Drug-induced edema refers to the disturbance of humoral balance caused by the clinical application of certain drugs. Body fluids stay in the interstitial spaces and there is swelling in the body or in the body. Mainly manifested as edema of the lower extremities or the face, and even severe systemic edema.
Clinically found that drug-induced edema is not uncommon, some drugs can dilate vascular smooth muscle, increase vascular permeability; or cause water and sodium retention, resulting in lower extremity edema. It is characterized by edema that occurs after medication and disappears shortly after discontinuation.
Types of drug-induced edema can be divided into: drug-induced renal edema, drug-induced cardiogenic edema, drug-induced allergic edema, drug-induced hepatic edema, drug-induced pulmonary edema, drug-induced cerebral edema, and drug-induced mucinous edema Wait.
I. Drugs that cause edema
This type of drug-induced edema is common in the face and lower extremities. It is slightly depressed edema, but also can be expressed as systemic edema, mostly accompanied by central obesity, hirsutism, acne, skin purple lines, high blood sugar, high blood pressure, low blood Potassium and other symptoms can generally disappear after drug withdrawal.
Mineralocorticoids cause edema by promoting reabsorption of sodium ions in the distal tubules. Glucocorticoids have a weak mineralocorticoid-like effect and can also cause edema by promoting protein breakdown and lowering plasma colloidal osmotic pressure.
2. Antihypertensive drugs:
Beta-blockers reduce cardiac output, renal blood flow, and glomerular filtration rate, increase secretion of renin and aldosterone, and cause sodium and sodium retention. Alpha-receptor antagonists (such as prazosin) and direct vasodilators (such as hydralazine) can cause fluid retention.
Angiotensin II receptor antagonists and angiotensin converting enzyme inhibitors cause lower incidence of lower extremity edema, but can also cause angioedema.
Therefore, long-term use of diuretics, vasoactive drugs, etc. should be gradually reduced the amount of withdrawal, so as not to trigger a sudden withdrawal caused by edema.
3. Calcium channel blockers:
As the inhibition of myocardial and vascular smooth muscle transmembrane calcium inflow to expand blood vessels, such as nifedipine, amlodipine and verapamil, etc., edema is characterized by light morning and afternoon weight, common in the double ankle, a few can be Occurs in the face or other areas. Use of diuretics can relieve symptoms but cannot cure them. Generally, they disappear gradually after drug withdrawal. Older blood vessels are less dense and more prone to occur.
4. Antidiabetic drugs:
The use of this type of drug-induced edema occurs in the control of poor diabetes, insulin treatment stage, common in the face and lower extremity edema, severe cases can affect the body, mostly transient, self-limiting. Generally, the higher the blood glucose level before treatment, the faster the blood glucose level drops after the use of insulin, and the greater the possibility of causing edema or the earlier the time.
Edema is also a common adverse reaction caused by thiazolidinedione insulin sensitizers, usually mild to moderate peripheral edema, most with weight gain, combined with sulfonylurea or metformin when the adverse reaction symptoms increased significantly, with Patients with insulin use or heart disease have the highest rates.
5. Non-steroidal anti-inflammatory drugs:
3% to 5% of patients who use non-steroidal anti-inflammatory drugs may have nerve endings edema. The use of indomethacin and phenylbutazone is more common and is commonly seen in limb edema.
Selective inhibition of the NSAIDs of cyclooxygenase-2, such as rofecismus, has a greater risk of triggering water salt retention, hypertension, and worsening congestive heart failure.
NSAID can also cause angioneurotic edema, mucosal edema and other allergic reactions. Salicylates are prone to cause non-cardiogenic pulmonary edema in the case of poisoning, and a few can cause brain edema, which occurs mostly in elderly, smokers, and long-term aspirin patients.
NSAIDs interfere with prostaglandin (PG) biosynthesis by inhibiting COX activity. PG in the kidney is related to the metabolism of water and salts. Insufficient secretion of PG by drugs can reduce the renal blood flow, reduce the glomerular filtration rate, and increase the sodium reabsorption and cause edema.
NSAID causes kidney damage, which can be expressed as sodium and water retention, edema, often mild or subclinical, usually occurs in the first week after treatment, and can return to normal after drug withdrawal.
6. Immunosuppressive agents:
Sirolimus can cause facial edema; growth hormone occasionally presents with temporary facial, surrounding mild to moderate edema, mostly occurring at the beginning of treatment. Certain drugs inhibit iodine uptake by the thyroid gland, inhibit thyroid hormone synthesis and secretion, inhibit T4 conversion to T3 in the surrounding tissue, or cause hypothyroidism through immune mechanisms, leading to mucinous edema, common drugs such as anti-thyroid drugs, paraaminopris Sodium and so on.
7. Anti-tumor drugs:
Imatinib, sorafenib, dasatinib, panitumumab, lenalidomide, etc. can cause peripheral edema.
Some drugs combine with the protein in the body in the form of hapten to form the whole antigen, which stimulates plasma cells to produce IgE antibodies. When these drugs are contacted again, the antigen binds to IgE, which causes mast cells to release allergenic substances, causing smooth muscle spasm and microvascular dilation of target organs. Vascular wall permeability increases, plasma extravasation leads to edema.
9. Chinese herbal medicine:
The long-term use of Chinese herbs such as licorice and ginseng can cause water and sodium retention in the body and cause edema. The mechanism is that the active ingredients such as glycyrrhizin and glycyrrhetinic acid contained in licorice have adrenocortical hormone-like effects and cause edema.
II. Treatment measures after edema
1. Renal function tests should be performed on edema, including urea nitrogen, serum creatinine, ultrasound examination of kidney size, renal cortex thickness or effective renal blood flow, 24h urine volume, glomerular filtration rate, etc. If the test is normal, then Should actively look for other possible reasons. Confirmed by the drug caused by edema, once a clear diagnosis, should first stop the drug, mild edema and more on their own after the withdrawal of withdrawal.
The following principles should be followed when using glucocorticoids: minimum effective dose; every other day; short-range impact medication; try local medication instead of systemic medication; if using NSAID is effective, do not use hormones. In addition, when a large number of hormone therapy is used, physiological saline should be avoided as a vehicle to reduce the occurrence of hypokalemia, high sodium, and edema. The edema caused by glucocorticoids should not be stopped immediately. It should be gradually reduced so as not to cause the primary disease to rebound.
2. For edema, limiting sodium intake is the basic measure for treating edema. If the edema is obvious, a small dose of diuretic can be used.
3. For drugs that cause sodium water retention should be used with caution in patients with heart failure, liver dysfunction and kidney disease to avoid causing edema or aggravating heart failure.
4. Drugs damage the edema caused by heart, lung, kidney, and liver. In addition to stopping the medication and applying diuretics, appropriate measures should be taken to improve organ function and eliminate edema.