Aa 3.5%-D10w-Calcium

Drug overview for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate):

Generic name: AMINO ACID 3.5 % NO.2 PED/DEXTROSE 10 %/CALCIUM GLUCONATE
Drug class: Calcium
Therapeutic class: Electrolyte Balance-Nutritional Products

Amino acid injections are caloric agents that provide the protein necessary Dextrose is a carbohydrate caloric agent. Electrolyte solutions provide electrolyte supplementation and water for hydration. in parenteral nutrition.

Amino acid injections are used in parenteral nutrition to prevent nitrogen Dextrose injections are used as a source of calories and water for For further information on chemistry and stability, pharmacology, uses, cautions, and dosage and administration of electrolyte solutions, hydration. Dextrose and sodium chloride injections are used as a source of loss or in the treatment of negative nitrogen balance when adequate calories, sodium chloride, and water for hydration. nutrition by mouth, gastric or duodenal tube, or ostomy (i.e., specialized references on fluids and electrolytes and the manufacturers' esophagostomy, gastrostomy, jejunostomy) is impossible or undesirable labeling should be consulted.

(e.g., when bowel rest is needed because of GI surgery or its complications 2.5-11.5% Dextrose injections are administered by peripheral IV infusion to provide calories and water for hydration; these injections may be admixed such as ileus, fistulas, or anastomotic leaks); when GI absorption of protein is impaired (e.g., in GI disorders); or when protein requirements with amino acids injections or other compatible IV fluids to provide are substantially increased (e.g., burns, sepsis, severe trauma) such that parenteral nutrition. Hypertonic dextrose injections (concentration greater than 5%) are used to provide adequate calories in a minimal volume of they cannot be met by enteral nutrition. Parenteral nutrition may be used to provide positive nitrogen balance and a source of calories, water.

40-70% Dextrose injections are concentrated sources of calories electrolytes, trace elements, vitamins, and other essential factors, which are admixed with amino acids injections or other compatible IV fluids and administered via central veins to provide parenteral nutrition. 50% particularly during long-term nutritional support. Parenteral nutrition is Dextrose injections are frequently used in adults and children to restore used for preoperative and postoperative patients in whom enteral nutrition blood glucose concentrations in the treatment of hypoglycemia resulting is undesirable or not tolerated and in patients with GI disorders such as from insulin excess or other causes.

10-25% Dextrose injections are used in mechanical or functional obstruction, developmental abnormalities, malabsorption states (e.g., short-bowel syndrome), inflammatory bowel neonates and infants to restore blood glucose concentrations in the disease, or GI fistulas; in patients with hypermetabolic conditions such as treatment of acute symptomatic hypoglycemia. extensive burns, sepsis, or severe trauma; and in patients with other conditions such as acute renal failure, hepatic insufficiency, anorexia Dextrose gel or chewable tablets are used orally for the management of hypoglycemia in conscious diabetics. nervosa, coma, or neoplastic disease in whom parenteral nutritional support is necessary.

Solutions of amino acids provide the protein necessary in parenteral nutrition. Amino acid injections vary in the amount of protein and nitrogen, in the presence and amount of essential and nonessential amino acids, in osmolarity, and in electrolyte concentrations. Nonprotein calories are generally provided as dextrose; however, fructose, alcohol, or fat are also used.

Fat and dextrose may be used in combination, particularly during peripheral parenteral nutrition or when essential fatty acids are required. Dosage, route of administration (peripheral or central IV), and concomitant infusion of nonprotein calories depend on various factors including nutritional and metabolic status of the patient, anticipated duration of parenteral nutritional support, and tolerance of the veins. Central venous nutrition (total parenteral nutrition, hyperalimentation) should be used when amino acid solutions are to be admixed with hypertonic dextrose and administered via a central venous catheter to promote protein synthesis in hypercatabolic or severely depleted patients or in those requiring long-term parenteral nutrition.

