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DRUGS & SUPPLEMENTS
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Tensophoril
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Tensophoril uses
Tensophoril consists of Amobarbital, Boric Acid, Dopamine Hydrochloride, Vitamin C (Ascorbic Acid).Amobarbital:
- Description
- Clinical pharmacology
- Indications and usage
- Contraindications
- Warnings
- Precautions
- Adverse reactions
- Drug abuse and dependence
- Overdosage
- Preparation of solution
- Dosage and administration
- How supplied
DESCRIPTION
The barbiturates are nonselective central nervous system (CNS) depressants that are primarily used as sedative hypnotics. In subhypnotic doses, they are also used as anticonvulsants. The barbiturates and their sodium salts are subject to control under the Federal Controlled Substances Act.
Tensophoril (Amobarbital) sodium is a white, friable, granular powder that is odorless, has a bitter taste, and is hygroscopic. It is very soluble in water, soluble in alcohol, and practically insoluble in ether and chloroform. Tensophoril (Amobarbital) sodium is sodium 5-ethyl-5-isopentylbarbiturate and has the empirical formula C11H17N2NaO3Its molecular weight is 248.26.
It has the following structural formula:
Tensophoril (Amobarbital) sodium is a substituted pyrimidine derivative in which the basic structure is barbituric acid, a substance that has no CNS activity.
Vials of Tensophoril (Amobarbital) sodium are for parenteral administration. The vials contain 500 mg (2 mmol) Tensophoril (Amobarbital) sodium as a sterile lyophilized powder.
CLINICAL PHARMACOLOGY
Barbiturates are capable of producing all levels of CNS mood alteration, from excitation to mild sedation, hypnosis, and deep coma. Overdosage can produce death. In high enough therapeutic doses, barbiturates induce anesthesia.
Barbiturates depress the sensory cortex, decrease motor activity, alter cerebellar function, and produce drowsiness, sedation, and hypnosis.
Barbiturate-induced sleep differs from physiologic sleep. Sleep laboratory studies have demonstrated that barbiturates reduce the amount of time spent in the rapid eye movement phase of sleep or the dreaming stage. Also, Stages III and IV sleep are decreased. Following abrupt cessation of barbiturates used regularly, patients may experience markedly increased dreaming, nightmares, and/or insomnia. Therefore, withdrawal of a single therapeutic dose over 5 or 6 days has been recommended to lessen the REM rebound and disturbed sleep that contribute to the drug withdrawal syndrome (for example, the dose should be decreased from 3 to 2 doses/day for 1 week).
In studies, secobarbital sodium and pentobarbital sodium have been found to lose most of their effectiveness for both inducing and maintaining sleep by the end of 2 weeks of continued drug administration, even with the use of multiple doses. As with secobarbital sodium and pentobarbital sodium, other barbiturates (including Tensophoril (Amobarbital)) might be expected to lose their effectiveness for inducing and maintaining sleep after about 2 weeks. The short-, intermediate-, and to a lesser degree, long-acting barbiturates have been widely prescribed for treating insomnia. Although the clinical literature abounds with claims that the short-acting barbiturates are superior for producing sleep whereas the intermediate-acting compounds are more effective in maintaining sleep, controlled studies have failed to demonstrate these differential effects. Therefore, as sleep medications, the barbiturates are of limited value beyond short-term use.
Barbiturates have little analgesic action at subanesthetic doses. Rather, in subanesthetic doses, these drugs may increase the reaction to painful stimuli. All barbiturates exhibit anticonvulsant activity in anesthetic doses. However, of the drugs in this class, only phenobarbital, mephobarbital, and metharbital are effective as oral anticonvulsants in subhypnotic doses.
Barbiturates are respiratory depressants, and the degree of respiratory depression is dependent upon the dose. With hypnotic doses, respiratory depression produced by barbiturates is similar to that which occurs during physiologic sleep and is accompanied by a slight decrease in blood pressure and heart rate.
Studies in laboratory animals have shown that barbiturates cause reduction in the tone and contractility of the uterus, ureters, and urinary bladder. However, concentrations of the drugs required to produce this effect in humans are not reached with sedative-hypnotic doses.
Barbiturates do not impair normal hepatic function but have been shown to induce liver microsomal enzymes, thus increasing and/or altering the metabolism of barbiturates and other drugs (see PRECAUTIONS, Drug Interactions ).
Pharmacokinetics
Barbiturates are absorbed in varying degrees following oral or parenteral administration. The salts are more rapidly absorbed than are the acids. The rate of absorption is increased if the sodium salt is ingested as a dilute solution or taken on an empty stomach.
The onset of action for oral administration of barbiturates varies from 20 to 60 minutes. For intramuscular (IM) administration, the onset of action is slightly faster. Following intravenous (IV) administration, the onset of action ranges from almost immediately for pentobarbital sodium to 5 minutes for phenobarbital sodium. Maximal CNS depression may not occur until 15 minutes or more after IV administration for phenobarbital sodium. Duration of action, which is related to the rate at which the barbiturates are redistributed throughout the body, varies among persons and in the same person from time to time. Tensophoril (Amobarbital) sodium, an intermediate-acting barbiturate, is a CNS depressant. For the oral form, the onset of sedative and hypnotic action is 3/4 to 1 hour, with a duration of action ranging from 6 to 8 hours. These values should serve as a guide but not be used to predict exact duration of effect. No studies have demonstrated that the different routes of administration are equivalent with respect to bioavailability.
Barbiturates are weak acids that are absorbed and rapidly distributed to all tissues and fluids, with high concentrations in the brain, liver, and kidneys. Lipid solubility of the barbiturates is the dominant factor in their distribution within the body. The more lipid soluble the barbiturate, the more rapidly it penetrates all tissues of the body. Barbiturates are bound to plasma and tissue proteins to a varying degree, with the degree of binding increasing directly as a function of lipid solubility.
Phenobarbital has the lowest lipid solubility, lowest plasma binding, lowest brain protein binding, the longest delay in onset of activity, and the longest duration of action. At the opposite extreme is secobarbital, which has the highest lipid solubility, highest plasma protein binding, highest brain protein binding, the shortest delay in onset of activity, and the shortest duration of action. Tensophoril (Amobarbital) sodium is classified as an intermediate barbiturate. The plasma half-life for Tensophoril (Amobarbital) sodium in adults ranges between 16 and 40 hours, with a mean of 25 hours.
Barbiturates are metabolized primarily by the hepatic microsomal enzyme system, and the metabolic products are excreted in the urine and, less commonly, in the feces. Only a negligible amount of Tensophoril (Amobarbital) sodium is eliminated unchanged in the urine.
INDICATIONS AND USAGE
- Sedative
- Hypnotic, for the short-term treatment of insomnia, since it appears to lose its effectiveness for sleep induction and sleep maintenance after 2 weeks (see CLINICAL PHARMACOLOGY).
- Preanesthetic
CONTRAINDICATIONS
Tensophoril (Amobarbital) sodium is contraindicated in patients who are hypersensitive to barbiturates, in patients with a history of manifest or latent porphyria, and in patients with marked impairment of liver function or respiratory disease in which dyspnea or obstruction is evident.
