THE MERCK MANUAL: The Merck Manual of Diagnosis and Therapy
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Acetylcysteine Drug Information Provided by Lexi-Comp

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Pronunciation

(a se teel SIS teen)

Generic Available (U.S.)

Yes: Solution for inhalation

Index Terms

  • N Acetylcysteine
  • N-Acetyl-L-cysteine
  • N-Acetylcysteine
  • Acetylcysteine Sodium
  • Mercapturic Acid
  • Mucomyst
  • NAC

Brand Names: U.S.

  • Acetadote®

Brand Names: Canada

  • Acetylcysteine Solution
  • Mucomyst®
  • Parvolex®

Pharmacologic Category

  • Antidote
  • Mucolytic Agent

Pharmacologic Category Synonyms

  • Expectorant, Mucolytic

Use: Labeled Indications

Antidote for acute acetaminophen poisoning; repeated supratherapeutic ingestion (RSTI) of acetaminophen; adjunctive mucolytic therapy in patients with abnormal or viscid mucous secretions in acute and chronic bronchopulmonary diseases; pulmonary complications of surgery and cystic fibrosis; diagnostic bronchial studies

Use: Unlabeled

Prevention of contrast-induced renal dysfunction (oral, I.V.); distal intestinal obstruction syndrome (DIOS, previously referred to as meconium ileus equivalent)

Pregnancy Risk Factor

B

Pregnancy Considerations

Based on limited reports using acetylcysteine to treat acetaminophen poisoning in pregnant women, acetylcysteine has been shown to cross the placenta and may provide protective levels in the fetus.

Lactation

Excretion in breast milk unknown/use caution

Contraindications

Hypersensitivity to acetylcysteine or any component of the formulation

Warnings/Precautions

Concerns related to adverse effects:

• Anaphylactoid reactions: Acute flushing and erythema have been reported; usually occurs within 30-60 minutes and may resolve spontaneously. Serious anaphylactoid reactions have also been reported and are more commonly associated with I.V. administration, but also occur with oral administration (Mroz, 1997). When used for acetaminophen poisoning, the incidence is reduced when the initial intravenous loading dose is administered over 60 minutes. The acetylcysteine infusion may be interrupted until the treatment of allergic symptoms is initiated; the infusion can then be carefully restarted. Treatment for anaphylactoid reactions should be immediately available. Use caution in patients with asthma or history of bronchospasm as these patients may be at increased risk. Conversely, patients with high acetaminophen levels (>150 mg/dL) may be at a reduced risk for anaphylactoid reactions (Pakravan, 2008; Sandilands, 2009; Waring, 2008).

Disease-related concerns:

• Acute acetaminophen poisoning: Appropriate use: Acetylcysteine is indicated in patients with a serum acetaminophen level that indicates they are at "possible" risk or greater for hepatotoxicity when plotted on the Rumack-Matthew nomogram. There are several situations where the nomogram is of limited use. Serum acetaminophen levels obtained <4 hours postingestion are not interpretable; patients presenting late may have undetectable serum concentrations, despite having received a toxic dose. The nomogram is less predictive of hepatic injury following an acute overdose with an extended release acetaminophen product. The nomogram also does not take into account patients who may be at higher risk of acetaminophen toxicity (eg, alcoholics, malnourished patients). Nevertheless, acetylcysteine should be administered to any patient with signs of hepatotoxicity, even if the serum acetaminophen level is low or undetectable. Patients who present >24 hours after an acute ingestion or patients who present following an acute ingestion at an unknown time may be candidates for acetylcysteine therapy; consultation with a poison control center or clinical toxicologist is highly recommended.

• Repeated supratherapeutic ingestion (RSTI) of acetaminophen: Appropriate use: The Rumack-Matthew nomogram is not designed to be used following RSTIs. In general, an accurate past medical history, including a comprehensive acetaminophen ingestion history, in conjunction with AST concentrations and serum acetaminophen levels, may give the clinician insight as to the patient's risk of acetaminophen toxicity. Some experts recommend that acetylcysteine be administered to any patient with "higher than expected" serum acetaminophen levels or serum acetaminophen level >10 mcg/mL, even in the absence of hepatic injury; others recommend treatment for patients with laboratory evidence and/or signs and symptoms of hepatotoxicity (Hendrickson, 2006; Jones, 2000). Consultation with a poison control center or a clinical toxicologist is highly recommended.

Dosage form specific issues:

• Inhalation: Since increased bronchial secretions may develop after inhalation, percussion, postural drainage, and suctioning should follow. If bronchospasm occurs, administer a bronchodilator; discontinue acetylcysteine if bronchospasm progresses.

Adverse Reactions

Inhalation: Frequency not defined.