Peripheral parenteral nutrition should be used in individuals who are moderately catabolic or depleted and in whom the central venous route is not indicated. Dilute amino acid solutions mixed with 5 or 10% dextrose injection may be infused by peripheral vein and supplemented with fat emulsion. Protein sparing involves peripheral infusion of dilute amino acid solutions, with or without nonprotein calories (e.g., dextrose) or electrolytes, and is used in well-nourished, mildly catabolic individuals, including routine postsurgical individuals who require only short-term parenteral nutrition.

Specialized amino acid injections (e.g., Aminess(R), Aminosyn RF(R), HepatAmine(R), NephrAmine(R), RenAmin(R)) are available for patients (e.g., those with renal or hepatic disease) who may have specialized requirements for amino acids or who may not tolerate amino acids contained in conventional solutions. For further information on chemistry and stability, pharmacology, uses, cautions, and dosage and administration of amino acid injections, specialized references on nutritional support and the manufacturers' labeling should be consulted.

DRUG IMAGES

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The following indications for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate) have been approved by the FDA:

Indications:
None.

Professional Synonyms:
None.

The following dosing information is available for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate):

Dosing
Administration
Dosing Information
Generic

Dosage of dextrose depends on the age, weight, clinical condition, and fluid, electrolyte, and acid-base balance of the patient. Dextrose may usually be administered IV to healthy individuals at a rate of 0.5 g/kg per hour without producing glycosuria; the maximum infusion rate should generally not exceed 0.8

g/kg per hour.

For the treatment of hypoglycemia resulting from insulin excess or other causes in adults and children, the usual dose is 20-50 mL of 50% dextrose injection administered slowly (e.g., 3 mL/minute) IV; repeated doses and supportive therapy may be required in severe cases. For the treatment of acute symptomatic hypoglycemia in neonates and infants, the usual dose is 2 mL/kg of 10-25% dextrose injection administered slowly IV; higher or repeated doses may be required in severe cases, and subsequent continuous IV infusion of 10-15% dextrose injection may be necessary to maintain sufficient blood glucose concentrations. When patients do not respond to or tolerate dextrose, the use of other drugs (e.g., glucagon, corticosteroids, epinephrine) should be considered.

For the management of hypoglycemia in conscious diabetics, 10-20 g of dextrose may be administered orally as a gel or chewable tablets; the dose may be repeated in 10-20 minutes if necessary. Self monitoring of blood glucose concentration may be useful in determining whether a repeat dose is necessary; some clinicians recommend that if hypoglycemic symptoms are still present and a blood glucose increase of at least 20 mg/dL is not achieved within 20 minutes after oral administration of dextrose, the patient should consider administration of a repeat dose. Each gram of the 40% (w/w) dextrose gel provides 400 mg of dextrose (i.e., 25 g of gel provides 10 g of dextrose).

For further information on chemistry and stability, pharmacology, uses, cautions, and dosage and administration of dextrose, specialized references and the manufacturers'; labeling should be consulted.

Dextrose injections are administered IV. Hypertonic dextrose solutions are preferably administered via an IV catheter placed into a large central vein. If hypertonic (10%) dextrose solutions are administered peripherally, a large arm vein should be used and, if possible, the injection site should be alternated daily.

Except in the emergency treatment of severe hypoglycemia, higher concentrations of dextrose injections (e.g., 20% and higher) should be administered via central veins and only after appropriate dilution. When used for the emergency treatment of hypoglycemia, hypertonic dextrose injections may be administered slowly via a peripheral vein. Concentrated dextrose gels and chewable dextrose tablets are administered orally in the management of acute symptomatic hypoglycemia.

No dosing information available.

No generic dosing information available.

The following drug interaction information is available for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate):

Contraindicated
Severe
Moderate

There are 3 contraindications. These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.

