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Components:
Dexmedetomidine Hydrochloride
Method of action:
Psycholeptics
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Medically reviewed by Oliinyk Elizabeth Ivanovna, Pharmacy. Last updated on 2019.12.11

Name of the medicinal product

Krunamina

Qualitative and quantitative composition

Dexmedetomidine Hydrochloride

Therapeutic indications

The information provided in Therapeutic indications of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Therapeutic indications in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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For sedation of adult ICU (Intensive Care Unit) patients requiring a sedation level not deeper than arousal in response to verbal stimulation (corresponding to Richmond Agitation-Sedation Scale (RASS) 0 to -3).

Dosage (Posology) and method of administration

The information provided in Dosage (Posology) and method of administration of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Dosage (Posology) and method of administration in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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For hospital use only. Krunamina should be administered by healthcare professionals skilled in the management of patients requiring intensive care.

Posology

Patients already intubated and sedated may switch to dexmedetomidine with an initial infusion rate of 0.7 micrograms/kg/h which may then be adjusted stepwise within the dose range 0.2 to 1.4 micrograms/kg/h in order to achieve the desired level of sedation, depending on the patient's response. A lower starting infusion rate should be considered for frail patients. Dexmedetomidine is very potent and the infusion rate is given per hour. After dose adjustment, a new steady state sedation level may not be reached for up to one hour.

Maximum dose

The maximum dose of 1.4 micrograms/kg/h should not be exceeded. Patients failing to achieve an adequate level of sedation with the maximum dose of dexmedetomidine should be switched to an alternative sedative agent.

Use of a loading dose of Krunamina is not recommended and is associated with increased adverse reactions. Propofol or midazolam may be administered if needed until clinical effects of dexmedetomidine are established.

Duration

There is no experience in the use of Krunamina for more than 14 days. The use of Krunamina for longer than this period should be regularly reassessed.

Special populations

Elderly

No dose adjustment is normally required for elderly patients.

Renal impairment

No dose adjustment is required for patients with renal impairment.

Hepatic impairment

Dexmedetomidine is metabolised in the liver and should be used with caution in patients with hepatic impairment. A reduced maintenance dose may be considered.

Paediatric population

The safety and efficacy of Krunamina in children aged 0 to 18 years have not been established.1 and 5.2 but no recommendation on a posology can be made.

Method of administration

Krunamina must be administered only as a diluted intravenous infusion using a controlled infusion device.

Contraindications

The information provided in Contraindications of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Contraindications in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Advanced heart block (grade 2 or 3) unless paced.

Uncontrolled hypotension.

Acute cerebrovascular conditions.

Special warnings and precautions for use

The information provided in Special warnings and precautions for use of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Special warnings and precautions for use in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Monitoring

Krunamina is intended for use in an intensive care setting and use in other environments is not recommended. All patients should have continuous cardiac monitoring during Krunamina infusion. Respiration should be monitored in non-intubated patients due to the risk of respiratory depression and in some case apnoea.

General precautions

Since Krunamina should not be administered by loading or bolus dose, users should be ready to use an alternative sedative for acute control of agitation or during procedures, especially during the first few hours of treatment.

Some patients receiving Krunamina have been observed to be arousable and alert when stimulated. This alone should not be considered as evidence of lack of efficacy in the absence of other clinical signs and symptoms.

Krunamina should not be used as an induction agent for intubation or to provide sedation during muscle relaxant use.

Dexmedetomidine lacks the anticonvulsant action of some other sedatives and so will not suppress underlying seizure activity.

Care should be taken if combining dexmedetomidine with other substances with sedative or cardiovascular actions as additive effects may occur.

Cardio-vascular effects and precautions

Dexmedetomidine reduces heart rate and blood pressure through central sympatholysis but at higher concentrations causes peripheral vasoconstriction leading to hypertension. Dexmedetomidine normally does not cause deep sedation and patients may be easily roused. Dexmedetomidine is therefore not suitable in patients who will not tolerate this profile of effects, for example those requiring continuous deep sedation or with severe cardiovascular instability.

Caution should be exercised when administering dexmedetomidine to patients with pre-existing bradycardia. Data on the effects of Krunamina in patients with heart rate <60 are very limited and particular care should be taken with such patients. Bradycardia does not normally require treatment, but has commonly responded to anti-cholinergic medicine or dose reduction where needed. Patients with high physical fitness and slow resting heart rate may be particularly sensitive to bradycardic effects of alpha-2 receptor agonists and cases of transient sinus arrest have been reported.