Central nervous system: Drowsiness, chills, fever

Gastrointestinal: Vomiting, nausea, stomatitis

Local: Irritation, stickiness on face following nebulization

Respiratory: Bronchospasm, rhinorrhea, hemoptysis

Miscellaneous: Acquired sensitization (rare), clamminess, unpleasant odor during administration

Intravenous:

>10%: Miscellaneous: Anaphylactoid reaction (8% to 18%; shorter infusion periods [eg, <60 minutes] associated with increased incidence)

1% to 10%:

Cardiovascular: Flushing (1% to 8%), tachycardia (1% to 4%), edema (1% to 2%)

Dermatologic: Urticaria (6% to 8%), rash (2% to 4%), pruritus (1% to 4%)

Gastrointestinal: Vomiting (2% to 10%), nausea (1% to 6%)

Respiratory: Pharyngitis (≤1%), rhinorrhea (≤1%), rhonchi (≤1%), throat tightness (≤1%)

<1%, postmarketing, and/or case reports (limited to important or life-threatening): Anaphylaxis, angioedema, bronchospasm, chest tightness, cough, dizziness, dyspnea, headache, hypotension, respiratory distress, stridor, wheezing

Metabolism/Transport Effects

None known.

Drug Interactions

There are no known significant interactions.

Storage

Solution for injection (Acetadote®): Store unopened vials at room temperature, 20°C to 25°C (68°F to 77°F). Following reconstitution with D5W, solution is stable for 24 hours at room temperature. A color change may occur in opened vials (light purple) and does not affect the safety or efficacy.

Solution for inhalation: Store unopened vials at room temperature; once opened, store under refrigeration and use within 96 hours. A color change may occur in opened vials (light purple) and does not affect the safety or efficacy.

Reconstitution

Solution for injection (Acetadote®):

Loading dose: Dilute 150 mg/kg in D5W 200 mL.

Second dose: Dilute 50 mg/kg in D5W 500 mL.

Third dose: Dilute 100 mg/kg in D5W 1000 mL.

Note: To avoid fluid overload in patients <40 kg and those requiring fluid restriction, decrease volume of D5W proportionally (see table in dosing section). Discard unused portion.

Solution for inhalation: The 20% solution may be diluted with sodium chloride or sterile water; the 10% solution may be used undiluted.

Intravenous administration of solution for inhalation (unlabeled route): Using D5W, dilute acetylcysteine 20% oral solution to a 3% solution.

Compatibility

Inhalation: Incompatible with rubber and metals (particularly iron, copper, and nickel); do not mix with ampicillin, oxytetracycline, erythromycin.

Intravenous: Stable in D5W.

Y-site administration: Incompatible with metals (particularly iron, copper, and nickel); cefepime, ceftazidime

Mechanism of Action

Exerts mucolytic action through its free sulfhydryl group which opens up the disulfide bonds in the mucoproteins thus lowering mucous viscosity.

In patients with acetaminophen toxicity, acetylcysteine acts as a hepatoprotective agent by restoring hepatic glutathione, serving as a glutathione substitute, and enhancing the nontoxic sulfate conjugation of acetaminophen.

The presumed mechanism in preventing contrast-induced nephropathy is its ability to scavenge oxygen-derived free radicals and improve endothelium-dependent vasodilation.

Pharmacodynamics/Kinetics

Onset of action: Inhalation: 5-10 minutes

Duration: Inhalation: >1 hour

Distribution: 0.47 L/kg

Protein binding: 83%

Half-life elimination:

Reduced acetylcysteine: 2 hours

Total acetylcysteine: Adults: 5.6 hours; Newborns: 11 hours

Time to peak, plasma: Oral: 1-2 hours

Excretion: Urine

Dosage

Acetaminophen poisoning: Note: Only the 72-hour oral and 21-hour I.V. regimens are FDA-approved. Ideally, in patients with an acute acetaminophen ingestion, treatment should begin within 8 hours of ingestion or as soon as possible after ingestion. In patients who present following RSTI and treatment is deemed appropriate, acetylcysteine should be initiated immediately.

Children and Adults:

Oral: Note: Consultation with a poison control center or clinical toxicologist is highly recommended when considering the discontinuation of oral acetylcysteine prior to the conclusion of a full 18-dose course of therapy.

72-hour regimen: Consists of 18 doses; total dose delivered: 1330 mg/kg

Loading dose: 140 mg/kg

Maintenance dose: 70 mg/kg every 4 hours; repeat dose if emesis occurs within 1 hour of administration

I.V. (Acetadote®):

21-hour regimen: Consists of 3 doses; total dose delivered: 300 mg/kg

Loading dose: 150 mg/kg (maximum: 15 g) infused over 60 minutes

Second dose: 50 mg/kg (maximum: 5 g) infused over 4 hours

Third dose: 100 mg/kg (maximum: 10 g) infused over 16 hours

Note: The fluid volume should be reduced in patients weighing <40 kg according to the following table:

Acetadote® Dosing / Fluid Volume Guidelines for Patients <40 kg Body Weight (kg) Loading Dose 150 mg/kg over 1 h Second Dose 50 mg/kg over 4 h Third Dose 100 mg/kg over 16 h Acetadote® (mL) D5W (mL) Acetadote® (mL) D5W (mL) Acetadote® (mL) D5W (mL) 30 22.5 100 7.5 250 15 500 25 18.75 100 6.25 250 12.5 500 20 15 60 5 140 10 280 15 11.25 45 3.75 105 7.5 210 10 7.5 30 2.5 70 5 140 Table has been converted to the following text. Acetadote® Dosing / Fluid Volume Guidelines for Patients <40 kg Body weight 30 kg: Loading dose (150 mg/kg over 1 hour): Acetadote® 22.5 mL in D5W 100 mL Second dose (50 mg/kg over 4 hours): Acetadote® 7.5 mL in D5W 250 mL Third dose (100 mg/kg over 16 hours): Acetadote® 15 mL in D5W 500 mL Body weight 25 kg: Loading dose (150 mg/kg over 1 hour): Acetadote® 18.75 mL in D5W 100 mL Second dose (50 mg/kg over 4 hours): Acetadote® 6.25 mL in D5W 250 mL Third dose (100 mg/kg over 16 hours): Acetadote® 12.5 mL in D5W 500 mL Body weight 20 kg: Loading dose (150 mg/kg over 1 hour): Acetadote® 15 mL in D5W 60 mL Second dose (50 mg/kg over 4 hours): Acetadote® 5 mL in D5W 140 mL Third dose (100 mg/kg over 16 hours): Acetadote® 10 mL in D5W 280 mL Body weight 15 kg: Loading dose (150 mg/kg over 1 hour): Acetadote® 11.25 mL in D5W 45 mL Second dose (50 mg/kg over 4 hours): Acetadote® 3.75 mL in D5W 105 mL Third dose (100 mg/kg over 16 hours): Acetadote® 7.5 mL in D5W 210 mL Body weight 10 kg: Loading dose (150 mg/kg over 1 hour): Acetadote® 7.5 mL in D5W 30 mL Second dose (50 mg/kg over 4 hours): Acetadote® 2.5 mL in D5W 70 mL Third dose (100 mg/kg over 16 hours): Acetadote® 5 mL in D5W 140 mL

Adjuvant therapy in respiratory conditions: Note: Patients should receive an aerosolized bronchodilator 10-15 minutes prior to acetylcysteine.

Inhalation, nebulization (face mask, mouth piece, tracheostomy): Acetylcysteine 10% and 20% solution (dilute 20% solution with sodium chloride or sterile water for inhalation); 10% solution may be used undiluted

Infants: 1-2 mL of 20% solution or 2-4 mL of 10% solution until nebulized given 3-4 times/day

Children and Adults: 3-5 mL of 20% solution or 6-10 mL of 10% solution until nebulized given 3-4 times/day; dosing range: 1-10 mL of 20% solution or 2-20 mL of 10% solution every 2-6 hours

Inhalation, nebulization (tent, croupette): Children and Adults: Dose must be individualized; may require up to 300 mL solution/treatment

Direct instillation: Adults:

Into tracheostomy: 1-2 mL of 10% to 20% solution every 1-4 hours

Through percutaneous intratracheal catheter: 1-2 mL of 20% or 2-4 mL of 10% solution every 1-4 hours via syringe attached to catheter

Diagnostic bronchogram: Nebulization or intratracheal: Adults: 1-2 mL of 20% solution or 2-4 mL of 10% solution administered 2-3 times prior to procedure

Prevention of contrast-induced nephropathy (CIN) (unlabeled use): Adults: Oral: 600-1200 mg twice daily for 2 days (beginning the day before the procedure); may be given as powder in capsules (some centers use solution, diluted in cola beverage or juice). Note: No longer recommended for use prior to percutaneous coronary intervention; instead adequate hydration is preferred (Levine, 2011).

Administration: Oral

Treatment of acetaminophen poisoning, administer orally as a 5% solution. Dilute the 20% solution 1:3 with a cola, orange juice, or other soft drink. Use within 1 hour of preparation. The unpleasant odor (sulfur-like) becomes less noticeable as treatment progresses. If patient vomits within 1 hour of dose, readminister. (Note: It is helpful to put the acetylcysteine on ice, in a cup with a cover, and drink through a straw; alternatively, administer via an NG tube).

Administration: I.V.

Acetadote®: Acetaminophen poisoning:

Loading dose: Dilute in D5W 200 mL; administer over 60 minutes.

Second dose: Dilute in D5W 500 mL; administer over 4 hours.

Third dose: Dilute in D5W 1000 mL; administer over 16 hours.

Note: To avoid fluid overload in patients <40 kg and those requiring fluid restriction, decrease volume of D5W proportionally (see table in dosing section). Discard unused portion.