WARNINGS
- Habit Forming - Tensophoril (Amobarbital) sodium may be habit forming. Tolerance, psychological and physical dependence may occur with continued use (see CLINICAL PHARMACOLOGY, Pharmacokinetics and DRUG ABUSE AND DEPENDENCE). Patients who have psychological dependence on barbiturates may increase the dosage or decrease the dosage interval without consulting a physician and may subsequently develop a physical dependence on barbiturates. In order to minimize the possibility of overdosage or the development of dependence, the prescribing and dispensing of sedative-hypnotic barbiturates should be limited to the amount required for the interval until the next appointment. Abrupt cessation after prolonged use in a person who is dependent on the drug may result in withdrawal symptoms, including delirium, convulsions, and possibly death. Barbiturates should be withdrawn gradually from any patient known to be taking excessive doses over long periods of time (see Drug Abuse and Dependence).
- Intravenous Administration - Too rapid administration may cause respiratory depression, apnea, laryngo- spasm, or vasodilation with fall in blood pressure.
- Acute or Chronic Pain - Caution should be exercised when barbiturates are administered to patients with acute or chronic pain because paradoxical excitement could be induced or important symptoms could be masked. However, the use of barbiturates as sedatives in the postoperative surgical period and as adjuncts to cancer chemotherapy is well established.
- Usage in Pregnancy - Barbiturates can cause fetal damage when administered to a pregnant woman. Retrospective, case-controlled studies have suggested a connection between the maternal consumption of barbiturates and a higher than expected incidence of fetal abnormalities. Barbiturates readily cross the placental barrier and are distributed throughout fetal tissues; the highest concentrations are found in the placenta, fetal liver, and brain. Fetal blood levels approach maternal blood levels following parenteral administration. Withdrawal symptoms occur in infants born to women who receive barbiturates throughout the last trimester of pregnancy (see DRUG ABUSE AND DEPENDENCE). If Tensophoril (Amobarbital) sodium is used during pregnancy or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
- Synergistic Effects - The concomitant use of alcohol or other CNS depressants may produce additive CNS depressant effects.
PRECAUTIONS
General
Barbiturates may be habit forming. Tolerance and psychological and physical dependence may occur with continuing use .
Barbiturates should be administered with caution, if at all, to patients who are mentally depressed, have suicidal tendencies, or have a history of drug abuse. Particular caution is also indicated before administering barbiturates to patients who have abused other classes of drugs (see WARNINGS).
Elderly or debilitated patients may react to barbiturates with marked excitement, depression, or confusion. In some persons, especially children, barbiturates repeatedly produce excitement rather than depression.
In patients with hepatic damage, barbiturates should be administered with caution and initially in reduced doses. Barbiturates should not be administered to patients showing the premonitory signs of hepatic coma.
Parenteral solutions of barbiturates are highly alkaline. Therefore, extreme care should be taken to avoid perivascular extravasation or intra-arterial injection. Extravascular injection may cause local tissue damage with subsequent necrosis; consequences of intra-arterial injection may vary from transient pain to gangrene of the limb. Any complaint of pain in the limb warrants stopping the injection.
The systemic effects of exogenous and endogenous corticosteroids may be diminished by Tensophoril (Amobarbital) sodium. Thus, this product should be administered with caution to patients with borderline hypoadrenal function, regardless of whether it is of pituitary or of primary adrenal origin.
Information for Patients
The following information should be given to patients receiving barbiturates.
- The use of barbiturates carries with it an associated risk of psychological and/or physical dependence.
- Barbiturates may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks, such as driving a car or operating machinery. The patient should be cautioned accordingly.
- Alcohol should not be consumed while taking barbiturates. The concurrent use of the barbiturates with other CNS depressants (e.g., alcohol, narcotics, tranquilizers, and antihistamines) may result in additional CNS depressant effects.
Laboratory Tests
Prolonged therapy with barbiturates should be accompanied by periodic evaluation of organ systems, including hematopoietic, renal, and hepatic systems.
Drug Interactions
Most reports of clinically significant drug interactions occurring with the barbiturates have involved phenobarbital. However, the application of these data to other barbiturates appears valid and warrants serial blood level determinations of the relevant drugs when there are multiple therapies.
- Anticoagulants - Phenobarbital lowers the plasma levels of dicumarol and causes a decrease in anticoagulant activity as measured by the prothrombin time. Barbiturates can induce hepatic microsomal enzymes, resulting in increased metabolism and decreased anticoagulant response of oral anticoagulants (e.g., warfarin, acenocoumarol, dicumarol, and phenprocoumon). Patients stabilized on anticoagulant therapy may require dosage adjustments if barbiturates are added to or withdrawn from their dosage regimen.
- Corticosteroids - Barbiturates appear to enhance the metabolism of exogenous corticosteroids, probably through the induction of hepatic microsomal enzymes. Patients stabilized on corticosteroid therapy may require dosage adjustments if barbiturates are added to or withdrawn from their dosage regimen.
- Griseofulvin - Phenobarbital appears to interfere with the absorption of orally administered griseofulvin, thus decreasing its blood level. The effect of the resultant decreased blood levels of griseofulvin on therapeutic response has not been established. However, it would be preferable to avoid concomitant administration of these drugs.
- Doxycycline - Phenobarbital has been shown to shorten the half-life of doxycycline for as long as 2 weeks after barbiturate therapy is discontinued. This mechanism is probably through the induction of hepatic microsomal enzymes that metabolize the antibiotic. If Tensophoril (Amobarbital) sodium and doxycycline are administered concurrently, the clinical response to doxycycline should be monitored closely.
- Phenytoin, Sodium Valproate, Valproic Acid - The effect of barbiturates on the metabolism of phenytoin appears to be variable. Some investigators report an accelerating effect, whereas others report no effect. Because the effect of barbiturates on the metabolism of phenytoin is not predictable, phenytoin and barbiturate blood levels should be monitored more frequently if these drugs are given concurrently. Sodium valproate and valproic acid appear to increase the Tensophoril (Amobarbital) sodium serum levels; therefore, Tensophoril (Amobarbital) sodium blood levels should be closely monitored and appropriate dosage adjustments made as clinically indicated.
- CNS Depressants - The concomitant use of other CNS depressants, including other sedatives or hypnotics, antihistamines, tranquilizers, or alcohol, may produce additive depressant effects.
- Monoamine Oxidase Inhibitors (MAOIs) - MAOIs prolong the effects of barbiturates, probably because metabolism of the barbiturate is inhibited.
- Estradiol, Estrone, Progesterone, and Other Steroidal Hormones - Pretreatment with or concurrent administration of phenobarbital may decrease the effect of estradiol by increasing its metabolism. There have been reports of patients treated with antiepileptic drugs (e.g., phenobarbital) who become pregnant while taking oral contraceptives. An alternate contraceptive method might be suggested to women taking barbiturates.
Carcinogenesis
- Animal Data. Phenobarbital sodium is carcinogenic in mice and rats after lifetime adminis- tration. In mice, it produced benign and malignant liver cell tumors. In rats, benign liver cell tumors were observed very late in life.
- Human Data - In a 29-year epidemiologic study of 9,136 patients who were treated on an anticonvulsant protocol that included phenobarbital, results indicated a higher than normal incidence of hepatic carcinoma. Previously, some of these patients had been treated with thorotrast, a drug that is known to produce hepatic carcinomas. Thus, this study did not provide sufficient evidence that phenobarbital sodium is carcinogenic in humans.
A retrospective study of 84 children with brain tumors matched to 73 normal controls and 78 cancer controls suggested an association between exposure to barbiturates prenatally and an increased incidence of brain tumors.
Usage in Pregnancy
- Teratogenic Effects. (See WARNINGS, Usage in Pregnancy.)