The hypotensive effects of dexmedetomidine may be of greater significance in those patients with pre-existing hypotension (especially if not responsive to vasopressors), hypovolaemia, chronic hypotension or reduced functional reserve such as patients with severe ventricular dysfunction and the elderly and special care is warranted in these cases. Hypotension does not normally require specific treatment but, where needed, users should be ready to intervene with dose reduction, fluids and/or vasoconstrictors.

Patients with impaired peripheral autonomic activity (e.g. due to spinal cord injury) may have more pronounced haemodynamic changes after starting dexmedetomidine and so should be treated with care.

Transient hypertension has been observed primarily during the loading dose in association with the peripheral vasoconstrictive effects of dexmedetomidine and a loading dose is not recommended. Treatment of hypertension has generally not been necessary but decreasing the continuous infusion rate may be advisable.

Local vasoconstriction at higher concentration may be of greater significance in patients with ischaemic heart disease or severe cerebrovascular disease who should be monitored closely. Dose reduction or discontinuation should be considered in a patient developing signs of myocardial or cerebral ischaemia.

Patients with hepatic impairment

Care should be taken in severe hepatic impairment as excessive dosing may increase the risk of adverse reactions, over-sedation or prolonged effect as a result of reduced dexmedetomidine clearance.

Patients with neurological disorders

Experience of dexmedetomidine in severe neurological disorders such as head injury and after neurosurgery is limited and it should be used with caution here, especially if deep sedation is required. Dexmedetomidine may reduce cerebral blood flow and intracranial pressure and this should be considered when selecting therapy.

Other

Alpha-2 agonists have rarely been associated with withdrawal reactions when stopped abruptly after prolonged use. This possibility should be considered if the patient develops agitation and hypertension shortly after stopping dexmedetomidine.

It is not known whether dexmedetomidine is safe to use in malignant hyperthermia-sensitive individuals therefore it is not recommended. Krunamina treatment should be discontinued in the event of a sustained unexplained fever.

Effects on ability to drive and use machines

The information provided in Effects on ability to drive and use machines of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Effects on ability to drive and use machines in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Not relevant.

Undesirable effects

The information provided in Undesirable effects of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Undesirable effects in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Summary of the safety profile

The most frequently reported adverse reactions with dexmedetomidine are hypotension, hypertension and bradycardia, occurring in approximately 25%, 15% and 13% of patients respectively.

Hypotension and bradycardia were also the most frequent dexmedetomidine-related serious adverse reactions occurring in 1.7% and 0.9% of randomised Intensive Care Unit (ICU) patients respectively.

Tabulated list of adverse reactions

The adverse reactions listed in Table 1 have been accumulated from pooled data of clinical trials in intensive care.

Adverse reactions are ranked under headings of frequency, the most frequent first, using the following convention: Very common (>1/10); common (>1/100 to <1/10); uncommon (>1/1,000 to <1/100); rare (>1/10,000 to <1/1,000), very rare (<1/10,000).

Table 1. Adverse reactions

Metabolism and nutrition disorders

Common:

Hyperglycaemia, hypoglycaemia

Uncommon:

Metabolic acidosis, hypoalbuminaemia

Psychiatric disorders

Common:

Agitation

Uncommon:

Hallucination

Cardiac disorders

Very common:

Bradycardia*

Common:

Myocardial ischaemia or infarction, tachycardia

Uncommon:

Atrioventricular block first degree, cardiac output decreased

Vascular disorders:

Very common:

Hypotension*, hypertension*

Respiratory, thoracic and mediastinal disorders

Common:

Respiratory depression

Uncommon:

Dyspnoea, apnoea

Gastrointestinal disorders

Common:

Nausea, vomiting, dry mouth

Uncommon:

Abdominal distension

General disorders and administration site conditions

Common:

Withdrawal syndrome, hyperthermia

Uncommon:

Drug ineffective, thirst

* See section on Description of selected adverse reactions

Description of selected adverse reactions

In relatively healthy non-ICU subjects treated with dexmedetomidine, bradycardia has occasionally led to sinus arrest or pause. The symptoms responded to leg raising and anticholinergics such as atropine or glycopyrrolate. In isolated cases bradycardia has progressed to periods of asystole in patients with pre-existing bradycardia.

Hypertension has been associated with the use of a loading dose and this reaction can be reduced by avoiding such a loading dose or reducing the infusion rate or size of the loading dose.