If the commercial I.V. form is unavailable, the solution for inhalation has been used; each dose should be infused through a 0.2 micron Millipore filter (in-line) over 60 minutes (Yip, 1998); intravenous administration of the solution for inhalation is not USP 797-compliant.

Administration: Inhalation

Acetylcysteine is incompatible with tetracyclines, erythromycin, amphotericin B, iodized oil, chymotrypsin, trypsin, and hydrogen peroxide. Administer separately. Intermittent aerosol treatments are commonly given when patient arises, before meals, and just before retiring at bedtime.

Monitoring Parameters

Acetaminophen poisoning: Monitor patient for the development of anaphylaxis or anaphylactoid reactions; monitor serum acetaminophen levels, AST, ALT, bilirubin, PT, INR, serum creatinine, BUN, serum glucose, hemoglobin, hematocrit, and electrolytes. Assess patient for nausea, vomiting, and skin rash following oral administration. Reassess LFTs for possible hepatotoxicity every 4-6 hours. An early elevation in the INR may be related to acetylcysteine therapy (Schmidt, 2002).

Acute ingestion: Obtain the first acetaminophen level 4 hours postingestion (or as soon as possible thereafter); plot on the Rumack-Matthew nomogram. In patients who have ingested an extended release formulation of acetaminophen or have coingested an agent known to delay gastric emptying, obtain a repeat serum acetaminophen measurement 4-6 hours following the first measurement if the original level (taken at 4-8 hours postingestion) when plotted on the Rumack-Matthew nomogram indicated that treatment was not necessary.

Patient Education

Pulmonary treatment: Prepare solution (may dilute with sterile water to reduce concentrate from impeding nebulizer) and use as directed. Clear airway by coughing deeply before using aerosol. Wash face and face mask after treatment to remove any residual. You may experience drowsiness, nausea, or vomiting. Report persistent chills or fever, adverse change in respiratory status, palpitations, or extreme anxiety or nervousness.

Anesthesia and Critical Care Concerns/Other Considerations

Clinical Pearls/Comments: Intravenous acetylcysteine may be indicated over oral formulation in treatment of acetaminophen overdose for a restricted number of indications (oral cannot be tolerated, coingested toxin requires ongoing gastrointestinal decontamination, gastrointestinal tract nonfunctional, late presentation of acetaminophen overdose, neonatal toxicity from maternal overdose) (Yip, 1998). A commercially manufactured intravenous product is now available in the United States. If this formulation is unavailable, the product normally administered by inhalation can be administered intravenously. The inhalation preparation is sterile, but not labeled “pyrogen free.”

Evidence-Based Information: Adverse Events Related to Administration: A retrospective case series was performed to determine adverse events associated with intravenous acetylcysteine. Adverse reactions occurred in four (~5%) cases. Flushing, pruritus, and phlebitis were reported; one was labeled as an “anaphylactic” reaction (Yip, 1998).

Another retrospective case series evaluated patients who received intravenous acetylcysteine and the literature to develop management guideline for anaphylactoid reactions (Bailey, 1998). Their recommendations for treatment of non-life-threatening allergic reactions include administering diphenhydramine (1 mg/kg I.V.; maximum dose: 50 mg) and reassessing the need for intravenous acetylcysteine. If the acetylcysteine infusion was stopped initially and symptoms resolved, consider restarting infusion 1 hour after diphenhydramine's administration. Anaphylactoid reactions have also been reported with the commercial I.V. formulation. Monitor closely for allergic reactions. Be prepared to handle anaphylactoid reaction if it occurs.

Cardiovascular Considerations

Contrast-Induced Nephropathy (CIN): Oral:

Oral administration: Although study results vary, acetylcysteine may be beneficial in prevention of CIN in patients undergoing cardiac catheterization (Curhan, 2003). Tepel (2000) and his group originally randomized 83 patients with chronic renal insufficiency to oral acetylcysteine (600 mg twice daily) and intravenous saline 0.45% or placebo and intravenous saline 0.45%. All patients were having a CT scan with iopromide contrast. Patients receiving acetylcysteine had a significant reduction in serum creatinine 48 hours after the procedure. Conversely, patients in the placebo arm had significant increase in serum creatinine.

A randomized, placebo-controlled trial in 200 Chinese patients with stable mild-to-moderate renal insufficiency also evaluated acetylcysteine in prevention of CIN (Kay, 2003). Patients were undergoing elective coronary angiography and/or intervention, and had serum creatinine concentrations >1.2 mg/dL or Clcr <60 mL/minute (estimated and measured). A low-osmolality nonionic contrast agent was used. All patients received saline 0.9% I.V. at 1 mL/kg/hour for 12 hours before and for 6 hours after contrast exposure. Three doses of acetylcysteine (600 mg twice daily) or matching placebo were given before and one dose after dye exposure. Contrast nephropathy developed more frequently in the control group (12%) than in the acetylcysteine group (4%). The average length of hospitalization was 0.5 days shorter in the acetylcysteine group. No adverse events related to acetylcysteine were reported.