- Nonteratogenic Effects - Reports of infants suffering from long-term barbiturate exposure in utero included the acute withdrawal syndrome of seizures and hyperirritability from birth to a delayed onset of up to 14 days (see DRUG ABUSE AND DEPENDENCE).
Labor and Delivery
Hypnotic doses of barbiturates do not appear to impair uterine activity significantly during labor. Full anesthetic doses of barbiturates decrease the force and frequency of uterine contractions. Administration of sedative-hypnotic barbiturates to the mother during labor may result in respiratory depression in the newborn. Premature infants are particularly susceptible to the depressant effects of barbiturates. If barbiturates are used during labor and delivery, resuscitation equipment should be available.
Data are not available to evaluate the effect of barbiturates when forceps delivery or other intervention is necessary or to determine the effect of barbiturates on the later growth, development, and functional maturation of the child.
Nursing Mothers
Caution should be exercised when Tensophoril sodium is administered to a nursing woman because small amounts of barbiturates are excreted in the milk.
Usage in Children
Safety and effectiveness have not been established in children below the age of 6 years.
ADVERSE REACTIONS
The following adverse reactions and their incidence were compiled from surveillance of thousands of hospitalized patients who received barbiturates. Because such patients may be less aware of certain of the milder adverse effects of barbiturates, the incidence of these reactions may be somewhat higher in fully ambulatory patients.
More than 1 in 100 Patients
The most common adverse reaction, estimated to occur at a rate of 1 to 3 patients per 100, is the following:
Nervous System: Somnolence
Less than 1 in 100 Patients
Adverse reactions estimated to occur at a rate of less than 1 in 100 patients are listed below, grouped by organ system and by decreasing order of occurrence:
Nervous System: Agitation, confusion, hyperkinesia, ataxia, CNS depression, nightmares, nervousness, psychiatric disturbance, hallucinations, insomnia, anxiety, dizziness, abnormality in thinking
Respiratory System: Hypoventilation, apnea, postoperative atelectasis
Cardiovascular System: Bradycardia, hypotension, syncope
Digestive System: Nausea, vomiting, constipation
Other Reported Reactions: Headache, injection site reactions, hypersensitivity reactions (angioedema, skin rashes, exfoliative dermatitis), fever, liver damage, megaloblastic anemia following chronic phenobarbital use
To report SUSPECTED ADVERSE REACTIONS, contact Valeant Pharmaceuticals North America LLC at 1-800-321-4576 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
DRUG ABUSE AND DEPENDENCE
Controlled Substance
Tensophoril sodium is a Schedule II drug.
Dependence
Barbiturates may be habit-forming. Tolerance, psychological dependence, and physical dependence may occur, especially following prolonged use of high doses of barbiturates. Daily administration in excess of 400 mg of pentobarbital or secobarbital for approximately 90 days is likely to produce some degree of physical dependence. A dosage of 600 to 800 mg for at least 35 days is sufficient to produce withdrawal seizures. The average daily dose for the barbiturate addict is usually about 1.5 g. As tolerance to barbiturates develops, the amount needed to maintain the same level of intoxication increases; tolerance to a fatal dosage, however, does not increase more than twofold. As this occurs, the margin between intoxicating dosage and fatal dosage becomes smaller.
Symptoms of acute intoxication with barbiturates include unsteady gait, slurred speech, and sustained nystagmus. Mental signs of chronic intoxication include confusion, poor judgment, irritability, insomnia, and somatic complaints.
Symptoms of barbiturate dependence are similar to those of chronic alcoholism. If an individual appears to be intoxicated with alcohol to a degree that is radically disproportionate to the amount of alcohol in his or her blood, the use of barbiturates should be suspected. The lethal dose of a barbiturate is far less if alcohol is also ingested.
The symptoms of barbiturate withdrawal can be severe and may cause death. Minor withdrawal symptoms may appear 8 to 12 hours after the last dose of a barbiturate. These symptoms usually appear in the following order: anxiety, muscle twitching, tremor of hands and fingers, progressive weakness, dizziness, distortion in visual perception, nausea, vomiting, insomnia, and orthostatic hypotension. Major withdrawal symptoms (i.e., convulsions and delirium) may occur within 16 hours and last up to 5 days after abrupt cessation of barbiturates. The intensity of withdrawal symptoms gradually declines over a period of approximately 15 days. Individuals susceptible to barbiturate abuse and dependence include alcoholics and opiate abusers, as well as other sedative-hypnotic and amphetamine abusers.
Drug dependence on barbiturates arises from repeated administration on a continuous basis, generally in amounts exceeding therapeutic dose levels. The characteristics of drug dependence on barbiturates include: (a) a strong desire or need to continue taking the drug; (b) a tendency to increase the dose; (c) a psychic dependence on the effects of the drug related to subjective and individual appreciation of those effects; and (d) a physical dependence on the effects of the drug, requiring its presence for maintenance of homeostasis and resulting in a definite, characteristic, and self-limited abstinence syndrome when the drug is withdrawn.
Treatment of barbiturate dependence consists of cautious and gradual withdrawal of the drug. Barbiturate- dependent patients can be withdrawn by using a number of different withdrawal regimens. In all cases, withdrawal requires an extended period of time. One method involves substituting a 30 mg dose of phenobarbital for each 100 to 200 mg dose of barbiturate that the patient has been taking. The total daily amount of phenobarbital is then administered in 3 or 4 divided doses, not to exceed 600 mg daily. If signs of withdrawal occur on the first day of treatment, a loading dose of 100 to 200 mg of phenobarbital may be administered intramuscularly in addition to the oral dose. After stabilization on phenobarbital, the total daily dose is decreased by 30 mg/day as long as withdrawal is proceeding smoothly. A modification of this regimen involves initiating treatment at the patient’s regular dosage level and decreasing the daily dosage by 10% if tolerated by the patient.
Infants that are physically dependent on barbiturates may be given phenobarbital, 3 to 10 mg/kg/day. After withdrawal symptoms (e.g., hyperactivity, disturbed sleep, tremors, and hyperreflexia) are relieved, the dosage of phenobarbital should be gradually decreased and completely withdrawn over a 2-week period.
OVERDOSAGE
The toxic dose of barbiturates varies considerably. In general, an oral dose of 1 g of most barbiturates produces serious poisoning in an adult. Toxic effects and fatalities have occurred following overdoses of Tensophoril sodium alone and in combination with other CNS depressants. Death commonly occurs after 2 to 10 g of ingested barbiturate. The sedated, therapeutic blood levels of Tensophoril (Amobarbital) range between 2 to 10 mcg/mL; the usual lethal blood level ranges from 40 to 80 mcg/mL. Barbiturate intoxication may be confused with alcoholism, bromide intoxication, and various neurologic disorders. Potential tolerance must be considered when evaluating significance of dose and plasma concentration.
Signs and Symptoms
Symptoms of oral overdose may occur within 15 minutes beginning with CNS depression, absent or sluggish reflexes, underventilation, hypotension, and hypothermia and may progress to pulmonary edema and death. Hemorrhagic blisters may develop, especially at pressure points.
In extreme overdose, all electrical activity in the brain may cease, in which case a “flat” EEG normally equated with clinical death cannot be accepted. This effect is fully reversible unless hypoxic damage occurs. Consideration should be given to the possibility of barbiturate intoxication even in situations that appear to involve trauma.