Paediatric population

Children > 1 month post-natal, predominantly post-operative, have been evaluated for treatment up to 24 hours in the ICU and demonstrated a similar safety profile as in adults. Data in new-born infants (28 - 44 weeks gestation) is very limited and restricted to maintenance doses ≤ 0.2 mcg/kg/h. A single case of hypothermic bradycardia in a neonate has been reported in the literature.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via:

Ireland

HPRA Pharmacovigilance, Earlsfort Terrace, IRL - Dublin 2; Tel: +353 1 6764971, Fax: +353 1 6762517. Website: www.hpra.ie e-mail: medsafety@hpra.ie

United Kingdom

Yellow Card Scheme

Website: www.mhra.gov.uk/yellowcard

Overdose

The information provided in Overdose of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Overdose in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Symptoms

Several cases of dexmedetomidine overdose have been reported both in the clinical trial and the post-marketing data. The reported highest infusion rates of dexmedetomidine in these cases have reached up to 60 µg/kg/h for 36 minutes and 30 µg/kg/h for 15 minutes in a 20-month-old child and in an adult, respectively. The most common adverse reactions reported in conjunction with overdose in these cases included bradycardia, hypotension, oversedation, somnolence and cardiac arrest.

Management

In cases of overdose with clinical symptoms, dexmedetomidine infusion should be reduced or stopped. Expected effects are primarily cardiovascular and should be treated as clinically indicated. At high concentration hypertension may be more prominent than hypotension. In clinical studies, cases of sinus arrest reversed spontaneously or responded to treatment with atropine and glycopyrrolate. Resuscitation was required in isolated cases of severe overdose resulting in cardiac arrest.

Pharmacodynamic properties

The information provided in Pharmacodynamic properties of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Pharmacodynamic properties in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Pharmacotherapeutic group: Psycholeptics, other hypnotics and sedatives, ATC code: N05CM18

Dexmedetomidine is a selective alpha-2 receptor agonist with a broad range of pharmacological properties. It has a sympatholytic effect through decrease of the release of noradrenaline in sympathetic nerve endings. The sedative effects are mediated through decreased firing of locus coeruleus, the predominant noradrenergic nucleus, situated in the brainstem. Dexmedetomidine has analgesic and anaesthetic/analgesic-sparing effects. The cardiovascular effects depend on the dose; with lower infusion rates the central effects dominate leading to decrease in heart rate and blood pressure. With higher doses, peripheral vasoconstricting effects prevail leading to an increase in systemic vascular resistance and blood pressure, while the bradycardic effect is further emphasised. Dexmedetomidine is relatively free from respiratory depressive effects when given as monotherapy to healthy subjects.

In placebo controlled trials in a post-operative ICU population previously intubated and sedated with midazolam or propofol, Krunamina significantly reduced the requirement for both rescue sedative (midazolam or propofol) and opioids during sedation for up to 24 hours. Most dexmedetomidine patients required no additional sedative treatment. Patients could be successfully extubated without stopping the Krunamina infusion. Studies from outside the ICU have confirmed that Krunamina can be administered safely to patients without endotracheal intubation provided adequate monitoring is in place.

Dexmedetomidine was similar to midazolam (Ratio 1.07; 95% CI 0.971, 1.176) and propofol (Ratio 1.00; 95% CI 0.922, 1.075) on the time in target sedation range in a predominently medical population requiring prolonged light to moderate sedation (RASS 0 to -3) in the ICU for up to 14 days, reduced the duration of mechanical ventilation compared to midazolam and reduced the time to extubation compared to midazolam and propofol. Compared to both propofol and midazolam, patients were more easily roused, more cooperative and better able to communicate whether or not they had pain. Dexmedetomidine treated patients had more frequent hypotension and bradycardia but less tachycardia than those receiving midazolam and more frequent tachycardia but similar hypotension to propofol-treated patients. Delirium measured by the CAM-ICU scale was reduced in a study compared to midazolam and delirium-related adverse events were lower on dexmedetomidine compared to propofol. Those patients who withdrew due to insufficient sedation were switched to either propofol or midazolam. The risk of insufficient sedation was increased in patients who were difficult to sedate with standard care immediately prior to switching.

Evidence of paediatric efficacy was seen in a dose-controlled ICU study in a largely post-operative population aged 1 month to ≤ 17 years. Approximately 50% of patients treated with dexmedetomidine did not require rescue addition of midazolam during a median treatment period of 20.3 hours, not exceeding 24 hours. Data on treatment for > 24 hours is not available. Data in new-born infants (28 - 44 weeks gestation) is very limited and restricted to low doses (≤ 0.2 mcg/kg/h). New-born infants may be particularly sensitive to the bradycardic effects of Krunamina in the presence of hypothermia and in conditions of heart rate-dependent cardiac output.

