Vecuronium Bromide-Water (vecuronium bromide/water for injection,sterile)
Neuromuscular Blockers Intravenous Syringe (ML)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Vecuronium bromide is an aminosteroid nondepolarizing neuromuscular blocking agent.
Vecuronium bromide is a nondepolarizing neuromuscular blocking agent that produces pharmacologic effects similar to those of other nondepolarizing neuromuscular blocking agents. The drug acts by competing for cholinergic receptors at the motor end-plate. Vecuronium appears to have little histamine-releasing activity when administered at usual clinical doses.
Unlike other nondepolarizing neuromuscular blocking agents, vecuronium has no clinically significant effects on hemodynamic parameters and does not significantly impact blood pressure, heart rate, cardiac output, systemic vascular resistance, or pulmonary capillary wedge pressure.
The manufacturer states that the ED90 (dose required to produce 90% suppression of the control twitch response) of vecuronium in patients undergoing balanced anesthesia averages 0.057 mg/kg; in several studies in patients undergoing balanced anesthesia, the ED90 has ranged from 0.049-0.062 mg/kg.
The onset and duration of, and the rate of recovery from, neuromuscular blockade induced by vecuronium vary among individuals, are dose dependent, and may be altered by the anesthetic agent (e.g., enflurane, isoflurane, halothane) employed. The time from injection to onset of neuromuscular blockade decreases as the dose of vecuronium bromide increases. The manufacturer states that following IV administration of a vecuronium bromide dose of 0.08-0.1 mg/kg, neuromuscular blockade begins within 1 minute and is maximal at 3-5 minutes; good to excellent intubating conditions typically occur within 2.5-3 minutes.
The duration of neuromuscular blockade increases as the dose of vecuronium bromide increases. The manufacturer states that the duration of clinically sufficient neuromuscular blockade (i.e., time from injection to 25% spontaneous recovery of control twitch response) induced by initial vecuronium bromide doses of 0.08-0.1 mg/kg under balanced anesthesia is about 25-40 minutes, and the duration of vecuronium-induced blockade (time from injection to 95% spontaneous recovery of control twitch response) is approximately 45-65 minutes. Repeated administration of maintenance doses of vecuronium bromide appears to have little, if any, cumulative effect on duration of the neuromuscular blockade.
In addition, since the time necessary to recover from maintenance doses of the same size generally does not change with each additional dose, doses may be administered at relatively regular intervals with predictable neuromuscular blocking results. The manufacturer states that the recovery time (the time necessary for spontaneous recovery of the twitch response from 25% to 75% of the control response) following administration of vecuronium bromide doses of 0.08-0.1 mg/kg under balanced or halothane anesthesia is about 15-25 minutes.
Vecuronium is approximately 60-80% bound to plasma proteins. The distribution half-life following a single IV dose of 0.025-0.28 mg/kg is approximately 4 minutes, and elimination half-life is approximately 65-75 minutes in healthy surgical patients and renal failure patients undergoing transplant surgery. In late pregnancy, the elimination half-life may be decreased to approximately 35-40 minutes.
In aqueous solution in vitro, vecuronium undergoes spontaneous deacetylation at the 3alpha- and/or 17beta-positions to form the hydroxy derivatives; following use of vecuronium during surgery, only unchanged vecuronium has been detected in human plasma, but the 3-desacetyl vecuronium metabolite has been rarely detected in human plasma following prolonged vecuronium use in the intensive care unit. The neuromuscular blocking activity of the 3alpha-hydroxy derivative appears to be at least 50% that of the unchanged drug. In vitro, the 3alpha-hydroxy derivative undergoes rapid conversion to the 3alpha,17beta-dihydroxy derivative.
Vecuronium and its metabolite(s) appear to be excreted principally in feces via biliary elimination; the drug and its metabolite(s) are also excreted in urine. Approximately 3-35% of an IV dose of vecuronium bromide is excreted in urine within 24 hours after administration in humans. In patients with a T-tube in the common bile duct, 25-50% of an IV dose of vecuronium was reportedly excreted in bile within 42 hours after administration.
The 3-desacetyl vecuronium metabolite has been recovered in the urine of some patients in quantities that account for up to 10% of the injected dose; 3-desacetyl vecuronium has also been recovered by T-tube in some patients, accounting for up to 25% of the injected dose.
