What is compounding?
Drug compounding is often regarded as the process of combining or mixing drugs to create a medication tailored to the needs of an individual patient.
The generic form of Vetmedin is Pimobendan.
Vetmedin is in limited supply. Orders placed will be shipped as product continues to come off backorder.
Aminocaproic Acid is used in the treatment of bleeding due to fibrinolysis. It is also used to treat bleeding episodes in patients with certain medical conditions such as aplastic anemia, cirrhosis of the liver, placenta abruptio and urinary bleeding.
Aminocaproic acid is a man-made form of a protein that occurs naturally in the body. This protein is responsible for blood clotting. Aminocaproic acid works as a synthetic inhibitor of the plasmin-plasminogen system. This aminocaproic acid prevents the breakdown of clots and stops excessive bleeding.
Aminocaproic Acid Injection, is useful in enhancing hemostasis when fibrinolysis contributes to bleeding. In life-threatening situations, fresh whole blood transfusions, fibrinogen infusions, and other emergency measures may be required.
Fibrinolytic bleeding may frequently be associated with surgical complications following heart surgery (with or without cardiac bypass procedures), and portacaval shunt; hematological disorders such as aplastic anemia; acute and life-threatening abruptio placentae; hepatic cirrhosis; and neoplastic disease such as carcinoma of the prostate, lung, stomach, and cervix.
Urinary fibrinolysis, usually a normal physiological phenomenon, may frequently be associated with life-threatening complications following severe trauma, anoxia, and shock. Symptomatic of such complications is surgical hematuria (following prostatectomy and nephrectomy) or nonsurgical hematuria (accompanying polycystic or neoplastic diseases of the genitourinary system).
Aminocaproic Acid Injection, USP is administered by infusion, utilizing the usual compatible intravenous vehicles (eg., Sterile Water for Injection, Sodium Chloride for Injection, 5% Dextrose or Ringer's Injection). Although Sterile Water for Injection is compatible with intravenous injection, the resultant solution is hupo-osmolar. RAPID INJECTION OF AMINOCAPROIC ACID INJECTION UNDILUTED INTO A VEIN IS NOT RECOMMENDED.
For the treatment of acute bleeding syndromes due to elevated fibrinolytic activity, it is suggested that 16 to 20 mL (4 to 5 g) of aminocaproic acid in 250 mL of diluent be administered by infusion during the first hour of treatment, followed by a continuous infusion at the rate of 4 mL (1 g) per hour in 50 mL of diluent. This method of treatment would ordinarily be continued for about 8 hours or until the bleeding situation has been controlled.
Parenteral drug products should be inspected visually for particulate matter and discoloration before administration, whenever solution and container permit. Do not administer unless the solution is clear and the seal is intact. Discard unused portion.
Aminocaproic acid should not be used when there is evidence of an active intravascular clotting process.
When there is uncertainty as to whether the cause of bleeding is primary fibrinolysis or disseminated intravascular coagulation (DIC), this distinction must be made before administering Aminocaproic Acid Injection.
The following tests can be applied to differentiate the two conditions:
Aminocaproic Acid Injection must not be used in the presence of DIC without concomitant heparin.
In patients with upper urinary tract bleeding, aminocaproic acid administration has been known to cause intrarenal obstruction in the form of glomerular capillary thrombosis or clots in the renal pelvis and ureters. For this reason, Aminocaproic Acid Injection, USP should not be used in hematuria of upper urinary tract origin, unless the possible benefits outweigh the risk.
Subendocardial hemorrhages have been observed in dogs given intravenous infusions of 0.2 times the maximum human therapeutic dose of aminocaproic acid and in monkeys given 8 times the maximum human therapeutic dose of aminocaproic acid.
Fatty degeneration of the myocardium has been reported in dogs given intravenous doses of aminocaproic acid at 0.8 to 3.3 times the maximum human therapeutic dose and in monkeys given intravenous doses of aminocaproic acid at 6 times the maximum human therapeutic dose.
Rarely, skeletal muscle weakness with necrosis of muscle fibers has been reported following prolonged administration. Clinical presentation may range from mild myalgias with weakness and fatigue to a severe proximal myopathy with rhabdomyolysis, myoglobinuria, and acute renal failure. Muscle enzymes, especially creatine phosphokinase (CPK) are elevated. CPK levels should be monitored in patients on long-term therapy. Aminocaproic Acid Injection administration should be stopped if a rise in CPK is noted. The resolution follows discontinuation of Aminocaproic Acid Injection; however, the syndrome may recur if Aminocaproic Acid Injection is restarted.
The possibility of cardiac muscle damage should also be considered when skeletal myopathy occurs. One case of cardiac and hepatic lesions observed in man has been reported. The patient received 2g of aminocaproic acid every 6 hours for a total dose of 26g. Death was due to continued cerebrovascular hemorrhage. Necrotic changes in the heart and liver were noted at autopsy.
A few cases of acute overdosage with Aminocaproic Acid Injection administered intravenously have been reported. The effects have ranged from no reaction to transient hypotension to severe acute renal failure leading to death. One patient with a history of brain tumor and seizures experienced seizures after receiving an 8-gram bolus injection of Aminocaproic Acid Injection. The single dose of Aminocaproic Acid Injection causing symptoms of overdosage or considered to be life-threatening is unknown. Patient have tolerated doses as high as 100 grams while acute renal failure has been reported following a dose of 12 grams.
The intravenous and oral LD50 of aminocaproic acid were 3 and 12 g/kg respectively, in the mouse and 3.2 and 16.4 g/kg respectively in the rat. An intravenous infusion dose of 2.3 g/kg was lethal in the dog. On intravenous administration, tonic-clonic convulsions were observed in dogs and mice.
No treatment for overdosage is known, although evidence exists that aminocaproic acid is removed by hemodialysis and may be removed by peritoneal dialysis. Pharmacokinetic studies have shown that total body clearance of aminocaproic acid is markedly decreased in patients with severe renal failure.