Drug Interaction	Drug Names
Sympathomimetics (Indirect & Mixed Acting)/MAOIs SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Catecholamine stores increased by MAOIs can be released by indirect acting sympathomimetics such as ephedrine and amphetamine. MAO inhibitors also interfere with gut and liver metabolism of direct acting sympathomimetics (e.g oral phenylephrine). CLINICAL EFFECTS: Concurrent use of MAOIs may result in potentiation of sympathomimetic effects, which may result in headaches, hypertensive crisis, toxic neurological effects, and malignant hyperpyrexia. Fatalities have occurred. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Concurrent use of monoamine oxidase inhibitors and sympathomimetics is contraindicated. The manufacturers of sympathomimetic agents recommend waiting 14 days after discontinuation of MAO inhibitors before initiating the sympathomimetic. DISCUSSION: Indirect acting sympathomimetic amines may cause abrupt elevation of blood pressure when administered to patients taking monoamine oxidase inhibitors, resulting in a potentially fatal hypertensive crisis. Mixed (direct and indirect) acting sympathomimetics have also been shown to interact with monoamine oxidase inhibitors depending on their degree of indirect action. The direct-acting sympathomimetics have not been reported to interact. Dopamine is metabolized by monoamine oxidase, and its pressor effect is enhanced by monoamine oxidase inhibitors. Since procarbazine, an antineoplastic agent, is a weak monoamine oxidase inhibitor, hypertensive reactions may result from its concurrent use with indirect and mixed acting sympathomimetics. Furazolidone, an antibacterial with monoamine oxidase inhibitor action, has also been shown to interact with indirect acting sympathomimetics. Linezolid is another antibacterial with monoamine oxidase inhibitor properties. Metaxalone is a weak inhibitor of MAO. Foods containing large amounts of tyramine have also been implicated in this interaction. Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A. At recommended dosages, rasagiline, oral selegiline, and transdermal selegiline up to 6mg/day are selective for MAO-B; however, at higher dosages they have been shown to lose their selectivity. One or more of the drug pairs linked to this monograph have been included in a list of interactions that should be considered "high-priority" for inclusion and should not be inactivated in EHR systems. This DDI subset was vetted by an expert panel commissioned by the U.S. Office of the National Coordinator (ONC) for Health Information Technology.	EMSAM, FURAZOLIDONE, MARPLAN, MATULANE, METAXALONE, METHYLENE BLUE, NARDIL, PARNATE, PHENELZINE SULFATE, PROCARBAZINE HCL, PROVAYBLUE, SELEGILINE HCL, TRANYLCYPROMINE SULFATE
MAO Inhibitors/Tryptophan SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Concurrent use may result in additive effects on serotonin levels. MAOIs may potentiate the effects of tryptophan.(1) CLINICAL EFFECTS: Concurrent administration of tryptophan with a MAO Inhibitor may result in serotonin syndrome and/or hypertensive crisis.(1) Symptoms of serotonin syndrome may include tremor, agitation, diaphoresis, hyperreflexia, clonus, tachycardia, hyperthermia, and muscle rigidity.(15) In addition to these effects, disorientation, delirium, agitation, hypomania, shivering, ocular oscillation, and Babinski signs have been reported with concurrent tryptophan and phenelzine.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving MAO Inhibitors should not take agents such as tryptophan. If concurrent therapy is warranted, patients should be monitored for signs and symptoms of serotonin syndrome. Instruct patients to report muscle twitching, tremors, shivering and stiffness, fever, heavy sweating, heart palpitations, restlessness, confusion, agitation, trouble with coordination, or severe diarrhea. DISCUSSION: In a study in nine subjects, the administration of a single intravenous dose of tryptophan with tranylcypromine significantly increased the normal prolactin response to tryptophan. Four of the nine subjects developed a distinctive neuromotor syndrome characterized by hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea.(2) Another set of authors reported eight cases of delirium, ranging from mild to severe, in patients who received concurrent tranylcypromine and tryptophan. Symptoms developed within two days to 4 weeks of beginning concurrent therapy.(3) In a case report, the addition of tryptophan to a tranylcypromine regimen resulted in hypomania.(4) In another report, a patient developed hyperventilation, shivering, hyperthermia, increased muscle tone, and hyperreflexia when tryptophan was added to tranylcypromine therapy.