Children's Sudafed Pe (phenylephrine HCl)
Amphetamines/Anorexiants/Stimulants Oral Solution, Oral
Last reviewed · Source: First Databank (FDB) drug data
Overview
Phenylephrine hydrochloride is an alpha1-adrenergic receptor agonist.
The phenylephrine activation of alpha1-adrenergic receptors on vascular smooth muscle cells results in vasoconstriction. Following IV administration of phenylephrine hydrochloride, systolic and diastolic blood pressure, mean arterial blood pressure, and total peripheral vascular resistance are increased. Vasoconstriction occurs in most vascular beds, including renal, pulmonary, and splanchnic arteries, but minimal to no effect is observed on cerebral blood vessels.
Hepatic vascular beds are also affected. In some patients, phenylephrine can substantially reduce cardiac output, presumably due to increased afterload; however, the exact effects of the drug on global cardiac output depend on the dose and contributory effects of the arterial and venous vasculature. Although phenylephrine reduces venous compliance and can potentially increase venous return, accompanying increases in arterial and venous resistance can negate this potential benefit.
With increased blood pressure following IV administration, there is increased vagal activity, resulting in reflex bradycardia. Phenylephrine constricts both arterial and venous blood vessels, although its effects on arterial vessels are more pronounced. At clinically relevant dosages, phenylephrine increases myocardial work and oxygen requirements.
Following an IV bolus of phenylephrine hydrochloride, blood pressure increase is rapid, typically occurring within minutes. Blood pressure effects from a phenylephrine bolus may persist for up to 20 minutes. Phenylephrine is widely distributed into organs and peripheral tissues.
It is not known if phenylephrine or its metabolite are distributed into human or animal milk following parenteral administration.
Phenylephrine is extensively metabolized in the liver. Phenylephrine primarily undergoes metabolism by sulfotransferase and monoamine oxidase (MAO) to pharmacologically inactive metabolites. The 2 major metabolites are m-hydroxymandelic acid and sulfate conjugates.
Following IV administration of phenylephrine, approximately 86% of the dose is excreted in urine within 48 hours, principally as metabolites; approximately 16% of the dose is excreted in urine as unchanged drug. The terminal elimination half-life of phenylephrine averages 2.5 hours following IV administration. The observed effective half-life is approximately 5 minutes following IV infusion of the drug.
Patients with hepatic cirrhosis may have a reduced response to phenylephrine, potentially requiring higher dosages of the drug. Patients with end-stage renal disease may have an increased response to phenylephrine, potentially requiring lower dosages of the drug.
Generic name: phenylephrine HCl
Drug class: Amphetamines/Anorexiants/Stimulants
Therapeutic class: Respiratory Therapy Agents
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
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Indications
The following indications are listed for Children's Sudafed Pe:
- Nasal Congestion
Also known as: Nasal Stuffiness.
Dosing
No dosing information is available for this tab.
Phenylephrine hydrochloride is administered by IV bolus or continuous IV infusion for the treatment of clinically important hypotension. The drug is available as a 10 mg/mL phenylephrine hydrochloride injection concentrate that must be diluted prior to administration and as a ready-to-use phenylephrine hydrochloride 100 mcg/mL (Immphentiv(R), Biorphen(R)) injection. Ready-to-use phenylephrine hydrochloride 100 mcg/mL (Immphentiv(R), Biorphen(R)) injection should not be further diluted before IV bolus administration.
For treatment of hypotension during anesthesia, the manufacturers recommend administration of phenylephrine hydrochloride as an IV bolus or continuous infusion; when used in the treatment of septic shock, the drug should be administered as a continuous IV infusion with no initial bolus dose. Phenylephrine hydrochloride injection should be stored at 20-25degreesC, but may be exposed to temperatures ranging from 15-30degreesC; single-dose and pharmacy bulk vials should be kept in their original carton until time of use and protected from light.
Commercially available phenylephrine hydrochloride injection concentrate must be diluted with a compatible IV solution prior to administration. Diluted solutions may be stored at room temperature for up to 4 hours or under refrigeration for up to 24 hours; any unused portions should be discarded.
