Iron Poisoning

Large amounts of ferrous salts are toxic, but fatalities in adults are rare. Most deaths occur in children, particularly between the ages of 12 and 24 months. As little as 1-2 g of iron may cause death, but 2-10 g usually is ingested in fatal cases. The frequency of iron poisoning relates to its availability in the household, particularly the supply that remains after a pregnancy. The colored sugar coating of many of the commercially available tablets gives them the appearance of candy. All iron preparations should be kept in childproof bottles.

Signs and symptoms of severe poisoning may occur within 30 minutes after ingestion or may be delayed for several hours. They include abdominal pain, diarrhea, or vomiting of brown or bloody stomach contents containing pills. Of particular concern are pallor or cyanosis, lassitude, drowsiness, hyperventilation due to acidosis, and cardiovascular collapse. The corrosive injury to the stomach may result in pyloric stenosis or gastric scarring. Hemorrhagic gastroenteritis and hepatic damage are prominent findings at autopsy. In the evaluation of a child thought to have ingested iron, a color test for iron in the gastric contents and an emergency determination of the concentration of iron in plasma can be performed. If the latter is <63 mm (3.5 mg/L), the child is not in immediate danger. However, vomiting should be induced when there is iron in the stomach, and an x-ray should be taken to evaluate the number of radio-opaque pills remaining in the small bowel. When the plasma concentration of iron exceeds the total iron-binding capacity (63 mm; 3.5 mg/L), deferoxamine should be administered (see Chapter 65). Shock, dehydration, and acid-base abnormalities should be treated in the conventional manner. Most important is the speed of diagnosis and therapy. With early effective treatment, the mortality from iron poisoning can be reduced from as high as 45% to ~1%.

therapy with parenteral iron When oral iron therapy fails, parenteral iron administration may be an effective alternative. Common indications are iron malabsorption (e.g., sprue, short bowel syndrome), severe intolerance of oral iron, as a routine supplement to total parenteral nutrition, and in patients who are receiving erythropoietin. Parenteral iron also has been given to iron-deficient patients and pregnant women to create iron stores, something that would take months to achieve by the oral route. Parenteral iron therapy should be used only when clearly indicated, since acute hypersensitivity, including anaphylactic reactions, can occur. The belief that the response to parenteral iron, especially iron dextran, is faster than oral iron is open to debate. In otherwise healthy individuals, the rate of Hb response is determined by the balance between the severity of the anemia (the level of erythropoietin stimulus) and the delivery of iron to the marrow from iron absorption and iron stores. When a large intravenous dose of iron dextran is given to a severely anemic patient, the hematologic response can exceed that seen with oral iron for 1-3 weeks. Subsequently, the response is no better than that seen with oral iron.

FDA-approved preparations for parenteral therapy include sodium ferric gluconate complex in sucrose (ferrlecit), iron sucrose (venofer), and iron dextran (infed, dexferrum). Unlike iron dextran, which requires macrophage processing that may require several weeks, ~80% of sodium ferric gluconate is delivered to transferrin with 24 hours. Sodium ferric gluconate has a much lower risk of serious anaphylactic reactions than iron dextran.

Iron dextran injection (infed, dexferrum) is a colloidal solution of ferric oxyhydroxide com-plexed with polymerized dextran (molecular weight ~180 kDa) that contains 50 mg/mL of elemental iron. It can be administered by either intravenous (preferred) or intramuscular injection. When given by deep intramuscular injection, it is gradually mobilized via the lymphatics and transported to reticuloendothelial cells; the iron then is released from the dextran complex. Intravenous administration gives a more reliable response. Given intravenously in a dose of less than 500 mg, the iron dextran complex is cleared with a plasma t1/2 of 6 hours. When 1 g or more is administered intravenously as total dose therapy, reticuloendothelial cell clearance is constant at 10—20 mg/h. This slow rate of clearance results in a brownish discoloration of the plasma for several days and an elevation of the serum iron for 1—2 weeks.

Intramuscular injection of iron dextran should only be initiated after a test dose of 0.5 mL (25 mg of iron). If no adverse reactions are observed, the injections can proceed. The daily dose ordinarily should not exceed 0.5 mL (25 mg of iron) for infants weighing less than 4.5 kg (10 lb), 1 mL (50 mg of iron) for children weighing less than 9 kg (20 lb), and 2 mL(100 mg of iron) for other patients. Iron dextran should be injected only into the muscle mass of the upper outer quadrant of the buttock using a z-track technique (displacement of the skin laterally before injection).

A test injection of 0.5 mL of undiluted iron dextran or an equivalent amount (25 mg of iron) diluted in saline also should precede intravenous administration of a therapeutic dose of iron dex-tran. The patient should be observed for signs of immediate anaphylaxis, and for an hour after injection for any signs of vascular instability or hypersensitivity, including respiratory distress, hypotension, tachycardia, or back or chest pain. When widely spaced, total-dose infusion therapy is given, a test dose injection should be given before each infusion because hypersensitivity can appear at any time. The patient should be monitored closely throughout the infusion for signs of cardiovascular instability. Delayed hypersensitivity reactions also are observed, especially in patients with rheumatoid arthritis or a history of allergies. Fever, malaise, lymphadenopathy, arthralgias, and urticaria can develop days or weeks following injection and last for prolonged periods of time. Therefore, iron dextran should be used with extreme caution in patients with rheumatoid arthritis or other connective tissue diseases, and during the acute phase of an inflammatory illness. once hypersensitivity is documented, iron dextran therapy must be abandoned.

When hemodialysis patients are started on erythropoietin, oral iron therapy alone generally is insufficient to guarantee an optimal Hb response. It therefore is recommended that sufficient parenteral iron be given to maintain a plasma ferritin level between 100 and 800 mg/L and a transferrin saturation of 20—50%. One approach is to administer an initial intravenous dose of 200—500 mg, followed by weekly or every-other-week injections of 25—100 mg of iron dextran to replace ongoing blood loss. With repeated doses of iron dextran—especially multiple, total-dose infusions such as those sometimes used in the treatment of chronic GI blood loss—accumulations of slowly metabolized iron dextran stores in reticuloendothelial cells can be impressive. The plasma ferritin level also can rise to levels associated with iron overload. While disease-related hemochromatosis has been associated with an increased risk of infections and cardiovascular disease, this has not been shown to be true in hemodialysis patients treated with iron dextran. It seems prudent, however, to withhold the drug if the plasma ferritin exceeds 800 mg/L.

Reactions to intravenous iron include headache, malaise, fever, generalized lymphadenopathy, arthralgias, urticaria, and in some patients with rheumatoid arthritis, exacerbation of the disease. Phlebitis may occur with prolonged infusions of a concentrated solution or when an intramuscular preparation containing 0.5% phenol is used in error. Of greatest concern is the rare anaphy-lactic reaction, which may be fatal despite treatment.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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