(5) There are two reports of fatalities following the concurrent administration of tryptophan and tranylcypromine. In the first report, a a patient had been receiving chlorpromazine, lithium, and tryptophan when phenelzine was initiated. Four weeks later, the patient developed neuroleptic malignant syndrome and expired despite resuscitation efforts.(6) In the second report, a patient had been receiving fluoxetine, levothyroxine, propranolol, quinidine, and hydroxyzine. Fluoxetine was discontinued and tranylcypromine, thioridazine, and tryptophan were initiated. The patient developed neuroleptic malignant syndrome two and one-half hours after the first tryptophan dose and expired 24 hours later. (7) In a case report, the addition of tryptophan to a regimen that included phenelzine resulted in an acute behavioral and neurologic syndrome. The patient's symptoms resolved 24 hours after the discontinuation of both agents.(8) In another report, a patient developed hypomania following the addition of tryptophan to phenelzine therapy.(4) Another report describes the development of delirium following the addition of tryptophan to phenelzine.(9) One set of authors reported three cases of myoclonus, hyperreflexia, and diaphoresis following the addition of tryptophan to phenelzine therapy.(10) Some studies have shown that the addition of tryptophan to MAO Inhibitor therapy may have beneficial results, including greater improvement in depression and faster onset of effects.(11,12) Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A.(13,14) Metaxalone is a weak inhibitor of MAO.(16,17)	AZILECT, EMSAM, FURAZOLIDONE, MARPLAN, MATULANE, METAXALONE, METHYLENE BLUE, NARDIL, PARNATE, PHENELZINE SULFATE, PROCARBAZINE HCL, PROVAYBLUE, RASAGILINE MESYLATE, SELEGILINE HCL, TRANYLCYPROMINE SULFATE, XADAGO, ZELAPAR
Sodium Oxybate/Sedative Hypnotics; Alcohol SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Oxybate may be associated with respiratory depression. As oxybate is taken at bedtime, concurrent use with alcohol or hypnotics may increase the risk for respiratory depression or loss of consciousness.(1-3) Primidone is metabolized to phenobarbital. CLINICAL EFFECTS: Concurrent use of sodium oxybate and sedative hypnotics or alcohol may further increase the risk for respiratory depression and profound sedation or coma.(1,2) Fatalities have been reported.(3) PREDISPOSING FACTORS: Based upon FDA evaluation of deaths in patients taking sodium oxybate, risk factors may include: use of multiple drugs which depress the CNS, more rapid than recommended oxybate dose titration, exceeding the maximum recommended oxybate dose, and prescribing for unapproved uses such as fibromyalgia, insomnia or migraine. Note that in oxybate clinical trials for narcolepsy 78% - 85% of patients were also receiving concomitant CNS stimulants.(1-3) PATIENT MANAGEMENT: The FDA states that sodium oxybate is contraindicated in patients also taking hypnotics or alcohol.(1,2) Significant quantities of alcohol may be present in medicinal products. Alcohol is is used to improve docetaxel and paclitaxel solubility. - The quantity of alcohol in paclitaxel injection formulations (0.385-0.396 grams/mL) is similar across manufacturers. A paclitaxel 200 mg dose contains approximately 13 grams of alcohol. - The quantity of alcohol in docetaxel formulations varies approximately 3-fold depending upon the manufacturer. FDA data on alcohol content (4): Product Manufacturer Alcohol/200 mg dose Docetaxel Inj. Pfizer 6.4 grams Docetaxel Inj. Sandoz 5.5 grams Docetaxel Inj. Accord 4.0 grams Taxotere-one vial Sanofi 4.0 grams formulation Docetaxel Inj. Hospira 3.7 grams Docefrez Sun Pharma 2.9 grams Taxotere-two vial Sanofi 2.0 grams formulation DISCUSSION: The FDA evaluated sodium oxybate postmarket fatal adverse event reports from the FDA Adverse Event Reporting System(AERS)and from the manufacturer. Although report documentation was not always optimal or complete, useful information was obtained. Factors which may have contributed to fatal outcome: concomitant use of one or more drugs which depress the CNS, more rapid than recommended upward dose titration, exceeding the maximum recommended oxybate dose, and prescribing for unapproved uses such as fibromyalgia, insomnia or migraine. Many deaths occurred in patients with serious psychiatric disorders such as depression and substance abuse. Other concomitant diseases may have also contributed to respiratory and CNS depressant effects of oxybate.(3)	LUMRYZ, LUMRYZ STARTER PACK, SODIUM OXYBATE, XYREM, XYWAV