Commercially available phenylephrine hydrochloride bulk vials are intended for use in a pharmacy admixture program for preparation of single doses to be dispensed to multiple patients. Each vial should be penetrated only one time with a suitable sterile transfer device or dispensing set. Dispensing from a pharmacy bulk vial should be completed within 4 hours after the vial is penetrated.
Prior to administration, phenylephrine hydrochloride solutions should be inspected visually for particulate matter and discoloration; the drug should be discarded if the solution is colored, cloudy, or contains any particulate matter.
Care should be taken to avoid extravasation and the infusion site should be checked for free flow.
No dosing information is available for this tab.
No dosing information is available for this tab.
Drug interactions
There is no enhanced messaging for this drug.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Mixed & Indirect Sympathomimetics; Oral Phenylephrine/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. 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.
Sympathomimetics/Dihydroergotamine
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 of dihydroergotamine and sympathomimetics may result in additive or synergistic effect on peripheral blood vessels.(1)
CLINICAL EFFECTS: Concurrent use of dihydroergotamine and sympathomimetics may result in increased blood pressure due to peripheral vasoconstriction.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Dihydroergotamine is contraindicated with sympathomimetics because the combination may result in additive or synergistic elevation of blood pressure.(1)
DISCUSSION: Significant elevation in blood pressure has been reported in patients treated with dihydroergotamine.(1) Sympathomimetics can be expected to have additional effects on blood pressure.
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Agents That Affect Catecholamines/Iobenguane I 123
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Many compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with iobenguane uptake into cells.(1)
CLINICAL EFFECTS: Compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with imaging completed with iobenguane.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discuss the use of agents that affect catecholamines. Discontinue drugs that reduce catecholamine uptake or deplete catecholamine stores prior to imaging with iobenguane. Before imaging with iobenguane, discontinue agents that affect catecholamines for at least 5 biological half-lives, as clinically tolerated.(1)
DISCUSSION: Many agents may reduce catecholamine uptake or deplete catecholamine stores.(1) Examples include: - CNS stimulants or amphetamines (e.g. cocaine, methylphenidate, dextroamphetamine) - norepinephrine and dopamine reuptake inhibitors (e.g. phentermine) - norepinephrine and serotonin reuptake inhibitors (e.g. tramadol) - monoamine oxidase inhibitors (e.g. phenelzine, linezolid) - central monoamine depleting drugs (e.g. reserpine) - non-select beta adrenergic blocking drugs (e.g. labetalol) - alpha agonists or alpha/beta agonists (e.g. pseudoephedrine, phenylephrine, ephedrine, phenylpropanolamine, naphazoline) - tricyclic antidepressants or norepinephrine reuptake inhibitors (e.g. amitriptyline, bupropion, duloxetine, mirtazapine, venlafaxine) - botanicals that may inhibit reuptake of norepinephrine, serotonin or dopamine (e.g. ephedra, ma huang, St. John's Wort, yohimbine)
Agents That Affect Catecholamines/Iobenguane I 131
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Many compounds that reduce catecholamine uptake or that deplete catecholamine stores may interfere with iobenguane uptake into cells.(1)
CLINICAL EFFECTS: Compounds that reduce catecholamine uptake or that deplete catecholamine stores may impact the dosimetry calculations or effectiveness of iobenguane.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Discuss the use of agents that affect catecholamines. Discontinue drugs that reduce catecholamine uptake or deplete catecholamine stores for at least 5 half-lives before administration of either the dosimetry or a therapeutic dose of iobenguane. Do not administer these drugs until at least 7 days after each iobenguane dose.(1)