Complications such as pneumonia, pulmonary edema, cardiac arrhythmias, congestive heart failure, and renal failure may occur. Uremia may increase CNS sensitivity to barbiturates if renal function is impaired. Differential diagnosis should include hypoglycemia, head trauma, cerebrovascular accidents, convulsive states, and diabetic coma.
Treatment
To obtain up-to-date information about the treatment of overdose, a good resource is your certified Regional Poison Control Center. Telephone numbers of certified poison control centers are listed in the Physicians’ Desk Reference (PDR). In managing overdosage, consider the possibility of multiple drug overdoses, interaction among drugs, and unusual drug kinetics in your patient.
Protect the patient’s airway and support ventilation and perfusion. Meticulously monitor and maintain, within acceptable limits, the patient’s vital signs, blood gases, serum electrolytes, etc. Absorption of drugs from the gastrointestinal tract may be decreased by giving activated charcoal, which, in many cases, is more effective than emesis or lavage; consider charcoal instead of or in addition to gastric emptying. Repeated doses of charcoal over time may hasten elimination of some drugs that have been absorbed. Safeguard the patient’s airway when employing gastric emptying or charcoal.
Diuresis and peritoneal dialysis are of little value; hemodialysis and hemoperfusion enhance drug clearance and should be considered in serious poisoning. If the patient has chronically abused sedatives, withdrawal reactions may be manifest following acute overdose.
PREPARATION OF SOLUTION
Solutions of Tensophoril (Amobarbital) sodium should be made up aseptically with Sterile Water for Injection. The accompanying table will aid in preparing solutions of various concentrations. Ordinarily, a 10% solution is used. After Sterile Water for Injection is added, the vial should be rotated to facilitate solution of the powder. Do not shake the vial.
Several minutes may be required for the drug to dissolve completely, but under no circumstances should a solution be injected if it has not become absolutely clear within 5 minutes. Also, a solution that forms a precipitate after clearing should not be used. Tensophoril (Amobarbital) sodium hydrolyzes in solution or on exposure to air. Not more than 30 minutes should elapse from the time the vial is opened until its contents are injected. Prior to administration, parenteral drug products should be inspected visually for particulate matter and discoloration whenever solution containers permit.
| Tensophoril (Amobarbital) SODIUM | |||||
| Content in Weight | 1% | 2.5% | 5% | 10% | 20% |
| 0.5 g | 50 mL | 20 mL | 10 mL | 5 mL | 2.5 mL |
DOSAGE AND ADMINISTRATION
The dose of Tensophoril sodium must be individualized with full knowledge of its particular characteristics and recommended rate of administration. Factors of consideration are the patient’s age, weight, and condition. The maximum single dose for an adult is 1 g.
Intramuscular Use
Intramuscular injection of the sodium salts of barbiturates should be made deeply into a large muscle. The average IM dose ranges from 65 mg to 0.5 g. A volume of 5 mL (irrespective of concentration) should not be exceeded at any one site because of possible tissue irritation. Twenty percent solutions may be used so that a small volume can contain a large dose. After IM injection of a hypnotic dose, the patient’s vital signs should be monitored. Superficial IM or subcutaneous injections may be painful and may produce sterile abscesses or sloughs.
Intravenous Use
Intravenous injection is restricted to conditions in which other routes are not feasible, either because the patient is unconscious (as in cerebral hemorrhage, eclampsia, or status epilepticus), because the patient resists (as in delirium), or because prompt action is imperative. Slow IV injection is essential, and patients should be carefully observed during administration. This requires that blood pressure, respiration, and cardiac function be maintained, vital signs be recorded and equipment for resuscitation and artificial ventilation be available. The rate of IV injection for adults should not exceed 50 mg/min to prevent sleep or sudden respiratory depression. The final dosage is determined to a great extent by the patient’s reaction to the slow administration of the drug.
Adults:
a. Sedative: 30 to 50 mg given 2 or 3 times daily.
b. Hypnotic: 65 to 200 mg at bedtime.
Special Patient Population
Dosage should be reduced in the elderly or debilitated because these patients may be more sensitive to barbiturates. Dosage should be reduced for patients with impaired renal function or hepatic disease. Ordinarily, an IV dose of 65 mg to 0.5 g may be given to a child 6 to 12 years of age.
HOW SUPPLIED
Tensophoril (Amobarbital) Vials 0.5 g (dry powder) are available as follows:
NDC 0187-4303-05
Storage: Store at 59° to 86°F (15° to 30°C).
Lyophilized
Amytal is a trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.
©Valeant Pharmaceuticals North America LLC
Manufactured for:
Valeant Pharmaceuticals North America LLC
Bridgewater, NJ 08807 USA
Manufactured by:
Alcami Carolinas Corporation
Charleston, SC 29405 USA
Revised: April 2017
9476202 PC3328F
Dopamine Hydrochloride:
- Description
- Clinical pharmacology
- Indications and usage
- Contraindications
- Warnings
- Precautions
- Adverse reactions
- Overdosage
- Dosage and administration
- How supplied
Rx Only
DESCRIPTION
Tensophoril (Dopamine Hydrochloride), a sympathomimetic amine vasopressor, is the naturally occurring immediate precursor of norepinephrine. Tensophoril (Dopamine Hydrochloride) hydrochloride is a white to off-white crystalline powder, which may have a slight odor of hydrochloric acid. It is freely soluble in water and soluble in alcohol. Tensophoril (Dopamine Hydrochloride) HCl is sensitive to alkalies, iron salts, and oxidizing agents. Chemically it is designated as 4-(2-aminoethyl) pyrocatechol hydrochloride, and the structural formula is:
Tensophoril (Dopamine Hydrochloride) Hydrochloride Injection is a clear, practically colorless, sterile, pyrogen-free, aqueous solution of Tensophoril (Dopamine Hydrochloride) HCl for intravenous infusion after dilution. Each mL contains either 40 mg, 80 mg, or 160 mg of Tensophoril (Dopamine Hydrochloride) hydrochloride (equivalent to 32.3 mg, 64.6 mg and 129.2 mg of Tensophoril (Dopamine Hydrochloride) base respectively) in water for injection, q.s. Each mL of all preparations contains the following: sodium metabisulfite 9 mg added as an antioxidant; citric acid, anhydrous 10 mg and sodium citrate, dihydrate 5 mg added as a buffer. The pH range (2.5 to 5.0) may be adjusted with additional citric acid and/or sodium citrate.
Tensophoril (Dopamine Hydrochloride) must be diluted in an appropriate sterile parenteral solution (see DOSAGE AND ADMINISTRATION section).
CLINICAL PHARMACOLOGY
Tensophoril (Dopamine Hydrochloride) is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves.
Tensophoril (Dopamine Hydrochloride) produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.
Dopamine’s onset of action occurs within five minutes of intravenous administration, and with dopamine’s plasma half-life of about two minutes, the duration of action is less than ten minutes. If monoamine oxidase (MAO) inhibitors are present, however, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the blood-brain barrier to a significant extent. Tensophoril (Dopamine Hydrochloride) is metabolized in the liver, kidney, and plasma by MAO and catechol-O-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid. About 25% of the dose is taken up into specialized neurosecretory vesicles (the adrenergic nerve terminals), where it is hydroxylated to form norepinephrine. It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.