There are 5 severe interactions. These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.

Drug Interaction	Drug Names
Aspartame; Phenylalanine; Tyrosine/Nitisinone SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Aspartame contains phenylalanine, which is metabolized into tyrosine. Nitisinone prevents the breakdown of tyrosine.(1) CLINICAL EFFECTS: Elevated levels of tyrosine can cause vision changes (cornea ulcers, corneal opacities, keratitis, conjunctivitis, eye pain, and photophobia), skin problems (painful hyperkeratotic plaques on the soles and palms), and nervous system toxicity (variable degrees of mental retardation and developmental delay). PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving nitisinone should following dietary restrictions concerning the consumption of aspartame, phenylalanine, and tyrosine, including medications that contain these ingredients.(1) DISCUSSION: In most patients, eye symptoms resulting from elevated tyrosine levels were transient, lasting less than one week; however, six patients had prolonged episodes lasting up to almost 2 years.(1)	NITISINONE, NITYR, ORFADIN
Intravenous Ceftriaxone/Intravenous Calcium Products SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Intravenous ceftriaxone and intravenous calcium may form an insoluble precipitate if administered too closely together. CLINICAL EFFECTS: Intravenous administration of calcium-containing products with intravenous ceftriaxone may have serious risks in all patients, especially in the neonate population. NEONATES: Intravenous administration of calcium-containing products within 48(1-2) to 120(3) hours of intravenous administration of ceftriaxone may result in damage to the lungs and/or kidneys in neonates. Fatalities in neonates have been reported.(1-7) OLDER CHILDREN and ADULTS: Sequential administration requires proper line flushing. Use within 48 hours may result in the formation of kidney stones in older children(5) and the formation of "sludge" in the gallbladder.(2) Simultaneous administration in patients older than 28 days may result in the formation of an insoluble ceftriaxone-calcium precipitate.(1-7) PREDISPOSING FACTORS: Neonates, both preterm and term, may be a greatest risk of death from this interaction.(1-4) Young age may predispose patients to formation of ceftriaxone-calcium precipitates in the kidney.(5) High doses of ceftriaxone may also increase the risk of precipitates.(6) PATIENT MANAGEMENT: The US manufacturer of ceftriaxone, Health Canada, and the US Food and Drug Administration (FDA) state that the concomitant use of ceftriaxone and intravenous calcium-containing products is contraindicated in neonates less than or equal to 28 days of age. Ceftriaxone should not be used in neonates less than or equal to 28 days of age if they are receiving or are expected to receive calcium-containing intravenous products.(2,3,7) The US manufacturer of ceftriaxone, Health Canada, and the US FDA state that in patients older than 28 days of age, ceftriaxone and calcium-containing products may be administered sequentially, provided the infusion lines are thoroughly flushed between infusions with a compatible fluid.(2,3,7) The US manufacturer of ceftriaxone, Health Canada, and the US FDA state that ceftriaxone must not be administered simultaneously with intravenous calcium-containing solutions via a Y-site in any age group.(2,3,7) DISCUSSION: Isolated reports of neonatal (both term and preterm infants) deaths have been associated with ceftriaxone-calcium precipitates in the lungs and kidneys. A total of 7 cases have been reported to the FDA, resulting in 5 deaths. All 5 deaths were in neonates of 3 weeks or less in age. Six of the 7 patients received calcium gluconate, 1 received calcium via hyperalimentation.(6) In some cases, ceftriaxone and the calcium product were administered by different routes,(1) lines,(2) and/or at different times.(1,2) Reports of a ceftriaxone-calcium salt precipitate in the gall-bladder have also been reported.(2) In in vitro studies in adult and neonatal plasma, ceftriaxone recovery was examined with ceftriaxone concentrations up to 1 mM (in excess of concentrations seen with 2 g ceftriaxone infused over 30 minutes) and calcium concentrations up to 12 mM (48 mg/dL). Ceftriaxone recovery was reduced with calcium concentrations of 6 mM (24 mg/dL) in adult plasma and 4 mM (16 mg/dL) in neonatal plasma. This may indicate ceftriaxone-calcium precipitation formation.(2,7) There have been no reports associated with concurrent use of oral calcium products and the US manufacturer of ceftriaxone states that there is no risk with oral calcium products or use of intramuscular ceftriaxone.(4)	CEFTRIAXONE, CEFTRIAXONE SODIUM
Digitalis Glycosides/Intravenous Calcium Products SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: The mechanism of action of digitalis glycosides involves its ability to cause an increase in excitation-contraction coupling mediated through the effects of calcium. Excitable tissues in the heart experience inhibition of sodium/potassium ATPase (the membrane "sodium pump") by digitalis glycosides and so attain relatively higher intracellular sodium and lower potassium concentrations. Higher intracellular sodium concentrations facilitate exchange of extracellular calcium ions and the inward and internal flux of calcium results in modified transmembrane potentials and stronger contractions of cardiac muscle. Elevated extracellular concentrations of calcium after parenteral calcium salts further facilitate these inward calcium fluxes. CLINICAL EFFECTS: Rapid administration of calcium via the intravenous route may result in digitalis toxicity, including arrhythmias.(1) PREDISPOSING FACTORS: Low body weight, advanced age, impaired renal function, hypokalemia, hypercalcemia, and/or hypomagnesemia may increase the risk of digoxin toxicity. PATIENT MANAGEMENT: In patients maintain on a digitalis glycosides, administer intravenous calcium slowly and with caution. If cardiac toxicity develops, supportive measures without additional antiarrhythmics may be sufficient. DISCUSSION: Effects of digitalis glycosides on the heart are increased by elevated extracellular concentrations of ionic calcium. Intravenous administration of calcium salts during digitalis therapy may result in altered cardiac electrophysiologic activity such as tachycardia or arrhythmias. Oral calcium carbonate has not been shown to affect the bioavailability of oral digitalis.	DIGITEK, DIGOXIN, DIGOXIN MICRONIZED, LANOXIN, LANOXIN PEDIATRIC
