Calcium therapy intravenous

The basis of the treatment of fluoride poisoning is intravenous or intramuscular calcium therapy [61,62]. 

Dalton BR, Zuege DJ, Shahpori R, Laupland KB. Concomitant ceftriaxone and high-concentration intravenous calcium therapy in adult critical care patients a matched cohort study. Aim Pharmacother 2010 44(7-8) 1158-63. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

For women whose breast cancer has metastasized to bone, bisphosphonates are recommended, in addition to chemotherapy or endocrine therapy, to reduce bone pain and fractures.28,64 Pamidronate (90 mg) and zoledronate (4 mg) can be given intravenously once each month. These bisphosphonates are given in combination with calcium and vitamin D. 

Several uses have been suggested for levulinic acid and its salts. Thus, calcium levulinate seems to have advantages as a calcium carrier in tuberculosis therapy, and it is said to be more suitable than calcium gluconate for intravenous injection. A mercury salt, phenyl mercury... 

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. 

Because of its toxicity, plicamycin (mithramycin) is not the drug of first choice for the treatment of hypercalcemia. However, when other forms of therapy fail, 25-50 mcg/kg given intravenously usually lowers serum calcium substantially within 24-48 hours. This effect can last several days. This dose can be repeated as necessary. The most dangerous toxic effect is sudden thrombocytopenia followed by hemorrhage. Hepatic and renal toxicity can also occur. Hypocalcemia, nausea, and vomiting may limit therapy. Use of this drug must be accompanied by careful monitoring of platelet counts, liver and kidney function, and serum calcium levels. 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

Acetylsalicylic acid is usually given by oral administration (0.5-8 g/day) for pain and inflammation and for antiplatelet therapy (75-100 mg/day). It is also available in rectal and topical formulations and as a soluble lysine derivative for intravenous or intramuscular application. Acetylsalicylic acid is often used in multi-drug preparations. The main side-effects are gastrointestinal disorders. Use in children is limited due to the risk of Reye s syndrome (Waldmann et al., 1982). The lithium, magnesium, calcium, and aluminium salts of acetylsalicylic acid are used in some special preparations. 

Adverse respiratory effects are uncommon with calcium channel blockers. However, three cases of acute broncho-spasm accompanied by urticaria and pruritus have been reported in patients taking verapamil (51), and a patient with Duchenne-type muscular dystrophy developed respiratory failure during intravenous verapamil therapy for supraventricular tachycardia (52). Recurrent exarcer-bations of asthma occurred in a 66-year-old lady with hypertension and bronchial asthma given modified-release verapamil (53). 

All were successfully treated with hyperinsulinemia/ euglycemia therapy. The authors described the mechanism of action of this form of therapy, which is mainly related to improvement in cardiac contractility and peripheral vascular resistance and reversal of acidosis. They proposed indications and dosing for this therapy consisting in most cases of intravenous glucose with an intravenous bolus dose of insulin 1 U/kg followed by an infusion of 0.5-1 U/kg/hour until the systolic blood pressure is over 100 mm/Hg and the heart rate over 50/minute. Hyperinsulinemia/euglycemia therapy is currently reserved as an adjunct to conventional therapy and is recommended only after an inadequate response to fluid resuscitation, high-dose calcium salts, and pressor agents. 

Shackney S, Hasson J. Preciptious Fall In Serum Calcium, Hypotension, and Acute Renal Failure After Intravenous Phosphate Therapy for Hypercalcemia. Ann of Intern Med 1967 5 906-16. 

The nondihydropyridine calcium channel blockers, such as verapamil and diltiazem, have efficacy rates similar to that of adenosine, but are considered second line. Intravenous calcium channel blockers have a few disadvantages. In contrast to adenosine, caution should be taken in hypotensive patients. Adenosine may cause hypotension, but appears to be safe in patients who present with hypotension due to the short half-life. In addition, calcium channel blockers also should be used with caution in patients with systolic heart failure, patients receiving concurrent beta-blocker therapy, and in those with accessory pathways. 

Some TCA masks have been presented as chelated TCA. Chelation is a medical therapy that aims to detoxify the body of harmful minerals and metals. Chemically, chelation is the process by which an organic substance (the chelator) binds metal ions (iron, copper, lead, calcium, etc.) into inactive, non-toxic and water-soluble complexes that are easily eliminated in the urine. Intravenous chelation therapy (e.g. with ethylenediamine tetra acetic acid, EDTA) is often used to treat poisoning with heavy metals, including lead. The use of the term chelation therefore seems inappropriate as far as TCA is concerned, and has no chemical basis since TCA is not a metal. The little information available states that chelation reduces the speed of penetration of TCA and therefore its depth of action. Might what we call chelation be partial inactivation of the TCA The directions of use for Accu Peel state that a process called chelation allows the TCA to reach an even depth at the same time as using lower concentrations of TCA . Might chelation, on the contrary, be a process that activates the TCA But how can TCA be activated ... 

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