Generic name: vecuronium bromide/water for injection,sterile
Drug class: Neuromuscular Blockers
Therapeutic class: Locomotor System
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Vecuronium Bromide-Water
Indications
The following indications are listed for Vecuronium Bromide-Water:
- General Anesthesia Adjunct
- Muscle Relaxation
- Skeletal Muscle Relaxation For Endotracheal Intubation
Also known as: Adjunct General Anesthesia, Muscle Flaccidity, Skeletal Muscle Relaxation For Endotracheal Tube Insertion, Skeletal Muscle Relaxation For Intratracheal Intubation, Skeletal Muscle Relaxation For Intubation Of Trachea.
Dosing
Dosage of vecuronium bromide is expressed in terms of the salt. The dosage must be carefully adjusted according to individual requirements and response. The use of a peripheral nerve stimulator is recommended to accurately monitor the degree of neuromuscular blockade and recovery, determine the need for additional doses, determine the adequacy of spontaneous recovery or antagonism, and minimize the complications of overdosage if additional doses are administered.
A reduction in the dosage of vecuronium bromide may be required in patients receiving general anesthetics (e.g., enflurane, isoflurane) that potentiate its neuromuscular blocking activity. Potentiation is minimal when vecuronium is administered prior to these anesthetics.
Vecuronium bromide is administered IV only.
The initial (intubating) dose is administered by rapid IV injection; maintenance doses may be administered by intermittent IV injection or by continuous IV infusion.
Store unopened vials of vecuronium bromide for injection at 20-25degreesC; protect vials from light and store in the original carton until the time of use.
For IV injection, commercially available vecuronium bromide for injection should be reconstituted with a compatible IV solution (e.g., 5% dextrose, 5% dextrose and 0.9% sodium chloride, 0.9% sodium chloride, Lactated ringer's, bacteriostatic water for injection, sterile water for injection). When reconstituted with bacteriostatic water for injection, the solution should be stored at room temperature or under refrigeration and used within 5 days; when reconstituted with other compatible solutions, the solution should be stored under refrigeration and used within 24 hours (any unused portions after this time period should be discarded).
For continuous IV infusion, the reconstituted vecuronium solution should be further diluted to the desired concentration (usually 0.1 or 0.2 mg/mL) in a compatible IV infusion solution such as 5% dextrose, 5% dextrose and 0.9% sodium chloride, 0.9% sodium chloride, or Lactated ringer's.
Reconstituted solutions of vecuronium and diluted solutions of the drug should be inspected visually for particulate matter and discoloration prior to administration whenever solution and container permit. Vecuronium should not be mixed in the same syringe nor administered simultaneously through the same needle as an alkaline solution (e.g., barbiturate solution).
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.
There are no contraindication interactions for this drug.
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Neuromuscular Blocking Agents/General Anesthetics (INHL)
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: General anesthetics enhance the pharmacologic effects of nondepolarizing muscle relaxants.
CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects of the nondepolarizing muscle relaxant including respiratory depression, bradycardia, hypotension, flushing, or muscle weakness.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: It may be necessary to decrease the dose of the nondepolarizing muscle relaxant. Monitor neuromuscular function and adjust the dose of the nondepolarizing muscle relaxant accordingly.
DISCUSSION: Concomitant administration of general anesthetics and nondepolarizing muscle relaxants has been shown to produce synergistic neuromuscular blocking effects of nondepolarizing muscle relaxants.
Neuromuscular Blocking Agents/Misc Antibiotics
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Aminoglycosides, bacitracin, clindamycin, lincomycin, and polymyxins may enhance the pharmacologic effects of neuromuscular blocking agents.
CLINICAL EFFECTS: May see an increase in the pharmacologic effects of neuromuscular blocking agents, including prolonged respiratory depression and apnea.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly.
DISCUSSION: Concomitant administration of aminoglycosides, bacitracin, clindamycin, lincomycin, and polymixins with neuromuscular blocking agents has been shown to produce synergism of the effects on skeletal muscles. Concurrent administration of these drugs has been associated with prolonged respiratory depression, respiratory paralysis, and fatal apnea. The interaction usually occurs when the antibiotic is given prior to or concurrently with the neuromuscular blocking drug, but it may also occur when given after administration. Any antibiotic dosage or route of administration may produce respiratory depression.
Neuromuscular Blocking Agents/Quinine Derivatives
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Synergistic or additive pharmacologic activity.
CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects, including profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Avoid concurrent administration of neuromuscular blocking agents and quinine derivatives during the first several hours of postoperative period. If administered, respiratory support may be needed. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Administration of quinidine during the immediate postoperative period has been associated with respiratory paralysis and apnea.
Neuromuscular Blocking Agents/Verapamil
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Unknown.