DISCUSSION: Many agents may reduce catecholamine uptake or deplete catecholamine stores.(1) Examples include: - CNS stimulants or amphetamines (e.g. cocaine, methylphenidate, dextroamphetamine) - norepinephrine and dopamine reuptake inhibitors (e.g. phentermine) - norepinephrine and serotonin reuptake inhibitors (e.g. tramadol) - monoamine oxidase inhibitors (e.g. phenelzine, linezolid) - central monoamine depleting drugs (e.g. reserpine) - non-select beta adrenergic blocking drugs (e.g. labetalol) - alpha agonists or alpha/beta agonists (e.g. pseudoephedrine, phenylephrine, ephedrine, phenylpropanolamine, naphazoline) - tricyclic antidepressants or norepinephrine reuptake inhibitors (e.g. amitriptyline, bupropion, duloxetine, mirtazapine, venlafaxine) - botanicals that may inhibit reuptake of norepinephrine, serotonin or dopamine (e.g. ephedra, ma huang, St. John's Wort, yohimbine) - calcium channel blockers
Mixed & Indirect Sympathomimet; Oral Phenylephrine/Slt Maois
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. Fatalities have occurred with combinations of sympathomimetics and MAO-A inhibitors.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Concurrent use of MAO-A inhibitors and sympathomimetics is contraindicated. The manufacturers of sympathomimetic agents recommend waiting 14 days after discontinuation of MAO inhibitors before initiating the sympathomimetic. Patients receiving indirect acting sympathomimetics should not receive linezolid unless they are monitored for potential increases in blood pressure. Initial dosages of dopamine should be reduced. At recommended dosages, 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. Patients receiving higher dosages of selegiline should be considered susceptive to this interaction.
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. Foods containing large amounts of tyramine have also been implicated in this interaction. A significant pressor response was observed in normal subjects receiving linezolid and tyramine doses of more than 100 mg. Administration of linezolid (600 mg BID for 3 days) with pseudoephedrine (60 mg q 4 hours for 2 doses) increased blood pressure by 32 mmHg. Administration of linezolid (600 mg BID for 3 days) with phenylpropanolamine (25 mg q 4 hours for 2 doses) increased blood pressure by 38 mmHg. 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.
Mixed & Indirect Sympathomimet;Oral Phenylephrine/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.
Selected Direct-Acting Sympathomimetics/Tricyclic Compounds
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Unknown. However, it is speculated that direct-acting sympathomimetic amines have an enhanced effect due to tricyclic blockage of norepinephrine reuptake.
CLINICAL EFFECTS: Increased effect of direct acting sympathomimetics.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Consider avoiding the concurrent use of direct-acting sympathomimetics and tricyclic compounds. If concurrent use of direct-acting sympathomimetics and tricyclic compounds is warranted, the initial dose of the sympathomimetic should be lowered and the patient should be monitored for adverse cardiovascular effects. Use of tricyclic compounds and other sympathomimetics should be approached with caution.
DISCUSSION: Epinephrine and other direct-acting sympathomimetic amines exert enhanced cardiovascular effects (e.g., arrhythmias, hypertension, and tachycardia) in individuals concurrently receiving or previously treated with tricyclic antidepressants. Other direct and mixed acting sympathomimetic amines have also been reported to interact with tricyclic antidepressants. These include norepinephrine, phenylephrine, dopamine, and methoxamine. Protriptyline, amitriptyline, and desipramine have also been reported to interact with direct-acting sympathomimetics.
Sympathomimetics/Ergot Alkaloids
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Concurrent use of ergot alkaloids and sympathomimetics may result in additive or synergistic effect on peripheral blood vessels.
CLINICAL EFFECTS: Concurrent use of ergot alkaloids and sympathomimetics may result in increased blood pressure due to peripheral vasoconstriction.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: When possible, avoid the concurrent use of ergot alkaloids and sympathomimetics. If concurrent use is warranted, monitor blood pressure and for signs of vasoconstriction. Decreasing the dose of one or both drugs may be necessary.
DISCUSSION: There have been reports of severe vasoconstriction resulting in gangrene in patients receiving intravenous ergonovine with dopamine or norepinephrine.