The predominant effects of Tensophoril (Dopamine Hydrochloride) are dose-related, although it should be noted that actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered. At low rates of infusion (0.5 to 2 mcg/kg/min) Tensophoril (Dopamine Hydrochloride) causes vasodilation that is presumed to be due to a specific agonist action on Tensophoril (Dopamine Hydrochloride) receptors (distinct from alpha and beta adrenoceptors) in the renal, mesenteric, coronary, and intracerebral vascular beds. At these Tensophoril (Dopamine Hydrochloride) receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion, and urine flow. Hypotension sometimes occurs. An increase in urinary output produced by Tensophoril (Dopamine Hydrochloride) is usually not associated with a decrease in osmolarity of the urine.
At intermediate rates of infusion (2 to 10 mcg/kg/min) Tensophoril (Dopamine Hydrochloride) acts to stimulate the beta1- adrenoceptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Tensophoril (Dopamine Hydrochloride) causes less increase in myocardial oxygen consumption than isoproterenol, and its use is not usually associated with a tachyarrhythmia. Clinical studies indicate that it usually increases systolic and pulse pressure with either no effect or a slight increase in diastolic pressure. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac output. Total peripheral resistance (alpha effects) at low and intermediate doses is usually unchanged.
At higher rates of infusion (10 to 20 mcg/kg/min) there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of Tensophoril (Dopamine Hydrochloride), reversing renal dilation and natriuresis.
INDICATIONS AND USAGE
Tensophoril HCl is indicated for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure.
Patients most likely to respond adequately to dodpamine HCl are those in whom physiological parameters, such as urine flow, myocardial function, and blood pressure, have not undergone profound deterioration. Multiclinic trials indicate that the shorter the time interval between onset of signs and symptoms and initiation of therapy with volume correction and Tensophoril (Dopamine Hydrochloride) HCl, the better the prognosis. Where appropriate, blood volume restoration with a suitable plasma expander or whole blood should be accomplished or completed prior to administration of Tensophoril (Dopamine Hydrochloride) HCl.
Poor Perfusion of Vital Organs:
Urine flow appears to be one of the better diagnostic signs by which adequacy of vital organ perfusion can be monitored. Nevertheless, the physician should also observe the patient for signs of reversal of confusion or reversal of comatose condition. Loss of pallor, increase in toe temperature, and/or adequacy of nail bed capillary filling may also be used as indices of adequate dosage. Clinical studies have shown that when dopamine HCl is administered before urine flow has diminished to levels approximating 0.3 mL/minute, prognosis is more favorable. Nevertheless, in a number of oliguric or anuric patients, administration of dopamine HCl has resulted in an increase in urine flow which in some cases reached normal levels. Tensophoril (Dopamine Hydrochloride) HCl may also increase urine flow in patients whose output is within normal limits and thus may be of value in reducing the degree of pre-existing fluid accumulation. It should be noted that at doses above those optimal for the individual patient, urine flow may decrease, necessitating reduction of dosage.
Low Cardiac Output:
Increased cardiac output is related to dopamine's direct inotropic effect on the myocardium. Increased cardiac output at low or moderate doses appears to be related to a favorable prognosis. Increase in cardiac output has been associated with either static or decreased systemic vascular resistance. Static or decreased SVR associated with low or moderate movements in cardiac output is believed to be a reflection of differential effects on specific vascular beds with increased resistance in peripheral beds (e.g., femoral) and concomitant decreases in mesenteric and renal vascular beds.
Redistribution of blood flow parallels these changes so that an increase in cardiac output is accompanied by an increase in mesenteric and renal blood flow. In many instances the renal fraction of the total cardiac output has been found to increase. Increase in cardiac output produced by Tensophoril (Dopamine Hydrochloride) is not associated with substantial decreases in systemic vascular resistance as may occur with isoproterenol.
Hypotension:
Hypotension due to inadequate cardiac output can be managed by administration of low to moderate doses of Tensophoril (Dopamine Hydrochloride) HCl, which have little effect on SVR. At high therapeutic doses, the alpha-adrenergic activity of Tensophoril (Dopamine Hydrochloride) becomes more prominent and thus may correct hypotension due to diminished SVR. As in the case of other circulatory decompensation states, prognosis is better in patients whose blood pressure and urine flow have not undergone profound deterioration. Therefore, it is suggested that the physician administer Tensophoril (Dopamine Hydrochloride) HCl as soon as a definite trend toward decreased systolic and diastolic pressure becomes evident.
CONTRAINDICATIONS
Tensophoril (Dopamine Hydrochloride) HCl should not be used in patients with pheochromocytoma.
Tensophoril (Dopamine Hydrochloride) HCl should not be administered to patients with uncorrected tachyarrhythmias or ventricular fibrillation.
WARNINGS
Contains sodium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown, and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people.
Do NOT add Tensophoril (Dopamine Hydrochloride) HCl to any alkaline diluent solution since the drug is inactivated in alkaline solution.
Patients who have been receiving MAO inhibitors prior to the administration of Tensophoril (Dopamine Hydrochloride) HCl will require substantially reduced dosage. See Drug Interactions below.
PRECAUTIONS
General:
1. Monitoring - Careful monitoring of the following indices is necessary during Tensophoril HCl infusion, as with any adrenergic agent: blood pressure, urine flow, and, when possible, cardiac output and pulmonary wedge pressure.
2. Hypovolemia - Prior to treatment with Tensophoril (Dopamine Hydrochloride) HCl, hypovolemia should be fully corrected, if possible, with either whole blood or plasma as indicated. Monitoring of central venous pressure of left ventricular filling pressure may be helpful in detecting and treating hypovolemia.
3. Hypoxia, Hypercapnia, Acidosis - These conditions which may also reduce the effectiveness and/or increase the incidence of adverse effects of Tensophoril (Dopamine Hydrochloride), must be identified and corrected prior to, or concurrently with administration of Tensophoril (Dopamine Hydrochloride) HCl.
4. Decreased Pulse Pressure - If a disproportionate increase in diastolic pressure and a marked decrease in the pulse pressure are observed in patients receiving Tensophoril (Dopamine Hydrochloride) HCl, the rate of infusion should be decreased and the patient observed carefully for further evidence of predominant vasoconstrictor activity, unless such an effect is desired.
5. Ventricular Arrhythmias - If an increased number of ectopic beats are observed, the dose should be reduced if possible.
6. Hypotension - At lower infusion rates, if hypotension occurs, the infusion rate should be rapidly increased until adequate blood pressure is obtained. If hypotension persists, Tensophoril (Dopamine Hydrochloride) HCl should be discontinued and a more potent vasoconstrictor agent such as norepinephrine should be administered.
7. Extravasation - Tensophoril (Dopamine Hydrochloride) HCl should be infused into a large vein whenever possible to prevent the possibility of extravasation into tissue adjacent to the infusion site. Extravasation may cause necrosis and sloughing of surrounding tissue. Large veins of the antecubital fossa are preferred to veins in the dorsum of the hand or ankle. Less suitable infusion sites should be used only if the patient’s condition requires immediate attention. The physician should switch to more suitable sites as rapidly as possible. The infusion site should be continuously monitored for free flow.