In double blind comparator controlled ICU studies the incidence of cortisol suppression in patients treated with dexmedetomidine (n=778) was 0.5% compared with 0% in patients treated with either midazolam (n=338) or propofol (n=275). The event was reported as mild in 1 and moderate in 3 cases.

Pharmacokinetic properties

The information provided in Pharmacokinetic properties of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Pharmacokinetic properties in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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The pharmacokinetics of dexmedetomidine has been assessed following short term IV administration in healthy volunteers and long term infusion in ICU population.

Distribution

Dexmedetomidine exhibits a two-compartment disposition model. In healthy volunteers it exhibits a rapid distribution phase with a central estimate of the distribution half-life (t1/2α) of about 6 minutes. The mean estimate of the terminal elimination half-life (t1/2) is approximately 1.9 to 2.5 h (min 1.35, max 3.68 h) and the mean estimate of the steady-state volume of distribution (Vss) is approximately 1.16 to 2.16 l/kg (90 to 151 litres). Plasma clearance (Cl) has a mean estimated value of 0.46 to 0.73 l/h/kg (35.7 to 51.1 l/h). The mean body weight associated with these Vss and Cl estimates was 69 kg. Plasma pharmacokinetics of dexmedetomidine is similar in the ICU population following infusion >24 h. The estimated pharmacokinetic parameters are: t1/2 approximately 1.5 hours, Vss approximately 93 litres and Cl approximately 43 l/h. The pharmacokinetics of dexmedetomidine is linear in the dosing range from 0.2 to 1.4 µg/kg/h and it does not accumulate in treatments lasting up to 14 days. Dexmedetomidine is 94% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 0.85 to 85 ng/ml. Dexmedetomidine binds to both human serum albumin and Alpha-1-acid glycoprotein with serum albumin as the major binding protein of dexmedetomidine in plasma.

Biotransformation and Elimination

Dexmedetomidine is eliminated by extensive metabolism in the liver. There are three types of initial metabolic reactions; direct N-glucuronidation, direct N-methylation and cytochrome P450 catalysed oxidation. The most abundant circulating dexmedetomidine metabolites are two isomeric N-glucuronides. Metabolite H-1, N-methyl 3-hydroxymethyl dexmedetomidine O-glucuronide, is also a major circulating product of dexmedetomidine biotransformation. Cytochrome P-450 catalyses the formation of two minor circulating metabolites, 3-hydroxymethyl dexmedetomidine produced by hydroxylation at the 3-methyl group of dexmedetomidine and H-3 produced by oxidation in the imidazole ring. Available data suggest that the formation of the oxidised metabolites is mediated by several CYP forms (CYP2A6, CYP1A2, CYP2E1, CYP2D6 and CYP2C19). These metabolites have negligible pharmacological activity.

Following IV administration of radiolabeled dexmedetomidine an average 95% of radioactivity was recovered in the urine and 4% in the faeces after nine days. The major urinary metabolites are the two isomeric N-glucuronides, which together accounted for approximately 34% of the dose and N-methyl 3-hydroxymethyl dexmedetomidine O-glucuronide that accounted for 14.51% of the dose. The minor metabolites dexmedetomidine carboxylic acid, 3-hydroxymethyl dexmedetomidine and its O-glucuronide individually comprised 1.11 to 7.66% of the dose. Less than 1% of unchanged parent drug was recovered in the urine. Approximately 28% of the urinary metabolites are unidentified minor metabolites.

Special Populations

No major pharmacokinetic differences have been observed based on gender or age.

Dexmedetomidine plasma protein binding is decreased in subjects with hepatic impairment compared with healthy subjects. The mean percentage of unbound dexmedetomidine in plasma ranged from 8.5% in healthy subjects to 17.9% in subjects with severe hepatic impairment. Subjects with varying degrees of hepatic impairment (Child-Pugh Class A, B, or C) had decreased hepatic clearance of dexmedetomidine and prolonged plasma elimination t1/2. The mean plasma clearance values of unbound dexmedetomidine for subjects with mild, moderate, and severe hepatic impairment were 59%, 51% and 32% of those observed in the normal healthy subjects, respectively. The mean t1/2 for the subjects with mild, moderate or severe hepatic impairment was prolonged to 3.9, 5.4, and 7.4 hours, respectively. Although dexmedetomidine is administered to effect, it may be necessary to consider initial/maintenance dose reduction in patients with hepatic impairment depending on the degree of impairment and the response.

The pharmacokinetics of dexmedetomidine in subjects with severe renal impairment (creatinine clearance <30 ml/min) is not altered relative to healthy subjects.