CLINICAL EFFECTS: The neuromuscular blocking effect of nondepolarizing muscle relaxants may be extended, producing profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If possible, avoid administration of nondepolarizing neuromuscular blocking agents to patients receiving verapamil. When both drugs must be given, carefully monitor respiratory function to avoid prolonged neuromuscular blockade. If needed, blockade may be reversed by giving edrophonium. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Patients receiving verapamil have experienced prolonged skeletal muscle paralysis after administration of usual therapeutic doses of a nondepolarizing neuromuscular blocking agent. While muscle paralysis was unresponsive to treatment with neostigmine, reversal of blockade has been achieved by administration of edrophonium.
Moderate Interaction: Assess the risk to the patient and take action as needed.
Anesthesia Agents/Glp-1 Receptor Agonists
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: GLP-1 receptor agonists can cause delayed gastric emptying.(1,2)
CLINICAL EFFECTS: Gastric contents may remain in the stomach after preoperative fasting, which could increase the risk of regurgitation and aspiration.(1,2)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The American Society of Anesthesiologists (ASA) recommends the following for patients receiving elective procedures: - For patients on daily dosing, consider holding GLP-1 agonists on the day of the procedure. For patients on weekly dosing, consider holding GLP-1 agonists a week prior to the procedure. - Consult an endocrinologist for patients taking GLP-1 agonists for diabetes management if the GLP-1 agonist is held longer than the dosing schedule to avoid hyperglycemia. - For patients requiring urgent or emergent procedures, proceed and treat the patient as 'full stomach.'(3)
DISCUSSION: In one case report, a 31-year-old patient taking semaglutide followed preoperative fasting guidelines but food residue was discovered upon endoscopy, leading to cancellation of the surgical procedure.(4) In a case report, a semaglutide-treated patient experienced regurgitation upon induction of general anesthesia despite a 20 hour preoperative fasting period. The patient received semaglutide two days before the scheduled procedure.(5) A case report of a 42-year-old patient after fasting for 18 hours showed substantial gastric content upon endoscopy. The patient experienced intraoperative pulmonary aspiration of gastric contents which were suctioned from the trachea and bronchi using bronchoscopy.(6)
Neuromuscular Blocking Agents/Lincosamides
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Lincosamides appear to augment the neuromuscular blocking effects of nondepolarizing muscle relaxants.
CLINICAL EFFECTS: The effects of nondepolarizing neuromuscular relaxants may be prolonged leading to profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Monitor respiratory function of the patient and provide the necessary support. In patients who have received nondepolarizing muscle relaxants, avoid use of lincosamides in the recovery room. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Lincomycin has been reported to augment the neuromuscular blocking effect of pancuronium in seven anesthetized patients. The effect was readily antagonized by neostigmine administration. In a case report, clindamycin produced prolonged neuromuscular blockade in a patient who had received pancuronium. Neostigmine was ineffective in antagonizing the blockade.
Neuromuscular Blocking Agents/Polypeptide Antibiotics
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Synergistic pharmacologic activity. Polymyxin B affects neuromuscular transmission by blocking acetylcholine receptors. Its action is thus post-synaptic and the neuromuscular block has no antagonists. Polymyxin B causes neostigmine resistance to d-tubocurarine blockade and calcium resistance to the blockade evoked by aminoglycoside antibiotics (1,2,3,4). A pre-synaptic mechanism may also be involved with decreased release of acetylcholine.
CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects, including profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Concomitant administration of polypeptide antibiotics and neuromuscular blocking agents has been shown to produce synergism of the effects on skeletal muscles. Concurrent administration of these drugs has been associated with prolonged respiratory depression, respiratory paralysis, and apnea. This interaction has been documented with colistimethate, polymyxin B, bacitracin, and vancomycin.
Neuromuscular Blocking Agents/Trimethaphan
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Additive pharmacologic effects.
CLINICAL EFFECTS: May see an increase in the neuromuscular blocking effects, including profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If it is necessary to administer these drugs concurrently, do so with extreme caution. Monitor neuromuscular function and adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Available data indicate that the neuromuscular blocking effects of tubocurarine and trimethaphan may be additive.
Nondepolarizing Muscle Relaxants/Magnesium Salts, Injectable
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Magnesium may reduce postjunctional membrane neuromuscular blocking action of nondepolarizing muscle relaxants. Parenterally administered magnesium may potentiate the effects of the nondepolarizing muscle relaxants.