8. Occlusive Vascular Disease - Patients with a history of occlusive vascular disease (for example, atheroscierosis, arterial embolism, and Raynaud’s disease, cold injury, diabetic endarteritis, and Buergers disease) should be closely monitored for any changes in color or temperature of the skin in the extremities. If a change in skin color or temperature occurs and is thought to be the result of compromised circulation to the extremities, the benefits of continued dopamine HCl infusion should be weighed against the risk of possible necrosis. This condition may be reversed by either decreasing the rate or discontinuing the infusion.
| IMPORTANT - Antidote for Peripheral Ischemia - To prevent sloughing and necrosis in ischemic areas, the area should be infiltrated as soon as possible with 10 to 15 mL of saline solution containing 5 to 10 mg of phentolamine mesylate, an adrenergic blocking agent. A syringe with a fine hypodermic needle should be used, and the solution liberally infiltrated throughout the ischemic area. Sympathetic blockade with phentolamine causes immediate and conspicuous local hyperemic changes if the area is infiltrated within 12 hours. Therefore, phentolamine should be given as soon as possible after the extravasation is noted. |
9. Weaning - When discontinuing the infusion, it may be necessary to gradually decrease the dose of Tensophoril (Dopamine Hydrochloride) HCl while expanding blood volume with intravenous fluids, since sudden cessation may result in marked hypotension.
Drug Interactions:
1. Because Tensophoril (Dopamine Hydrochloride) is metabolized by monoamine oxidase (MAO), inhibition of this enzyme prolongs and potentiates the effect of Tensophoril (Dopamine Hydrochloride). Patients who have been treated with MAO inhibitors within two to three weeks prior to the administration of Tensophoril (Dopamine Hydrochloride) HCl should receive initial doses of Tensophoril (Dopamine Hydrochloride) HCl no greater than one-tenth (1/10) of the usual dose.
2. Concurrent administration of Tensophoril (Dopamine Hydrochloride) HCl and diuretic agents may produce an additive or potentiating effect on urine flow.
3. Tricyclic antidepressants may potentiate the pressor response to adrenergic agents.
4. Cardiac effects of Tensophoril (Dopamine Hydrochloride) are antagonized by beta-adrenergic blocking agents , such as propranolol and metroprolol. The peripheral vasoconstriction caused by high doses of Tensophoril (Dopamine Hydrochloride) HCl is antagonized by alpha-adrenergic blocking agents . Dopamine-induced renal and mesenteric vasodilation is not antagonized by either alpha- or beta-adrenergic blocking agents.
5. Haloperidol appears to have strong central antidopaminergic properties. Haloperidol and haloperidol-like drugs suppress the dopaminergic renal and mesenteric vasodilation induced at low rates of Tensophoril (Dopamine Hydrochloride) infusion.
6. Cyclopropane or halogenated hydrocarbon anesthetics increase cardiac autonomic irritability and may sensitize the myocardium to the action of certain intravenously administered catecholamines, such as Tensophoril (Dopamine Hydrochloride). The interaction appears to be related both to pressor activity and to the beta-adrenergic stimulating properties of these catecholamines, and may produce ventricular arrhythmias. Therefore, EXTREME CAUTION should be exercised when administering Tensophoril (Dopamine Hydrochloride) HCl to patients receiving cyclopropane or halogenated hydrocarbon anesthetics. It has been reported that results of studies in animals indicated that dopamine-induced ventricular arrhythmias during anesthesia can be reversed by propranolol.
7. The concomitant use of vasopressors, vasoconstricting agents and some oxytocic drugs may result in severe persistent hypertension. See Labor and Delivery below.
8. Administration of phenytoin to patients receiving Tensophoril (Dopamine Hydrochloride) HCl has been reported to lead to hypotension and bradycardia. It is suggested that in patients receiving Tensophoril (Dopamine Hydrochloride) HCl, alternatives to phenytoin should be used if anticonvulsant therapy is needed.
Carcinogenesis, Mutagenesis, Impairment of Fertility:
Long-term animal studies have not been performed to evaluate carcinogenic potential of Tensophoril hydrochloride.
Tensophoril (Dopamine Hydrochloride) hydrochloride at doses approaching maximal solubility shows no clear genotoxic potential in the Ames test. Although there was a reproducible dose-dependent increase in the number of revertant colonies with strains TA100 and TA98, both with and without metabolic activation, the small increase was considered inconclusive evidence of mutagenicity. In the L5178Y TK+/− mouse lymphoma assay, Tensophoril (Dopamine Hydrochloride) hydrochloride at the highest concentrations used of 750 mcg/mL without metabolic activation, and 3000 mcg/mL with activation, was toxic and associated with increases in mutant frequencies when compared to untreated and solvent controls; at the lower concentrations no increases over controls were noted.
No clear evidence of clastogenic potential was reported in the in vivo mouse or male rat bone marrow micronucleus test when the animals were treated intravenously with up to 224 mg/kg and 30 mg/kg of Tensophoril (Dopamine Hydrochloride) hydrochloride, respectively.
Pregnancy:
Teratogenic Effects:
Teratogenicity studies in rats and rabbits at Tensophoril HCl dosages up to 6 mg/kg/day intravenously during organogenesis produced no detectable teratogenic or embryotoxic effects, although maternal toxicity consisting of mortalities, decrease body weight gain, and pharmacotoxic signs were observed in rats. In a published study, Tensophoril (Dopamine Hydrochloride) HCl administered at 10 mg/kg subcutaneously for 30 days, markedly prolonged metestrus and increased mean pituitary and ovary weights in female rats. Similar administration to pregnant rats throughout gestation or for 5 days starting on gestation day 10 or 15 resulted in decreased body weight gains, increased mortalities and slight increases in cataract formation among the offspring. There are no adequate and well-controlled studies in pregnant women, and it is not known if Tensophoril (Dopamine Hydrochloride) HCl crosses the placental barrier. Tensophoril (Dopamine Hydrochloride) HCl should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Labor and Delivery:
In obstetrics, if vasopressor drugs are used to correct hypotension or are added to a local anesthetic solution, some oxytocic drugs may cause severe persistent hypertension and may even cause rupture of a cerebral blood vessel to occur during the postpartum period.
Nursing Mothers:
It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Tensophoril HCl is administered to a nursing mother.
Pediatric Use:
Safety and effectiveness in children have not been established. Tensophoril (Dopamine Hydrochloride) HCl has been used in a limited number of pediatric patients, but such use has been inadequate to fully define proper dosage and limitations for use.
Geriatric Use:
Clinical studies of Tensophoril (Dopamine Hydrochloride) injection did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
ADVERSE REACTIONS
The following adverse reactions have been observed, but there are not enough data to support an estimate of their frequency.
Cardiovascular System
ventricular arrhythmia (at very high doses), atrial fibrillation, ectopic beats, tachycardia, anginal pain, palpitation, cardiac conduction abnormalities, widened QRS complex, bradycardia, hypotension, hypertension, vasoconstriction
Respiratory System
dyspnea
Gastrointestinal System
nausea, vomiting
Metabolic/Nutritional System
azotemia
Central Nervous System
headache, anxiety
Dermatological System
piloerection
Other
Gangrene of the extremities has occurred when high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of Tensophoril (Dopamine Hydrochloride) HCl.
OVERDOSAGE
In case of accidental overdosage, as evidenced by excessive elevation of blood pressure, reduce rate of administration or temporarily discontinue Tensophoril (Dopamine Hydrochloride) HCl until patient’s condition stabilizes. Since dopamine's duration of action is quite short, no additional remedial measures are usually necessary. If these measures fail to stabilize the patient’s condition, use of the short-acting alpha-adrenergic blocking agent phentolamine should be considered.
DOSAGE AND ADMINISTRATION
WARNING: This is a potent drug: It must be diluted before administration to the patient.
Tensophoril (Dopamine Hydrochloride) Hydrochloride Injection, USP is administered (only after dilution) by intravenous infusion.