Data in new-born infants (28 - 44 weeks gestation) to children 17 years of age are limited. Dexmedetomidine half life in children (1 months to 17 years) appears similar to that seen in adults, but in new-born infants (under 1 month) it appears higher. In the age groups 1 months to 6 years, body weight-adjusted plasma clearance appeared higher but decreased in older children. Body weight-adjusted plasma clearance in new-born infants (under 1 month) appeared lower (0.9 l/h/kg) than in the older groups due to immaturity. The available data is summarised in the following table;

Mean (95% CI)

Age

N

Cl (l/h/kg)

t1/2 (h)

Under 1 month

28

0.93

(0.76, 1.14)

4.47

(3.81, 5.25)

1 to < 6 months

14

1.21

(0.99, 1.48)

2.05

(1.59, 2.65)

6 to < 12 months

15

1.11

(0.94, 1.31)

2.01

(1.81, 2.22)

12 to < 24 months

13

1.06

(0.87, 1.29)

1.97

(1.62, 2.39)

2 to < 6 years

26

1.11

(1.00, 1.23)

1.75

(1.57, 1.96)

6 to < 17 years

28

0.80

(0.69, 0.92)

2.03

(1.78, 2.31)

Pharmacotherapeutic group

The information provided in Pharmacotherapeutic group of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Pharmacotherapeutic group in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Psycholeptics, other hypnotics and sedatives, ATC code: N05CM18

Preclinical safety data

The information provided in Preclinical safety data of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Preclinical safety data in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, single and repeated dose toxicity and genotoxicity.

In the reproductive toxicity studies, dexmedetomidine had no effect on male or female fertility in the rat, and no teratogenic effects were observed in the rat or rabbit. In the rabbit study intravenous administration of the maximum dose, 96 µg/kg/day, produced exposures that are similar to those observed clinically. In the rat, subcutaneous administration at the maximum dose, 200 µg/kg/day, caused an increase in embryofetal death and reduced the fetal body weight. These effects were associated with clear maternal toxicity. Reduced fetal body weight was noted also in the rat fertility study at dose 18 µg/kg/day and was accompanied with delayed ossification at dose 54 µg/kg/day. The observed exposure levels in the rat are below the clinical exposure range.

Incompatibilities

The information provided in Incompatibilities of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Incompatibilities in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Compatibility studies have shown potential for adsorption of dexmedetomidine to some types of natural rubber. Although dexmedetomidine is dosed to effect, it is advisable to use components with synthetic or coated natural rubber gaskets.

Special precautions for disposal and other handling

The information provided in Special precautions for disposal and other handling of Krunamina is based on data of another medicine with exactly the same composition as the Krunamina of the medicine (Dexmedetomidine Hydrochloride). Be careful and be sure to specify the information on the section Special precautions for disposal and other handling in the instructions to the drug Krunamina directly from the package or from the pharmacist at the pharmacy.
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Ampoules and vials are intended for single patient use only.

Preparation of solution

Krunamina can be diluted in glucose 50 mg/ml (5%), Ringers, mannitol or sodium chloride 9 mg/ml (0.9%) solution for injection to achieve the required concentration of either 4 micrograms/ml or 8 micrograms/ml prior to administration. Please see below in tabulated form the volumes needed to prepare the infusion.

In case the required concentration is 4 micrograms/ml:

Volume of Krunamina 100 micrograms/ml concentrate for solution for infusion

Volume of diluent

Total volume of infusion

2 ml

48 ml

50 ml

4 ml

96 ml

100 ml

10 ml

240 ml

250 ml

20 ml

480 ml

500 ml

In case the required concentration is 8 micrograms/ml:

Volume of Krunamina 100 micrograms/ml concentrate for solution for infusion

Volume of diluent

Total volume of infusion

4 ml

46 ml

50 ml

8 ml

92 ml

100 ml

20 ml

230 ml

250 ml

40 ml

460 ml

500 ml

The solution should be shaken gently to mix well.

Krunamina should be inspected visually for particulate matter and discoloration prior to administration.

Krunamina has been shown to be compatible when administered with the following intravenous fluids and medicinal products:

Lactated Ringers, 5% glucose solution, sodium chloride 9 mg/ml (0.9%) solution for injection, mannitol 200 mg/ml (20%), thiopental sodium, etomidate, vecuronium bromide, pancuronium bromide, succinylcholine, atracurium besylate, mivacurium chloride, rocuronium bromide, glycopyrrolate bromide, phenylephrine HCl, atropine sulfate, dopamine, noradrenaline, dobutamine, midazolam, morphine sulfate, fentanyl citrate, and a plasma-substitute.

Any unused medicinal product or waste material should be disposed of in accordance with local requirements.

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