However, these results differed from those in another prospective, randomized trial (Allaqaband, 2002) that compared the efficacy of acetylcysteine (600 mg twice daily for 48 hours) plus saline 0.45% versus fenoldopam (0.1 mcg/kg/minute) plus saline 0.45% versus saline 0.45% alone (at 1 mL/kg/hour for 12 hours before procedure, during procedure, and 12 hours afterwards) in preventing CIN. Patients were high-risk (serum creatinine >1.6 mg/dL or Clcr <60 mL/minute) and undergoing cardiovascular procedures using low-osmolality nonionic contrast. Authors concluded that there was no benefit in either oral acetylcysteine or fenoldopam over saline in preventing CIN.

Marenzi, et al (2006) showed that acetylcysteine's effect may be dose dependent. Patients with acute MI requiring emergent cardiac catheterization for possible PCI received either high-dose acetylcysteine (1200 mg I.V. bolus over 5-10 minutes followed by 1200 mg administered orally twice daily for 48 hours), a low-dose regimen (600 mg I.V. bolus followed by 600 mg administered orally twice daily for 48 hours) or placebo. The group that received the high-dose regimen developed CIN (defined as an increase in serum creatinine concentration of ≥25% from baseline within 72 hour) less often than the low-dose group (p<0.001). All patients received saline 0.9% NaCl at 1 mL/kg/hour (0.5 mL/kg/hour for cases of overt heart failure) for 12 hours.

Briguori, et al (2007) evaluated three prophylactic regimens (normal saline and acetylcysteine (NAC); sodium bicarbonate and NAC; normal saline, ascorbic acid and NAC) in 326 patients with chronic kidney disease (serum creatinine ≥2 mg/dL) undergoing coronary and/or peripheral procedures with iodixanol. Saline was given I.V. at 1 mL/kg/hour (0.5 ml/kg/hour for LVEF <40%) for 12 hours before and 12 hours after contrast administration. Sodium bicarbonate administration was similar to that in the Merten trial. The oral NAC dose was 1200 mg twice daily given the day before and the day of contrast administration (4 doses total). The ascorbic acid dose was given I.V. as 3 g 2 hours before the procedure followed by 2 g the night of and the morning after the procedure. The amount of contrast administered and the contrast nephropathy risk scores were similar in each group. Contrast induced nephropathy (CIN) occurred in 9.9% (11/111 of patients) of saline/NAC group, 2% (2/108 of patients) of bicarbonate/NAC group and 10.3 % (11/107 of patients) in saline/NAC/ascorbic acid group. The bicarbonate/NAC group had significantly fewer episodes of CIN when compared to saline/NAC group in this patient population.

In the largest trial to date, oral NAC was compared to placebo in patients undergoing coronary and vascular angiography. The Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT) randomized 2308 patients to either NAC 1200 mg twice daily, 2 doses administered prior to the procedure and 2 doses after the procedure, or placebo. Patients enrolled in the study included those with diabetes mellitus (60.4%), age >70 years (52.1%), estimated Clcr <60 mL/minute (49%), or an acute coronary syndrome (35.4%); groups were well balanced. Hydration with 0.9% NaCl 1 mL/kg/hour starting 6-12 hours prior to procedure and 6-12 hours after procedure was strongly encouraged. Although administration of hydration was at the discretion of the managing physician, ~47% of patients in each group received the suggested 0.9% NaCl regimen, between 93% and 94% of all patients receiving some sort of 0.9% NaCl hydration, and ~5% in each group received sodium bicarbonate infusion. The ACT trial demonstrated no difference in the primary end point of contrast-induced nephropathy, defined as a 25% elevation of serum creatinine above baseline between 48 and 96 hours after angiography, and no difference in the secondary end point of serum creatinine doubling within 30 days. Additionally, no difference was seen in the 30-day clinical end points of mortality, need for dialysis, or cardiovascular mortality (ACT Investigators, 2011).

Parameters used to define CIN varied among studies.

I.V. administration: Note: Itching, flushing, and rash, as well as more serious allergic reactions, may occur with intravenous acetylcysteine. Several studies have evaluated intravenous acetylcysteine in the prevention of CIN. Three different dosing regimens were used. The initial study (Baker, 2003) randomized patients with stable renal function undergoing cardiac catheterization to intravenous acetylcysteine 150 mg/kg over 30 minutes followed by 50 mg/kg over 4 hours or placebo. The study was stopped when an interim analysis indicated borderline statistical significance (p= 0.045). Hydration volumes were different between the groups as well. The mean serum creatinine level in the active treatment group was lower after administration when compared to baseline. Acetylcysteine may have a direct affect on creatinine levels.