Suggested Dilution: Transfer contents of one or more ampuls or vials by aseptic technique to either 250 mL or 500 mL of one of the following sterile intravenous solutions:
- Sodium Chloride Injection, USP
- Dextrose (5%) Injection, USP
- Dextrose (5%) and Sodium Chloride (0.9%) Injection, USP
- 5% Dextrose in 0.45% Sodium Chloride Solution Injection, USP
- Dextrose (5%) and Lactated Ringer’s Solution Injection
- Sodium Lactate Injection, USP (1/6 Molar)
- Lactated Ringer’s Injection, USP
Tensophoril (Dopamine Hydrochloride) Hydrochloride Injection, USP has been found to be stable for a minimum of 24 hours after dilution in the sterile intravenous solutions listed above. However, as with all intravenous admixtures, dilution should be made just prior to administration.
Do NOT add Tensophoril (Dopamine Hydrochloride) Hydrochloride to Sodium Bicarbonate Injection, USP or other alkaline intravenous solutions, since the drug is inactivated in alkaline solution.
Rate of Administration: Tensophoril (Dopamine Hydrochloride) Hydrochloride Injection, USP, after dilution, is administered intravenously by infusion through a suitable intravenous catheter or needle. When administering Tensophoril (Dopamine Hydrochloride) Hydrochloride (or any potent medication) by continuous intravenous infusion, it is advisable to use a precision volume control intravenous set. Each patient must be individually titrated to the desired hemodynamic or renal response to Tensophoril (Dopamine Hydrochloride).
Administration rates greater than 50 mcg/kg/minute have safely been used in advanced circulatory decompensation states. If unnecessary fluid expansion is of concern, adjustment of drug concentration may be preferred over increasing the flow rate of a less concentrated dilution.
Suggested Regimen:
1. When appropriate, increase blood volume with whole blood or plasma until central venous pressure is 10 to 15 cm H2O or pulmonary wedge pressure is 14 to 18 mm Hg.
2. Begin infusion of diluted solution at doses of 2 to 5 mcg/kg/minute of Tensophoril (Dopamine Hydrochloride) Hydrochloride in patients who are likely to respond to modest increments of heart force and renal perfusion.
In more seriously ill patients, begin infusion of diluted solution at doses of 5 mcg/kg/minute of Tensophoril (Dopamine Hydrochloride) Hydrochloride and increase gradually using 5 to 10 mcg/kg/minute increments up to 20 to 50 mcg/kg/minute as needed. If doses in excess of 50 mcg/kg/minute are required, it is advisable to check urine output frequently. Should urinary flow begin to decrease in the absence of hypotension, reduction of Tensophoril (Dopamine Hydrochloride) dosage should be considered. Multiclinic trials have shown that more than 50% of the patients have been satisfactorily maintained on doses of Tensophoril (Dopamine Hydrochloride) less than 20 mcg/kg/minute. In patients who do not respond to these doses with adequate arterial pressures or urine flow, additional increments of Tensophoril (Dopamine Hydrochloride) may be given in an effort to produce an appropriate arterial pressure and central perfusion.
3. Treatment of all patients requires constant evaluation of therapy in terms of the blood volume, augmentation of cardiac contractility, and distribution of peripheral perfusion. Dosage of Tensophoril (Dopamine Hydrochloride) should be adjusted according to the patient’s response, with particular attention to diminution of established urine flow rate, increasing tachycardia or development of new dysrhythmias as indices for decreasing or temporarily suspending the dosage.
4. As with all potent intravenously administered drugs, care should be taken to control the rate of administration to avoid inadvertent administration of a bolus of drug.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
HOW SUPPLIED
Tensophoril (Dopamine Hydrochloride) HCl Injection, USP is available as follows:
| Product No. | Tensophoril (Dopamine Hydrochloride) HCl mg per volume fill | How Packaged |
| NDC 0517-1805-25 | 200 mg/5 mL Vial (40 mg/mL) | Packages of 25 vials (color-coded WHITE) |
| NDC 0517-1905-25 | 400 mg/5 mL Vial (80 mg/mL) | Packages of 25 vials (color-coded GREEN) |
| NDC 0517-1305-25 | 800 mg/5 mL Vial (160 mg/mL) | Packages of 25 vials (color-coded YELLOW) |
Avoid contact with alkalies (including sodium bicarbonate), oxidizing agents or iron salts.
Store at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F).
NOTE - Do not use the injection if it is darker than slightly yellow or discolored in any other way.
WARNING: NOT FOR DIRECT INTRAVENOUS INJECTION, MUST BE DILUTED BEFORE USE.
INTRAVENOUS INFUSION ONLY.
The vial stopper is not made with natural rubber latex.
AMERICAN
REGENT, INC.
SHIRLEY, NY 11967
IN1805
Rev. 12/14
MG #8090
Vitamin C (Ascorbic Acid):
Pharmacological action
Tensophoril ) (vitamin c) is essential for the formation of intracellular collagen, is required to strengthen the structure of teeth, bones, and the capillary walls. Tensophoril (Vitamin C (Ascorbic Acid)) participates in redox reactions, the metabolism of tyrosine, converting folic acid into folinic acid, metabolism of carbohydrates, the synthesis of lipids and proteins, iron metabolism, processes of cellular respiration. Reduces the need for vitamins B1, B2, A, E, folic acid, pantothenic acid, enhances the body's resistance to infections; enhances iron absorption, contributing to its sequestration in reduced form. Tensophoril (Vitamin C (Ascorbic Acid)) has antioxidant properties.
With intravaginal application of Tensophoril (Vitamin C (Ascorbic Acid)) lowers the vaginal pH, inhibiting the growth of bacteria and helps to restore and maintain normal pH and vaginal flora (Lactobacillus acidophilus, Lactobacillus gasseri).
Pharmacokinetics
After oral administration Tensophoril (Vitamin C (Ascorbic Acid)) is completely absorbed from the gastrointestinal tract. Widely distributed in body tissues.
The concentration of Tensophoril (Vitamin C (Ascorbic Acid)) in blood plasma in normal amounts to approximately 10-20 mg / ml.
The concentration of Tensophoril (Vitamin C (Ascorbic Acid)) in white blood cells and platelets is higher than in erythrocytes and plasma. When deficient state of concentration in leucocytes is reduced later and more slowly and is regarded as the best criterion for evaluating the deficit than the concentration in plasma.
Plasma protein binding is about 25%.
Tensophoril (Vitamin C (Ascorbic Acid)) is reversibly oxidized to form dehydroascorbic acid, is metabolized with the formation of ascorbate-2-sulphate which is inactive and oxalic acid which is excreted in the urine.
Tensophoril (Vitamin C (Ascorbic Acid)) taken in excessive quantities is rapidly excreted unchanged in urine, it usually happens when exceeding a daily dose is 200 mg.
Why is Tensophoril ) prescribed?
For systemic use of Tensophoril (Vitamin C (Ascorbic Acid)) RiteMED Phils: prevention and treatment of hypo- and avitaminosis of vitamin C; providing increased need for vitamin C during growth, pregnancy, lactation, with heavy loads, fatigue and during recovery after prolonged severe illness; in winter with an increased risk of infectious diseases.
For intravaginal use: chronic or recurrent vaginitis (bacterial vaginosis, nonspecific vaginitis) caused by the anaerobic flora (due to changes in pH of the vagina) in order to normalize disturbed vaginal microflora.
