in high concentrations by cannula, face mask, or nonrebreather mask) should be administered immediately. Assisted ventilation (continuous positive airway pressure, noninvasive pressure support ventilation, or intubation with mechanical ventilation) may be needed to reach acceptable levels of PaO2 and improve acid-base balance. Morphine sulfate, nitrate vasodilators (IV nitroglycerin or nitroprusside), and loop diuretics are typically given to patients with cardiogenic pulmonary edema to improve dyspnea, alter preload and afterload on the heart, and promote diuresis. Angiotensin-converting enzyme inhibitors, inotropic drugs (digoxin), antiarrhythmic agents, beta-adrenergic blockers, human B-type natriuretic peptide (BNP), and phosphodiesterase inhibitors may be used in selected circumstances. Bronchodilators may also be administered. Depending on the underlying cause, invasive interventions may occasionally include coronary angiography, intra-aortic balloon pump therapy, or surgical interventions such as coronary artery revascularization or valve repair, or ventricular assist device therapy.

The outlook is good if the condition is stabilized or reversed with treatment.

The patient's head is elevated, and his or her respirations and ventilatory effort are assessed. Oxygen is administered as prescribed, with care taken to limit the flow rate in patients whose respiratory drive is compromised. The lungs are auscultated for adventitious breath sounds such as crackles, gurgles, and wheezes, and the heart is assessed for apical rate and gallops. The patient is monitored for a cough productive of pink, frothy sputum. The skin is checked for diaphoresis and pallor or cyanosis. A medication history is collected, esp. for the use of cardiac or respiratory drugs and recreational drugs. The patient's cardiac rate and rhythm, blood pressure, and oxygen saturation levels are monitored continuously. An IV line administering normal saline solution is inserted at a keep-vein-open rate to provide access for medication administration. Prescribed first-line drug therapy is administered, and the patient's response to the drugs is evaluated. IV morphine slows respirations, improves hemodynamics, and reduces anxiety. It should be administered before initiating continuous positive air pressure (CPAP). CPAP improves oxygenation and decreases cardiac workload, thus decreasing the need for intubation and ventilation with positive end-expiratory pressure. An indwelling urinary catheter is inserted to monitor the patient's fluid status; diuresis should begin within 30 min of administration of an IV loop diuretic. Pulmonary edema is a life-threatening respiratory emergency. Everyone involved with the patient must remain calm and quiet, provide ongoing reassurance, and validate everything occurring through basic and simply understood explanations. After the crisis resolves, health care providers should discuss with the patient his or her feelings about the episode and give a thorough explanation of what occurred. The at-risk patient is taught to recognize early warning signs to act on immediately (such as weight gain or increasing peripheral edema), in an effort to recognize and prevent future episodes. Medications and dietary and lifestyle restrictions are explained (low-sodium diet, weight loss, smoking cessation), and written information provided for home review. The patient should be encouraged to enroll in a cardiac rehabilitation program (as applicable) for regular exercise tailored to his or her condition.

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PULMONARY EDEMA This radiograph is consistent with mild noncardiogenic interstitial pulmonary edema. Note the elevation of the left hemidiaphragm resulting from subsegmental atelectasis.
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PULMONARY EDEMA This radiograph is consistent with noncardiogenic pulmonary edema with probable right-sided pleural effusion.

purulent edema

Edema caused by a local collection of pus.

reexpansion pulmonary edema

ABBR: RPE, REPE Alveolar flooding that occurs after a collapsed or trapped lung reinflates, e.g., after the draining of a pleural effusion or the evacuation of a pneumothorax.

Reinke edema

SEE: Reinke edema

salt-induced edema

A form of edema worsened by excess sodium in the diet.

traumatic edema

Tissue swelling occurring after blunt or penetrating injury.
SYN: SEE: post-traumatic edema