Another trial (Webb, 2004) studied 500 mg of intravenous acetylcysteine administered immediately before cardiac catheterization. No significant difference was seen between acetylcysteine and placebo. Rashid (2004) randomized patients with peripheral vascular disease to 1 g acetylcysteine in 500 mL of normal saline 6-12 hours before and after the procedure. No significant differences were seen in renal function. Marenzi, et al (2006) evaluated the use of an initial I.V. push dose (high and low dose) of acetylcysteine prior to cardiac catheterization in acute MI patients followed by an oral regimen (high and low dose) compared to placebo. This trial is described above.

The 2011 ACCF/AHA/SCAI PCI clinical practice guidelines recommend against using acetylcysteine (I.V. or oral) to prevent CIN; instead, patients should be adequately hydrated prior to the procedure. A hydration regimen using I.V. isotonic crystalloid (eg, 0.9% NaCl) administered at 1-1.5 mL/kg/hour for 3-12 hours prior to procedure and for 6-24 hours after the procedure is reasonable (Levine, 2011).

Dental Health: Effects on Dental Treatment

Key adverse event(s) related to dental treatment: Stomatitis, drowsiness, fever, vomiting, nausea, bronchospasm, rhinorrhea, hemoptysis, and dizziness

Dental Health: Vasoconstrictor/Local Anesthetic Precautions

No information available to require special precautions

Mental Health: Effects on Mental Status

May cause drowsiness

Mental Health: Effects on Psychiatric Treatment

Sedative effects may be potentiated by psychotropic agents

Nursing: Physical Assessment/Monitoring

Monitor pulmonary function and response to therapy. If giving I.V., monitor for possible anaphylactoid reactions and be prepared to treat appropriately if needed.

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Injection, solution:

Acetadote®: 20% [200 mg/mL] (30 mL [DSC]) [contains edetate disodium]

Injection, solution [preservative free]:

Acetadote®: 20% [200 mg/mL] (30 mL)

Solution, for inhalation/oral: 10% [100 mg/mL] (10 mL, 30 mL); 20% [200 mg/mL] (10 mL, 30 mL)

Solution, for inhalation/oral [preservative free]: 10% [100 mg/mL] (4 mL, 10 mL); 20% [200 mg/mL] (4 mL, 10 mL, 30 mL)

Pricing: U.S. (www.drugstore.com)

Solution (Acetylcysteine)

10% (4): $12.99

10% (30): $20.30

10% (30): $25.99

20% (4): $16.99

20% (10): $22.99

20% (30): $29.99

References

ACT Investigators, “Acetylcysteine for Prevention of Renal Outcomes in Patients Undergoing Coronary and Peripheral Vascular Angiography: Main Results from the Randomized Acetylcysteine for Contrast-induced Nephropathy Trial (ACT),” Circulation, 2011, 124(11):1250-9.

Allaqaband S, Tumuluri R, Malik AM, et al, “Prospective Randomized Study of N-Acetylcysteine, Fenoldopam, and Saline for Prevention of Radiocontrast-Induced Nephropathy,” Catheter Cardiovasc Interv, 2002, 57(3):279-83.

Appelboam AV, Dargan PI, and Knighton J, “Fatal Anaphylactoid Reaction to N-Acetylcysteine: Caution in Patients With Asthma,” Emerg Med J, 2002, 19(6):594-5.

Bailey B and McGuigan MA, “Management of Anaphylactoid Reactions to Intravenous N-Acetylcysteine,” Ann Emerg Med, 1998, 31(6):710-5.

Baker CS, Wragg A, Kumar S, et al, "A Rapid Protocol for the Prevention of Contrast-Induced Renal Dysfunction: The RAPPID Study,” J Am Coll Cardiol, 2003, 41(12):2114-8.

Briguori C, Airoldi F, D'Andrea D, et al, “Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL). A Randomized Comparison of 3 Preventive Strategies,” Circulation, 2007, 115(10):1211-17.

Curhan GC, “Prevention of Contrast Nephropathy,” JAMA, 2003, 289(5):606-8.

Dart RC, Erdman AR, Olson KR, et al, “Acetaminophen Poisoning: An Evidence-Based Consensus Guideline for Out-of-Hospital Management,” Clin Toxicol (Phila), 2006, 44(1):1-18.

Douglas D and Smilkstein M, “Deferoxamine-Iron Induced Pulmonary Injury and N-Acetylcysteine,” J Toxicol Clin Toxicol, 1995, 33(5):495.

Falk JL, “Oral N-Acetylcysteine Given Intravenously for Acetaminophen Overdose: We Shouldn't Have To, But We Must,” Crit Care Med, 1998, 26(1):7.

Harrison PM, Keays R, Bray BP, et al, “Improved Outcome of Paracetamol-Induced Fulminant Hepatic Failure by Late Administration of Acetylcysteine,” Lancet, 1990, 335(8705):1572-3.