Linezolid/Tryptophan SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use may result in additive effects on serotonin levels. MAOIs may potentiate the effects of tryptophan.(1) CLINICAL EFFECTS: Concurrent administration of tryptophan with a MAO Inhibitor may result in serotonin syndrome and/or hypertensive crisis.(1) Symptoms of serotonin syndrome may include tremor, agitation, diaphoresis, hyperreflexia, clonus, tachycardia, hyperthermia, and muscle rigidity.(2) In addition to these effects, disorientation, delirium, agitation, hypomania, shivering, ocular oscillation, and Babinski signs have been reported with concurrent tryptophan and phenelzine.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving linezolid should not be administered tryptophan unless they can be closely monitored for serotonin syndrome. If concurrent therapy is warranted, patients should be monitored for signs and symptoms of serotonin syndrome. Instruct patients to report muscle twitching, tremors, shivering and stiffness, fever, heavy sweating, heart palpitations, restlessness, confusion, agitation, trouble with coordination, or severe diarrhea. DISCUSSION: In a case report, a patient receiving metoclopramide and a TPN containing tryptophan developed serotonin syndrome following the addition of linezolid to therapy.(3) In a study in nine subjects, the administration of a single intravenous dose of tryptophan with tranylcypromine significantly increased the normal prolactin response to tryptophan. Four of the nine subjects developed a distinctive neuromotor syndrome characterized by hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea.(4) Another set of authors reported eight cases of delirium, ranging from mild to severe, in patients who received concurrent tranylcypromine and tryptophan. Symptoms developed within two days to 4 weeks of beginning concurrent therapy.(5) In a case report, the addition of tryptophan to a tranylcypromine regimen resulted in hypomania.(6) In another report, a patient developed hyperventilation, shivering, hyperthermia, increased muscle tone, and hyperreflexia when tryptophan was added to tranylcypromine therapy.(7) There are two reports of fatalities following the concurrent administration of tryptophan and tranylcypromine. In the first report, a a patient had been receiving chlorpromazine, lithium, and tryptophan when phenelzine was initiated. Four weeks later, the patient developed neuroleptic malignant syndrome and expired despite resuscitation efforts.(8) In the second report, a patient had been receiving fluoxetine, levothyroxine, propranolol, quinidine, and hydroxyzine. Fluoxetine was discontinued and tranylcypromine, thioridazine, and tryptophan were initiated. The patient developed neuroleptic malignant syndrome two and one-half hours after the first tryptophan dose and expired 24 hours later. (9) In a case report, the addition of tryptophan to a regimen that included phenelzine resulted in an acute behavioral and neurologic syndrome. The patient's symptoms resolved 24 hours after the discontinuation of both agents.(10) In another report, a patient developed hypomania following the addition of tryptophan to phenelzine therapy.(6) Another report describes the development of delirium following the addition of tryptophan to phenelzine.(11) One set of authors reported three cases of myoclonus, hyperreflexia, and diaphoresis following the addition of tryptophan to phenelzine therapy.(12) Some studies have shown that the addition of tryptophan to MAO Inhibitor therapy may have beneficial results, including greater improvement in depression and faster onset of effects.(13,14)	LINEZOLID, LINEZOLID-0.9% NACL, LINEZOLID-D5W, ZYVOX
Mixed;Indirect Sympathomimetics/Rasagiline SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Catecholamine stores increased by MAOIs can be released by indirect acting sympathomimetics such as ephedrine and amphetamine. MAO inhibitors also interfere with gut and liver metabolism of direct acting sympathomimetics (e.g oral phenylephrine). CLINICAL EFFECTS: Concurrent use of MAOIs may result in potentiation of sympathomimetic effects, which may result in headaches, hypertensive crisis, toxic neurological effects, and malignant hyperpyrexia. Hypertensive crisis has been reported in patients taking recommended doses of rasagiline with sympathomimetic agents. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: At recommended dosages, rasagiline is selective for MAO-B; however, at higher dosages it has been shown to lose its selectivity. Patients receiving higher dosages of rasagiline should be considered susceptive to this interaction. Concurrent use should be approached with caution. DISCUSSION: Indirect acting sympathomimetic amines may cause abrupt elevation of blood pressure when administered to patients taking monoamine oxidase inhibitors, resulting in a potentially fatal hypertensive crisis. Mixed (direct and indirect) acting sympathomimetics have also been shown to interact with monoamine oxidase inhibitors depending on their degree of indirect action. The direct-acting sympathomimetics have not been reported to interact. Dopamine is metabolized by monoamine oxidase, and its pressor effect is enhanced by monoamine oxidase inhibitors.	AZILECT, RASAGILINE MESYLATE

