Sudafed Sinus 12Hr Pressr-Pain (naproxen sodium/pseudoephedrine HCl)

The lowest possible effective dosage and shortest duration of therapy consistent with treatment goals of the patient should be employed. Dosage of naproxen must be carefully adjusted according to individual requirements and response, using the lowest possible effective dosage.

Lower dosages of the drug should be considered in patients with renal or hepatic impairment or in geriatric patients. Use of naproxen or naproxen sodium in patients with moderate to severe renal impairment (creatinine clearance less than 30 mL/minute) is not recommended. Caution is advised when high dosages are required in patients with hepatic impairment. The commercially available preparation containing naproxen in fixed combination with esomeprazole magnesium is not recommended for patients with severe hepatic impairment because the appropriate esomeprazole dosage is not available as a fixed-ratio preparation for twice-daily dosing. In addition, the commercially available preparation containing naproxen sodium in fixed combination with sumatriptan succinate should not be used in patients with hepatic impairment since sumatriptan dosage cannot be appropriately adjusted.

Patients receiving naproxen for self-medication should be advised to use the lowest effective dosage and not to exceed the recommended dosage or duration of therapy. (See Precautions for Self-medication under Cautions.)

Each 220, 275, 412.5, 550, or 825 mg of naproxen sodium is approximately equivalent to 200, 250, 375, 500, or 750 mg of naproxen, respectively.

Different dose strengths and formulations are not necessarily bioequivalent, and this should be considered when changing from one strength to another or from one formulation to another.

The potential benefits and risks of naproxen therapy as well as alternative therapies should be considered prior to initiating naproxen therapy.

Naproxen and naproxen sodium are administered orally. Enteric-coated tablets of naproxen should not be broken, crushed, or chewed, so that the delayed-release properties of this formulation are maintained. Adverse GI effects may be minimized by administering the drugs with meals or milk. When used for self-medication, the manufacturer recommends that each dose of naproxen sodium be taken with a full glass of water. Tablets containing naproxen sodium in fixed combination with sumatriptan succinate may be administered without regard to meals; the tablets should not be split, crushed, or chewed. Naproxen oral suspension should be shaken gently prior to use; to ensure accurate measurement of the dose, a calibrated measuring device should always be used to administer the oral suspension. Tablets containing delayed-release naproxen in fixed combination with immediate-release esomeprazole magnesium should be swallowed whole with liquid and administered at least 30 minutes before meals; the tablets should not be split, chewed, crushed, or dissolved.

Because of the delayed-release properties of enteric-coated formulations, enteric-coated preparations of naproxen are not recommended for the management of acute pain. Also, the manufacturer states that because naproxen sodium is absorbed more rapidly than naproxen, the sodium salt conventional tablet formulation is recommended for the management of acute painful conditions when prompt onset of pain relief is desired.

Pseudoephedrine hydrochloride and sulfate are administered orally.

Pseudoephedrine hydrochloride 240-mg extended-release tablets should be administered orally once daily and swallowed whole with water; the extended-release tablets should not be divided, crushed, chewed, or dissolved. Patients should be advised that the tablet does not completely dissolve and may be passed in the stool.

No dosing information is available for this tab.

No dosing information is available for this tab.

There is no enhanced messaging for this drug.

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

Naproxen is contraindicated in patients with known hypersensitivity (e.g., anaphylaxis, serious dermatologic reactions) to the drug or any ingredient in the formulation. In addition, NSAIAs, including naproxen, generally are contraindicated in patients in whom asthma, urticaria, or other sensitivity reactions are precipitated by aspirin or other NSAIAs, since there is potential for cross-sensitivity between NSAIAs and aspirin, and severe, rarely fatal, anaphylactic reactions to NSAIAs have been reported in these patients. Although NSAIAs generally are contraindicated in these patients, the drugs have occasionally been used in NSAIA-sensitive patients who have undergone desensitization. Because patients with asthma may have aspirin-sensitivity asthma, patients with asthma but without known aspirin sensitivity who are receiving naproxen should be monitored for changes in manifestations of asthma. In patients with asthma, aspirin sensitivity is manifested principally as bronchospasm and usually is associated with nasal polyps; the association of aspirin sensitivity, asthma, and nasal polyps is known as the aspirin triad. Patients who are considering use of naproxen for self-medication should be advised that naproxen is contraindicated in patients who have experienced asthma, urticaria, or other sensitivity reaction to other analgesics or antipyretics. For a further discussion of cross-sensitivity of NSAIAs, see Cautions: Sensitivity Reactions, in the Salicylates General Statement 28:08.04.24.