Toxicology Investigator Network Authorship Group, "A Multicenter Comparison of the Safety of Oral Versus Intravenous Acetylcysteine for Treatment of Acetaminophen Overdose," Clin Toxicol (Phila), 2010, 48(5):424-30.

Hendrickson RG and Bizovi KE, “Acetaminophen,” Goldfrank's Toxicologic Emergencies, 8th edition, Flomenbaum NE, Goldfrank LR, Hoffman RS, et al, eds, New York: The McGraw-Hill Companies, Inc, 2006, 523-43.

Jones AL, “Mechanism of Action and Value of N-Acetylcysteine in the Treatment of Early and Late Acetaminophen Poisoning: A Critical Review,” J Toxicol Clin Toxicol, 1998, 36(4):277-85.

Jones AL, “Recent Advances in the Management of Late Paracetamol Poisoning,” Emerg Med, 2000, 12(1):14-21.

Kay J, Chow WH, Chan TM, et al, “Acetylcysteine for Prevention of Acute Deterioration of Renal Function Following Elective Coronary Angiography and Intervention: A Randomized Controlled Trial,” JAMA, 2003, 289(5):553-8.

Keays R, Harrison PM, Wendon JA, et al, “Intravenous Acetylcysteine in Paracetamol Induced Fulminant Hepatic Failure: A Prospective Controlled Trial,” BMJ, 1991, 303(6809):1026-9.

Levine GN, Bates ER, Blankenship JC, et al, “2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions,” Circulation, 2011, 124(23):e574-651.

Marenzi G, Assanelli E, Marana I, et al, “N-Acetylcysteine and Contrast-Induced Nephropathy in Primary Angioplasty,” N Engl J Med, 2006, 354(26):2773-82.

Mascarenhas MR, “Treatment of Gastrointestinal Problems in Cystic Fibrosis,” Curr Treat Options Gastroenterol, 2003, 6(5):427-41.

Mohammed S, Jamal AZ, and Robison LR, “Serum Sickness-Like Illness Associated With N-Acetylcysteine Therapy,” Ann Pharmacother, 1994, 28(2):285.

Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922.

Mroz L, Benitez JG, and Krenzelok E, “Angioedema With Oral Acetylcysteine,” Ann Emerg Med, 1997, 30(2):240-1.

Pakravan N, Waring WS, Sharma S, et al, “Risk Factors and Mechanisms of Anaphylactoid Reactions to Acetylcysteine in Acetaminophen Overdose,” Clin Toxicol, 2008, 46(8):697-702.

Prescott LF, Donovan JW, Jarvie DR, et al, “The Disposition and Kinetics of Intravenous N-Acetylcysteine in Patients With Paracetamol Overdosage,” Eur J Clin Pharmacol, 1989, 37(5):501-6.

Prescott LF, Illingworth RN, Critchley JA, et al, “Intravenous N-Acetylcysteine: The Treatment of Choice for Paracetamol Poisoning,” BMJ, 1979, 2:1097-1100.

Rashid ST, Salman M, Myint F, et al,“Prevention of Contrast-Induced Nephropathy in Vascular Patients Undergoing Angiography: A Randomized Controlled Trial of Intravenous N-Acetylcysteine," J Vasc Surg, 2004, 40(6):1136-41.

“Rationale, Design, and Baseline Characteristics of the Acetylcystein for Contrast-Induced NephropaThy (ACT) Trial: A Pragmatic Randomized Controlled Trial to Evaluate the Efficacy of Acetylcysteine for the Prevention of Contrast-Induced Nephropathy,” Trials, 2009, 10:38-45.

Rodgers G, Matyunas N, Ross M, et al, “Sulfhemoglobinemia Associated With N-Acetylcysteine (NAC) Therapy of Acetaminophen (APAP) Overdose: A Case Report,” Clin Toxicol, 1995, 33(5):530.

Sandilands EA and Bateman DN, “Adverse Reactions Associated With Acetylcysteine,” Clin Toxicol (Phila), 2009, 47(2):81-8.

Schmidt LE, Knudsen TT, Dalhoff K, et al, “Effect of Acetylcysteine on Prothrombin Index in Paracetamol Poisoning Without Hepatocellular Injury,” Lancet, 2002, 360(9340):1151-2.

Smilkstein MJ, Bronstein AC, Linden C, “Acetaminophen Overdose: A 48-Hour Intravenous N-Acetylcysteine Treatment Protocol," Ann Emerg Med, 1991, 20(10):1058-63.

Smilkstein MJ, Knapp GL, Kulig KW, et al, “Efficacy of N-Acetylcysteine in the Treatment of Acetaminophen Overdose: Analysis of the National Multicenter Study (1976 to 1985),” N Engl J Med, 1988, 319(24):1557-62.

Tepel M, van der Giet M, Schwarzfeld C, et al, “Prevention of Radiographic-Contrast-Agent-Induced Reductions in Renal Function by Acetylcysteine,” N Engl J Med, 2000, 343(3):180-4.