Sympathomimetics/Selected Inhalation Anesthetic Agents
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The exact mechanism is unknown. The anesthetics produce conduction changes that increase impulse re-entry into the myocardial tissue.(1) The anesthetics' ability to precipitate arrhythmias is enhanced by elevated arterial blood pressure, tachycardia, hypercapnia, and/or hypoxia, events that stimulate the release of endogenous catecholamines.(1)
CLINICAL EFFECTS: Concurrent use of inhalation anesthetic agents and sympathomimetics may result in ventricular arrhythmias or sudden blood pressure and heart rate increase during surgery.(2)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Monitor blood pressure and avoid use of sympathomimetics in patients being treated with anesthetics on the day of surgery.(2) Intravenous use of epinephrine during surgery with halothane and related halogenated general anesthetics should be strongly discouraged. When intravenous epinephrine is necessary, nitrous oxide anesthesia supplemented with ether, muscle relaxants, or opioids should be used instead of halothane.(3,4) Epinephrine may safely be used subcutaneously with the following precautions: the patient is adequately ventilated to prevent hypoxia or respiratory acidosis; the total dose of epinephrine is limited to 100 mcg/10 minute period or 300 mcg/hour in adults, 3.5 mcg/Kg in infants, 2.5 mcg/Kg in children up to two years of age, and 1.45 mcg/Kg in children over two years of age; a minimum effective concentration of anesthetic is maintained; the drugs are not co-administered in patients with hypertension or other cardiovascular disorders; and the cardiac rhythm is continuously monitored during and after injection.(3-10) If arrhythmias occur after the administration of the epinephrine, the drugs of choice are lidocaine or propranolol, depending on the type of arrhythmia.(1)
DISCUSSION: Administration of epinephrine during halothane anesthesia may may lead to serious ventricular arrhythmias.(3-6,11-18) This has occurred when epinephrine was administered intravenously,(6) when it was administered with lidocaine as a dental block,(11,14) or when it was administered supraperiosteally.(5) Norepinephrine has been shown to interact with halothane in a manner similar to epinephrine.(1) In two case reports, patients were given terbutaline (0.25 to 0.35 mg) for wheezing following induction of anesthesia with halothane. One patient's heart rate increased from 68 to 100 beats/minute, and the ECG showed premature ventricular contractions and bigeminy, while the other patient developed multiple unifocal premature ventricular contractions and bigeminy. The arrhythmias resolved in both patients following lidocaine administration.(19) Although not documented, isoproterenol causes effects on the heart similar to terbutaline(20) and would probably interact with halothane in a similar manner. Other inhalation anesthetics that increase the incidence of arrhythmias with epinephrine include chloroform,(20) methoxyflurane,(20) and enflurane.(12) A similar interaction may be expected between the other inhalation anesthetics and sympathomimetics.
Moderate Interaction: Assess the risk to the patient and take action as needed.
Sympathomimetics (Direct, Mixed-Acting)/Guanethidine
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Direct or mixed-acting sympathomimetics may inhibit uptake of guanethidine at the adrenergic neuron.
CLINICAL EFFECTS: Decreased antihypertensive effectiveness. Effects may be seen for several days after discontinuation of the direct or mixed-acting sympathomimetic.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Avoid concomitant administration of these drugs. If both drugs are administered, adjust the guanethidine dose as needed based on blood pressure.
DISCUSSION: Documentation supports routine monitoring of this interaction. It should be noted that this interaction can occur quickly.
Sympathomimetics (Direct, Mixed-Acting)/Methyldopa
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Unknown.
CLINICAL EFFECTS: The pressor response to sympathomimetics may be increased.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Start with low doses of sympathomimetics and monitor blood pressure of patients during concurrent administration of sympathomimetics and methyldopa.
DISCUSSION: The pressor response to sympathomimetics has been reported to be increased during methyldopa administration. In addition to increased duration of pressor response, severe hypertension has been reported.
Sympathomimetics/Rauwolfia Alkaloids
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Reserpine depletes catecholamine stores within the peripheral vascular adrenergic nerve endings, thus indirect acting sympathomimetics are unable to trigger the release of catecholamines. The reserpine-induced catecholamine release increases sensitivity to the effects of direct acting sympathomimetics.