CLINICAL EFFECTS: Increased neuromuscular blockade with profound sedation, respiratory depression, coma, and/or death.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Monitor respiratory function when parenteral magnesium and nondepolarizing muscle relaxants are administered concurrently. Adjust the dose of the neuromuscular blocking agent accordingly. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: The effects of nondepolarizing muscle relaxants have been reported to be increased in laboratory animals and in humans by concomitant administration of magnesium sulfate. Respiratory depression has been reported.
Nondepolarizing Muscle Relaxants/Piperacillin
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Piperacillin may prolong the neuromuscular blockade of the nondepolarizing muscle relaxants.(1,2)
CLINICAL EFFECTS: Concurrent use of nondepolarizing muscle relaxants and piperacillin may result in prolonged neuromuscular blockade including profound sedation, respiratory depression, coma, and/or death.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Patients should be monitored for increased or unexpected prolongation of neuromuscular blockade when using piperacillin with nondepolarizing muscle relaxants. Assure monitoring protocols are in place for patients receiving neuromuscular blocking agents. If concurrent use is necessary, monitor patients for unusual dizziness or lightheadedness, extreme sleepiness, slowed or difficult breathing, or unresponsiveness.
DISCUSSION: Concurrent use of nondepolarizing muscle relaxants and piperacillin may result in increased or prolonged neuromuscular blockage.(1,2) If these agents are used together, patients should be monitored closely for increased neuromuscular blockage.
Select Neuromuscular Blocking Agents/Hydantoins
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: It has been suggested that phenytoin increases end-plate anticholinesterase activity, resulting in higher acetylcholine concentration at the neuromuscular junction.(1)
CLINICAL EFFECTS: A higher plasma concentration of the neuromuscular blocking agent was required to effect a given level of neuromuscular blockade in patients receiving phenytoin.(2,3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Patients receiving hydantoin anticonvulsants should be monitored for a decreased response to the neuromuscular blocking agent. The dose of the neuromuscular blocking agent may need to be increased and/or given more frequently.(9)
DISCUSSION: In a study, patients receiving phenytoin were administered metocurine, attained 83% of maximum neuromuscular blockade compared with 98% in the control group.(1) In another study, patients maintained on phenytoin for more than one week had a significantly higher pancuronium requirement than those patients not receiving phenytoin.(1) In two separate case reports, patients maintained on phenytoin demonstrated a resistance to pancuronium and a decreased duration of neuromuscular blockade.(3,4) In a study, patients maintained on phenytoin and receiving vecuronium had a significantly shorter total duration and effect of neuromuscular blockade compared to those patients not receiving phenytoin.(5) In contrast, neither the effect nor duration of atracurium's neuromuscular blockade was affected by phenytoin.(5) Two in vitro studies showed that the neuromuscular blockade of curare and tubocurarine was potentiated by the use of phenytoin.(6,7) Ten children received a bolus dose of vecuronium 0.15mg/Kg while on phenytoin and showed a significantly increased clearance of vecuronium compared to the control group, 15.1 and 9.0 ml/Kg/min, respectively.(8) In a case report, a 58 year-old male previously stabilized on phenytoin (400 mg daily) was given an injection of vecuronium (8 mg) to induce muscle blockade during bowel surgery. While monitoring the effectiveness of vecuronium only 75% twitch height blockade was noted after seven minutes. The medication, due to its short duration and impaired effectiveness, had to be given more frequently throughout the surgery in order to maintain adequate muscle block.(9) A separate case report records a decreased response to pancuronium in a 15 year-old male, previously stabilized on phenytoin (350 mg daily), while undergoing surgery to remove a parietal tumor. Pancuronium (0.7 mg/kg) was given as a relaxant during the surgery and monitored using the train-of-four method. Intermittent doses of pancuronium (0.17 mg/kg) were given for the first hour of surgery without successful blockade apparent by the return of all four twitches within ten minutes of each dose. A second attempt at muscular blockade was made with continuous infusion atracurium (0.26-0.55 mg/kg/hour) for the duration of the surgery. Only 16 minutes after stopping the infusion, all four twitches were visible.(10)
Vecuronium/Dexamethasone; Methylprednisolone
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The mechanism of action is not clear.
CLINICAL EFFECTS: Concurrent use may increase the risk for critical illness polyneuromyopathy (CIPM).
PREDISPOSING FACTORS: Possible risk factors include: extended (> 48 hour) duration of continuous paralysis, high dose corticosteroids, and use in patients with septic shock.
PATIENT MANAGEMENT: For patients receiving combination therapy, it would be prudent to limit use of high-dose corticosteroids to conditions where the benefit is clear, and to use vecuronium for the shortest duration possible, preferably < 48 hours. When possible, avoid concomitant use of vecuronium and high-dose corticosteroids in patients with septic shock. Closely monitor magnitude and duration of paralysis as per institutional protocol.