Walson PD and Groth JF Jr, “Acetaminophen Hepatotoxicity After Prolonged Ingestion,” Pediatrics, 1993, 91(5):1021-2.

Waring WS, Stephen AF, Robinson OD, et al,“Lower Incidence of Anaphylactoid Reactions to N-Acetylcysteine in Patients With High Acetaminophen Concentrations After Overdose,” Clin Toxicol (Phila), 2008, 46(6):496-500.

Webb JG, Pate GE, Humphries KH, et al, “A Randomized Controlled Trial of Intravenous N-Acetylcysteine for the Prevention of Contrast-Induced Nephropathy After Cardiac Catheterization: Lack of Effect,” Am Heart J, 2004, 148(3):422-9.

Woo OF, Anderson IB, Kim SY, et al, “Shorter Duration of N-Acetylcysteine (NAC) for Acute Acetaminophen Poisoning,” Clin Toxicol, 1995, 33(5):508.

Woo OF, Mueller PD, Olson KR, et al, “Shorter Duration of Oral N-Acetylcysteine Therapy for Acute Acetaminophen Overdose,” Ann Emerg Med, 2000, 35(4):363-8.

Yankaskas JR, Marshall BC, Sufian B, et al, “Cystic Fibrosis Adult Care: Consensus Conference Report,” Chest, 2004, 125(1 Suppl):1-39.

Yip L, Dart RC, and Hurlbut KM, “Intravenous Administration of Oral N-Acetylcysteine,” Crit Care Med, 1998, 26(1):40-3.

Zyoud SH, Awang R, Sulaiman SA, et al, “Incidence of Adverse Drug Reactions Induced by N-Acetylcysteine in Patients With Acetaminophen Overdose,” Hum Exp Toxicol, 2010, 29(3):153-60.

Zyoud SH, Awang R, Sulaiman SA, et al, “N-Acetylcysteine-Induced Headache in Hospitalized Patients With Acute Acetaminophen Overdose,” Fundam Clin Pharmacol, 2011, 25(3):405-10.

International Brand Names

  • ACC (AR, HU, LU, MX, RU, ZA)
  • ACC 200 (EE)
  • Acemuk (AR)
  • Acetadote (AU, NZ)
  • Acetain (KP)
  • Acetin (MY)
  • Acetylcystein NM Pharma (SE)
  • Acetylcystein Tika (SE)
  • Acypront (HK)
  • Aerosolv (AT)
  • Bromuc (BR)
  • Broncoflem (PH)
  • Cystaline (TH)
  • Ecomucyl (CH)
  • Eloamin (CZ)
  • Exomuc (FR, HK, LU)
  • Fabrol (AT, GR)
  • Flemex AC (TH)
  • Flucil (TH)
  • Fluimicil (CH, DE)
  • Fluimiquil (LU)
  • Fluimucil (AR, BG, BR, CL, CO, CZ, EC, HK, HU, ID, IT, MA, NL, PE, PL, RU, TH, TW)
  • Fluimucil A (MY, PK)
  • Fluimukan (HR)
  • Flumil (ES)
  • Flutafin (TW)
  • Hidonac (ID, MY, PH, TH, TW)
  • Icystein (TW)
  • L-Cimexyl (SG)
  • Lubrisec (AR)
  • Lysomucil (LU)
  • Lysox (LU)
  • Madame Pearl's Mucolytic (HK)
  • Menaxol (CR, DO, GT, HN, NI, PA, SV)
  • Menaxol Forte (CR, DO, GT, HN, NI, PA, SV)
  • Mucofillin (JP)
  • Mucolair (LU)
  • Mucolator (LU, MY)
  • Mucolitico (CN)
  • Mucomiste (PT)
  • Mucomyst (AT, AU, BE, DK, FI, FR, KP, LU, NL, NO, SE)
  • Mucomystendo (FR)
  • Mucoserin (KP)
  • Mucosof (CL)
  • Mucosten (KP)
  • Mucosys (IN)
  • Mucoza (TH)
  • Mucylin (ID)
  • Mukolit (ID)
  • Muterin (KP)
  • Muxatil (PY)
  • Mysoven (TH)
  • NAC (TR)
  • NAC-ratiopharm (LU)
  • Parvolex (GB, IE, NZ, PH)
  • Pectocil (ID)
  • Pectomucil (LU)
  • Reolin (IL)
  • Rumicil (LU)
  • Savocel (CO)
  • Sebron (KP)
  • Simucil (ID)
  • Simucin (TH)
  • Siran 200 (IL)
  • Solmucol (HU, LU)
  • Spatam (SG)
  • Sputopur (HU)
  • Stecin (KP)
  • Stenac (MY, TH)
  • Tancore (TW)
  • Touxium Mucolyticum (LU)
  • Viskoferm (SE)

Lexi-Comp.com

Last full review/revision March 2012

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