NSAIAs are contraindicated in the setting of CABG surgery.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

There is no enhanced messaging for this drug.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

No enhanced messaging available.

No enhanced messaging available.

Use of NSAIAs during pregnancy at about 30 weeks of gestation or later can cause premature closure of the fetal ductus arteriosus, and use at about 20 weeks of gestation or later has been associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, use of NSAIAs should be avoided in pregnant women at about 30 weeks of gestation or later; if NSAIA therapy is necessary between about 20 and 30 weeks of gestation, the lowest effective dosage and shortest possible duration of treatment should be used. Monitoring of amniotic fluid volume via ultrasound examination should be considered if the duration of NSAIA treatment exceeds 48 hours; if oligohydramnios occurs, the drug should be discontinued and follow-up instituted according to clinical practice. Pregnant women should be advised to avoid use of NSAIAs beginning at 20 weeks' gestation unless otherwise advised by a clinician; they should be informed that NSAIAs should be avoided beginning at 30 weeks' gestation because of the risk of premature closure of the fetal ductus arteriosus and that monitoring for oligohydramnios may be necessary if NSAIA therapy is required for longer than 48 hours' duration between about 20 and 30 weeks of gestation.

Known effects of NSAIAs on the human fetus during the third trimester of pregnancy include prenatal constriction of the ductus arteriosus, tricuspid incompetence, and pulmonary hypertension; nonclosure of the ductus arteriosus during the postnatal period (which may be resistant to medical management); and myocardial degenerative changes, platelet dysfunction with resultant bleeding, intracranial bleeding, renal dysfunction or renal failure, renal injury or dysgenesis potentially resulting in prolonged or permanent renal failure, oligohydramnios, GI bleeding or perforation, and increased risk of necrotizing enterocolitis.

Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment has been observed, on average, following days to weeks of maternal NSAIA use, although oligohydramnios has been observed infrequently as early as 48 hours after initiation of NSAIA therapy. Oligohydramnios is often, but not always, reversible (generally within 3-6 days) following discontinuance of NSAIA therapy. Complications of prolonged oligohydramnios may include limb contracture and delayed lung maturation. A limited number of case reports have described maternal NSAIA use and neonatal renal dysfunction, in some cases irreversible, without oligohydramnios. Some cases of neonatal renal dysfunction have required treatment with invasive procedures such as exchange transfusion or dialysis. Deaths associated with neonatal renal failure have been reported. Methodologic limitations of these postmarketing studies and case reports include lack of a control group; limited information regarding dosage, duration, and timing of drug exposure; and concomitant use of other drugs. These limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants, and the extent to which certain reported risks can be generalized to full-term infants is uncertain.

Animal data indicate that prostaglandins have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, inhibitors of prostaglandin synthesis, such as naproxen, were associated with increased pre- and post-implantation losses. Prostaglandins also have an important role in fetal kidney development. In animal studies, inhibitors of prostaglandin synthesis impaired kidney development at clinically relevant doses.

Reproduction studies of naproxen in rats at 20 mg/kg daily (125 mg/m2, 0.23 times the human systemic exposure), rabbits at 20 mg/kg daily (220 mg/m2, 0.27 times the human systemic exposure), and mice at 170 mg/kg daily (510 mg/m2, 0.28 times the human systemic exposure) have not revealed evidence of harm to the fetus. Severe hypoxemia due to persistent pulmonary hypertension has occurred in infants whose mothers received naproxen to delay parturition. Neonatal death also has been reported when the drug was used to prevent preterm labor; autopsy of a neonate showed brain hemorrhage, multiple gastric ulcers, extensive GI bleeding, and an adverse cardiovascular effect known to be associated with use of NSAIAs. In addition, severe hyponatremia, water retention, cerebral irritation, and paralytic ileus was reported in a neonate whose mother ingested 5 g of naproxen 8 hours before delivery; it has been suggested that naproxen adversely affected renal function. Renal dysfunction and abnormal prostaglandin E concentrations in premature infants also have been reported.

Effects of naproxen during labor or delivery have not been studied. In animal studies, NSAIAs, including naproxen, inhibited prostaglandin synthesis, delayed parturition, and increased the incidence of stillbirth.

Naproxen is distributed into milk at concentrations of approximately 1% of peak plasma concentrations of the drug.

The developmental and health benefits of breast-feeding should be considered along with the mother's clinical need for naproxen and any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.

No enhanced messaging available.