CLINICAL EFFECTS: Increased effects of direct acting sympathomimetics. Decreased effects of indirect acting sympathomimetics. Mixed acting sympathomimetics will show effects based on the predominance of either direct or indirect activity.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If these agents are administered concurrently, monitor blood pressure. The dose of the sympathomimetic may need to be adjusted.
DISCUSSION: This interaction has been well documented in animal studies and human case reports have confirmed the interaction. Reserpine has been shown to decrease the response to epinephrine administered for hypotension. Reserpine has also been shown to decrease the effectiveness of ophthalmic epinephrine, a direct acting sympathomimetic. Ophthalmic phenylephrine has been shown to decrease the hypotensive effects of reserpine.
Contraindications
*Known hypersensitivity to phenylephrine or to any ingredient in the respective formulation.
- Severe uncontrolled hypertension
- Benign prostatic hyperplasia
- Coronary artery disease
- Hypertension
- Hyperthyroidism
- Chronic heart failure
Adverse reactions
The most commonly reported adverse effects in patients receiving IV phenylephrine hydrochloride were nausea, vomiting, and headache.
Rare or Very Rare
- Cardiac arrhythmia
- Dizziness
- Headache disorder
- Hyperhidrosis
- Insomnia
- Nervousness
- Pallor
- Tachycardia
- Tremor
There are no less severe adverse reactions for this drug.
Precautions
No enhanced messaging available.
The manufacturers state that safety and efficacy of parenteral preparations of phenylephrine hydrochloride have not been established in pediatric patients.
Data from randomized trials and meta-analyses with phenylephrine injection in pregnant women undergoing Cesarean section have not established a drug-associated risk of major birth defects or miscarriage. Additionally, the data did not identify adverse effects on maternal outcomes or infant Apgar scores. At recommended doses, phenylephrine does not appear to significantly affect fetal heart rate or fetal heart rate variability. Data are not available on phenylephrine use during the first or second trimester.
Untreated hypotension in pregnant women undergoing Cesarean delivery with neuraxial anesthesia has been associated with increased maternal nausea and vomiting. A sustained decrease in uterine blood flow caused by maternal hypotension has also been associated with fetal bradycardia and acidosis.
No data are available on the safety of phenylephrine injection during the period of organogenesis; therefore, conclusions cannot be drawn regarding the risk of birth defects from drug exposure. In addition, no data are available on the risk of miscarriage following fetal exposure to phenylephrine injection.
In animal studies, fetal malformations were observed following phenylephrine infusion over 1 hour during the period of organogenesis at a dosage of 1.2 times the human daily dosage. Decreased pup weight was also observed in offspring of pregnant rats who received 2.9 times the human daily dose of phenylephrine.
If a vasopressor is used in conjunction with oxytocic drugs, the vasopressor effect is potentiated and may result in serious adverse effects.
There are no data on whether phenylephrine or its metabolite is distributed into human or animal milk following parenteral administration. The effects on the breast-fed infant and milk production are not known.
The developmental and health benefits of breast-feeding should be weighed along with the mother's clinical need for the drug and any potential adverse effects on the breast-fed infant from phenylephrine or from the underlying maternal condition.
If phenylephrine is used in geriatric patients, dosage should be selected carefully, usually starting at the low end of the dosage range, since renal, hepatic, and cardiovascular dysfunction and concomitant disease or other drug therapy are more common in this age group.
Clinical studies of phenylephrine hydrochloride did not include sufficient numbers of patients >=65 years of age to determine whether geriatric patients respond differently than younger patients. Clinical experience to date has not identified any differences in response between geriatric and younger patients.
If phenylephrine is used in geriatric patients, dosage should be selected carefully, usually starting at the low end of the dosage range, since renal, hepatic, and cardiovascular dysfunction and concomitant disease or other drug therapy are more common in this age group.
ICD codes
| Code | Type | Description |
|---|---|---|
| Nasal congestion | ||
| R09.81 | ICD10CM | Nasal congestion |
ICD code information from First Databank (FDB).
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Last reviewed · Source: First Databank (FDB) drug data
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