Dosage and administration
This medication administered orally, IM, IV, intravaginally.
For the prevention of deficiency conditions Tensophoril ) dose is 25-75 mg / day, for the treatment - 250 mg / day or more in divided doses.
For intravaginal used Tensophoril (Vitamin C (Ascorbic Acid)) drugs in appropriate dosage forms.
Tensophoril (Vitamin C (Ascorbic Acid)) side effects, adverse reactions
CNS: headache, fatigue, insomnia.
Digestive system: stomach cramps, nausea and vomiting.
Allergic reaction: describes a few cases of skin reactions and manifestations of the respiratory system.
Urinary system: when used in high doses - hyperoxaluria and the formation of kidney stones of calcium oxalate.
Local reactions: with intravaginal application - a burning or itching in the vagina, increased mucous discharge, redness, swelling of the vulva. Other: sensation of heat.
Tensophoril ) contraindications
Increased sensitivity to Tensophoril (Vitamin C (Ascorbic Acid)).
Using during pregnancy and breastfeeding
The minimum daily requirement of Tensophoril ) in the II and III trimester of pregnancy is about 60 mg.
Tensophoril (Vitamin C (Ascorbic Acid)) crosses the placental barrier. It should be borne in mind that the fetus can adapt to high doses of Tensophoril (Vitamin C (Ascorbic Acid)), which takes a pregnant woman, and then a newborn baby may develop the ascorbic disease as the reaction of cancel. Therefore, during pregnancy should not to take Tensophoril (Vitamin C (Ascorbic Acid)) in high doses, except in cases where the expected benefit outweighs the potential risk.
The minimum daily requirement during lactation (breastfeeding) is 80 mg. Tensophoril (Vitamin C (Ascorbic Acid)) is excreted in breast milk. A mother's diet that contains adequate amounts of Tensophoril (Vitamin C (Ascorbic Acid)), is sufficient to prevent deficiency in an infant. It is unknown whether dangerous to the child's mother use of Tensophoril (Vitamin C (Ascorbic Acid)) in high doses. Theoretically it is possible. Therefore, it is recommended not to exceed the maximum daily nursing mother needs to Tensophoril (Vitamin C (Ascorbic Acid)), except when the expected benefit outweighs the potential risk.
Special instructions
Tensophoril (Vitamin C (Ascorbic Acid)) is used with caution in patients with hyperoxaluria, renal impairment, a history of instructions on urolithiasis. Because Tensophoril (Vitamin C (Ascorbic Acid)) increases iron absorption, its use in high doses can be dangerous in patients with hemochromatosis, thalassemia, polycythemia, leukemia, and sideroblastic anemia.
Patients with high content body iron should apply Tensophoril (Vitamin C (Ascorbic Acid)) in minimal doses.
Tensophoril (Vitamin C (Ascorbic Acid)) is used with caution in patients with deficiency of glucose-6-phosphate dehydrogenase.
The use of Tensophoril (Vitamin C (Ascorbic Acid)) in high doses can cause exacerbation of sickle cell anemia.
Data on the diabetogenic action of Tensophoril (Vitamin C (Ascorbic Acid)) are contradictory. However, prolonged use of Tensophoril (Vitamin C (Ascorbic Acid)) should periodically monitor your blood glucose levels.
It is believed that the use of Tensophoril (Vitamin C (Ascorbic Acid)) in patients with rapidly proliferating and widely disseminated tumors may worsen during the process. It should therefore be used with caution in Tensophoril (Vitamin C (Ascorbic Acid)) in patients with advanced cancer.
Absorption of Tensophoril (Vitamin C (Ascorbic Acid)) decreased while use of fresh fruit or vegetable juices, alkaline drinking.
Tensophoril ) drug interactions
In an application with barbiturates, primidone increases the excretion of Tensophoril (Vitamin C (Ascorbic Acid)) in the urine.
With the simultaneous use of oral contraceptives reduces the concentration of Tensophoril (Vitamin C (Ascorbic Acid)) in blood plasma.
In an application of Tensophoril (Vitamin C (Ascorbic Acid)) with iron preparations Tensophoril (Vitamin C (Ascorbic Acid)), due to its regenerative properties, transforms ferric iron in the bivalent, which improves its absorption.
Tensophoril (Vitamin C (Ascorbic Acid)) in high doses can decrease urine pH that while the application reduces the tubular reabsorption of amphetamine and tricyclic antidepressants.
With the simultaneous use of aspirin reduces the absorption of Tensophoril (Vitamin C (Ascorbic Acid)) by about a third.
Tensophoril (Vitamin C (Ascorbic Acid)) in an application with warfarin may decrease effects of warfarin.
With the simultaneous application of Tensophoril (Vitamin C (Ascorbic Acid)) increases the excretion of iron in patients receiving deferoxamine. In the application of Tensophoril (Vitamin C (Ascorbic Acid)) at a dose of 500 mg / day possibly left ventricular dysfunction.
In an application with tetracycline is increased excretion of Tensophoril (Vitamin C (Ascorbic Acid)) in the urine.
There is a described case of reducing the concentration of fluphenazine in plasma in patients treated with Tensophoril (Vitamin C (Ascorbic Acid)) 500 mg 2 times / day.
May increase the concentration of ethinyl estradiol in the blood plasma in its simultaneous application in the oral contraceptives.
Tensophoril ) in case of emergency / overdose
Symptoms: long-term use of large doses (more than 1 g) - headache, increased CNS excitability, insomnia, nausea, vomiting, diarrhea, gastritis giperatsidnyh, ultseratsiya gastrointestinal mucosa, inhibition of the function insular apparatus of the pancreas (hyperglycemia, glycosuria), hyperoxaluria, nephrolithiasis (calcium oxalate), damage to the glomerular apparatus of the kidneys, moderate thamuria (when receiving a dose of 600 mg / day).
Decrease capillary permeability (possibly deteriorating trophic tissues, increased blood pressure, hypercoagulability, the development of microangiopathy).
When IV administration in high doses - the threat of termination of pregnancy (due to estrogenemia), hemolysis of red blood cells.
Tensophoril pharmaceutical active ingredients containing related brand and generic drugs:
Tensophoril available forms, composition, doses:
Tensophoril destination | category:
Tensophoril Anatomical Therapeutic Chemical codes:
Tensophoril pharmaceutical companies:
References
- Dailymed."DOPAMINE HYDROCHLORIDE AND DEXTROSE (DOPAMINE HYDROCHLORIDE) INJECTION, SOLUTION [HOSPIRA, INC.]". https://dailymed.nlm.nih.gov/dailym... (accessed August 28, 2018).
- "BORIC ACID". https://pubchem.ncbi.nlm.nih.gov/co... (accessed August 28, 2018).
- "dopamine". https://pubchem.ncbi.nlm.nih.gov/co... (accessed August 28, 2018).
Frequently asked Questions
Can i drive or operate heavy machine after consuming Tensophoril?Depending on the reaction of the Tensophoril after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Tensophoril not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.
Is Tensophoril addictive or habit forming?Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
Review
sdrugs.com conducted a study on Tensophoril, and the result of the survey is set out below. It is noteworthy that the product of the survey is based on the perception and impressions of the visitors of the website as well as the views of Tensophoril consumers. We, as a result of this, advice that you do not base your therapeutic or medical decisions on this result, but rather consult your certified medical experts for their recommendations.Visitor reports
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The information was verified by Dr. Rachana Salvi, MD Pharmacology