There are 1 moderate interactions. The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.

Drug Interaction	Drug Names
Ziprasidone/Serotonergic Agents SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Ziprasidone is a 5-HT1A agonist and serotonin and norepinephrine reuptake inhibitor. Concurrent administration with one or more serotonergic agents may increase serotonin effects, resulting in serotonin toxicity.(1,2) CLINICAL EFFECTS: Concurrent use of ziprasidone and other serotonergic agents may result in serotonin syndrome, a potentially life-threatening condition with symptoms including altered mental status, hypertension, restlessness, myoclonus, hyperthermia, hyperreflexia, diaphoresis, shivering, and tremor.(1) PREDISPOSING FACTORS: Serotonin syndrome risk is dose-related. Higher systemic concentrations of either drug would be predicted to increase risk for serotonin toxicity.(2) Concomitant therapy with multiple agents which increase brain serotonin concentrations may also increase risk for serotonin syndrome.(2) PATIENT MANAGEMENT: Caution patients about the risk of serotonin syndrome with the concomitant use of ziprasidone with other serotonergic drugs. Instruct patients to contact their healthcare provider, or report to the emergency room, should they experience signs or symptoms of serotonin syndrome.(1) DISCUSSION: Several cases of serotonin syndrome have been reported in patients receiving ziprasidone.(4-6)	GEODON, ZIPRASIDONE HCL, ZIPRASIDONE MESYLATE