DISCUSSION: Although the pathophysiology of CIPM is incompletely understood, authors generally agree that concurrent use of vecuronium and high dose corticosteroids is associated with additive or synergistic risk for CIPM.
Contraindications
*Known hypersensitivity to vecuronium bromide.
There are no contraindication contraindications for this drug.
- Eaton-lambert syndrome
- Myasthenia gravis
- Cholestasis
- Hepatic cirrhosis
- Hypocalcemia
- Hypokalemia
- Hypomagnesemia
- Morbid obesity
- Neuromuscular disease
Adverse reactions
Adverse effects of vecuronium bromide generally are manifestations of the drug's pharmacologic action beyond the time period needed; this may vary from skeletal muscle weakness to profound and prolonged skeletal muscle paralysis resulting in respiration insufficiency or apnea.
There have also been postmarketing reports of severe allergic reactions (anaphylactic and anaphylactoid reactions) associated with neuromuscular blocking agents, including vecuronium; in some cases, these reactions have been life-threatening or fatal.
Rare or Very Rare
- Acute respiratory failure
- Allergic dermatitis
- Anaphylaxis
- Apnea
- Bradycardia
- Bronchospastic pulmonary disease
- Cardiogenic shock
- Hypotension
- Tachycardia
Rare or Very Rare
- Edema
- Erythema
- Flushing
- Muscle weakness
- Pruritus of skin
- Skin rash
Precautions
No enhanced messaging available.
The safety and effectiveness of vecuronium have been established in pediatric patients >=7 weeks of age. Infants 7 weeks to 1 year of age are moderately more sensitive to vecuronium on a mg/kg basis than adults and take approximately 1.5 times as long to recover. Pediatric patients 1 to <10 years of age may require a slightly higher initial dosage and may require slightly more frequent maintenance doses than adult patients.
Animal reproduction studies have not been conducted with vecuronium. It is not known whether vecuronium can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Administer vecuronium to a pregnant woman only if clearly needed.
The use of vecuronium in patients undergoing cesarean section has been reported; the umbilical venous plasma concentrations were 11% of maternal concentrations at delivery and mean neonate APGAR scores at 5 minutes were >=9. The action of neuromuscular blocking agents may be enhanced by magnesium salts administered for the management of preeclampsia.
Vecuronium crosses the placenta minimally.
It is not known whether vecuronium is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when vecuronium is administered to a breast-feeding woman.
The manufacturer recommends cautious dosage selection in elderly patients, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function in this patient population. Advanced age or other conditions associated with slower circulation time may result in delayed onset of neuromuscular blockade; however, the manufacturer does not recommend increasing the dosage of vecuronium bromide to reduce onset time, as higher dosages produce a longer duration of action. Close monitoring of neuromuscular function is recommended when vecuronium is administered in geriatric patients.
Clinical studies of vecuronium did not include sufficient numbers of patients >=65 years of age to determine whether they respond differently from younger patients. Some published studies report an increased effect and longer duration of action for vecuronium in geriatric patients compared with younger patients; however, other reports have found no significant differences between healthy elderly patients and younger adults. Advanced age or other conditions associated with slower circulation time may be associated with a delay in onset of action; however, recommended doses of vecuronium bromide should not be increased to reduce onset time, as higher doses produce a longer duration of action.
Select dosage cautiously in geriatric patients and monitor neuromuscular function closely.
ICD codes
| Code | Type | Description |
|---|---|---|
| General anesthesia adjunct | ||
| 3E030FZ | ICD10PCS | Introduction of intracirculatory anesthetic into peripheral vein, open approach |
| 3E033FZ | ICD10PCS | Introduction of intracirculatory anesthetic into peripheral vein, percutaneous approach |
| 3E040FZ | ICD10PCS | Introduction of intracirculatory anesthetic into central vein, open approach |
| 3E043FZ | ICD10PCS | Introduction of intracirculatory anesthetic into central vein, percutaneous approach |
| 3E050FZ | ICD10PCS | Introduction of intracirculatory anesthetic into peripheral artery, open approach |
| 3E053FZ | ICD10PCS | Introduction of intracirculatory anesthetic into peripheral artery, percutaneous approach |
| 3E060FZ | ICD10PCS | Introduction of intracirculatory anesthetic into central artery, open approach |
| 3E063FZ | ICD10PCS | Introduction of intracirculatory anesthetic into central artery, percutaneous approach |
ICD code information from First Databank (FDB).
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Last reviewed · Source: First Databank (FDB) drug data
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