Drug Interaction

Drug Names

Ziprasidone/Serotonergic Agents

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Ziprasidone is a 5-HT1A agonist and serotonin and norepinephrine reuptake inhibitor. Concurrent administration with one or more serotonergic agents may increase serotonin effects, resulting in serotonin toxicity.(1,2)

CLINICAL EFFECTS: Concurrent use of ziprasidone and other serotonergic agents may result in serotonin syndrome, a potentially life-threatening condition with symptoms including altered mental status, hypertension, restlessness, myoclonus, hyperthermia, hyperreflexia, diaphoresis, shivering, and tremor.(1)

PREDISPOSING FACTORS: Serotonin syndrome risk is dose-related. Higher systemic concentrations of either drug would be predicted to increase risk for serotonin toxicity.(2) Concomitant therapy with multiple agents which increase brain serotonin concentrations may also increase risk for serotonin syndrome.(2)

PATIENT MANAGEMENT: Caution patients about the risk of serotonin syndrome with the concomitant use of ziprasidone with other serotonergic drugs. Instruct patients to contact their healthcare provider, or report to the emergency room, should they experience signs or symptoms of serotonin syndrome.(1)

DISCUSSION: Several cases of serotonin syndrome have been reported in patients receiving ziprasidone.(4-6)

GEODON, ZIPRASIDONE HCL, ZIPRASIDONE MESYLATE

The following contraindication information is available for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate):

Overview
Contraindicated
Severe
Moderate

Drug contraindication overview.

No enhanced Contraindications information available for this drug.

There are 3 contraindications. Absolute contraindication.

Contraindication List
Digitalis toxicity
Hypercalcemia
Phenylketonuria

There are 3 severe contraindications. Adequate patient monitoring is recommended for safer drug use.

Severe List
Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min
Chronic kidney disease stage 5 (failure) GFr<15 ml/min
Hypercalcinuria

There are 3 moderate contraindications. Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.

Moderate List
Chronic kidney disease stage 3B (moderate) GFR 30-44 ml/min
Kidney disease with reduction in glomerular filtration rate (GFr)
Sarcoidosis

The following precautions are available for AA 3.5%-D10W-CALCIUM (amino acid 3.5 % no.2 ped/dextrose 10 %/calcium gluconate):

Pediatric
Pregnant
Lactation
Geriatric

No enhanced Pediatric Use information available for this drug.

Contraindicated

None

Severe Precaution

None

Management or Monitoring Precaution

None

No enhanced Pregnancy information available for this drug.

No enhanced Lactation information available for this drug.

No enhanced Geriatric Use information available for this drug.