Xylocaine CO2 (Lidocaine Hydrocarbonate)

XYLOCAINE® CO2

Astra

Lidocaine Hydrocarbonate

Local Anesthetic

Action And Clinical Pharmacology: Mechanism of Action: Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action. Local anesthetics of the amide type are thought to act within sodium channels of the nerve membrane.

Onset of Action: The onset of action with Xylocaine CO2 is faster than regular lidocaine HCl solutions. The rapid diffusion of the carbon dioxide released from the injectate results in a lowering of intracellular pH. This, in turn, causes faster absorption of the lidocaine base, the active form of Xylocaine CO2. In addition, the carbon dioxide may have an additive effect on the conduction block, resulting in a more intense motor block.

Hemodynamics: Lidocaine, like other local anesthetics, may also have effects on excitable membranes in the brain and myocardium. If excessive amounts of drug reach systemic circulation rapidly, symptoms and signs of toxicity will appear, emanating from the central nervous and cardiovascular systems.

CNS toxicity (see Overdose: Symptoms and Treatment) usually precedes the cardiovascular effects since it occurs at lower plasma concentrations. Direct effects of local anesthetics on the heart include slow conduction, negative inotropism and eventually cardiac arrest.

Indirect cardiovascular effects (hypotension, bradycardia) may occur after epidural or spinal administration depending on the extent of the concomitant sympathetic block.

Pharmacokinetics: Lidocaine is completely absorbed following parenteral administration. The rate of absorption depends on the dose, route of administration and the vascularity of the injection site. The highest peak plasma levels are obtained following intercostal nerve block (approximately 1.5 g/mL per 100 mg injected), while abdominal s.c. injections give the lowest (approximately 0.5 g/mL per 100 mg injected). Epidural and major nerve blocks are intermediate.

Absorption is considerably slowed by the addition of epinephrine, although it also depends on the site of injection. Peak plasma concentrations are reduced by 50% following s.c. injection, by 30% following epidural injection and by 20% following intercostal block if epinephrine 5 g/mL is added.

Lidocaine shows complete and biphasic absorption from the epidural space with half-lives in the order of 9.3 minutes and 82 minutes respectively. The slow absorption is rate-limiting in the elimination of lidocaine, which explains the slower elimination following epidural injection compared to i.v. injection.

Lidocaine has a total plasma clearance of 0.95 L/min, a volume of distribution at steady state of 91 L, an elimination half-life of 1.6 h and an estimated hepatic extraction ratio of 0.65. The clearance of lidocaine is almost entirely due to liver metabolism, and depends both on liver blood flow and the activity of metabolizing enzymes.

The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 g of free base per mL, 60 to 80% of lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein.

Lidocaine readily crosses the placenta, and equilibrium in regard to free, unbound drug will be reached. Because the degree of plasma protein binding in the fetus is less than in the mother, the total plasma concentration will be greater in the mother, but the free concentrations will be the same.

Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. Only 2% of lidocaine is excreted unchanged. Most of it is metabolized first to monoethylglycinexylidide (MEGX) and then to glycinexylidide (GX) and 2,6-xylidine. Up to 70% appears in the urine as 4-hydroxy-2,6-xylidine.

The elimination half-life of lidocaine following i.v. bolus injection is typically 1.5 to 2.0 hours. The elimination half-life in neonates (3.2 h) is approximately twice that of adults. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites.

Acidosis increases the systemic toxicity of lidocaine while the use of CNS depressants may increase the levels of lidocaine required to produce overt CNS effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6.0 g free base per mL.

Indications And Clinical Uses: For production of local or regional anesthesia by peripheral nerve block techniques such as brachial plexus block and by central neural techniques including epidural and caudal blocks, when the accepted procedures for these techniques, as described in standard textbooks, are observed.

Contra-Indications: In patients with a known history of hypersensitivity to local anesthetics of the amide type or to other components of the solution.

Xylocaine CO2 is not for spinal use.

Children: Xylocaine CO2 is not recommended in children as the pediatric dose schedule has not been established.

Manufacturers’ Warnings In Clinical States: Local anesthetics should only be employed by clinicians who are well versed in diagnosis and management of dose-related toxicity and other acute emergencies that might arise from the block to be employed and then only after ensuring the immediate availability of oxygen, other resuscitative drugs, cardiopulmonary equipment and the personnel needed for proper management of toxic reactions and related emergencies (see also Adverse Effects and Precautions). Delay in proper management of dose-related toxicity, underventilation from any cause, and/or altered sensitivity may lead to the development of acidosis, cardiac arrest and possibly, death.

It is essential that aspiration for blood or cerebrospinal fluid (where applicable) be done prior to injecting any local anesthetics, both the original and all subsequent doses, to avoid intravascular or subarachnoid injection. However, a negative aspiration does not ensure against an intravascular or subarachnoid injection.

Precautions: The safety and effectiveness of Xylocaine CO2 depend on proper dosage, correct technique, adequate precautions and readiness for emergencies. Standard textbooks should be consulted for specific techniques and precautions for various regional anesthetic procedures.

Resuscitative equipment, oxygen, and other resuscitative drugs should be available for immediate use (see Warnings and Overdose: Symptoms and Treatment). During major regional nerve blocks, the patients should have i.v. fluids running via an indwelling catheter to assure a functioning i.v. pathway. The lowest dosage that results in effective anesthesia should be used to avoid high plasma levels and serious adverse effects. Injections should be made slowly, with frequent aspirations before and during the injection to avoid intravascular injection.

During the administration of epidural anesthesia, it is recommended that a test dose be administered initially and that the patient be monitored for CNS toxicity and cardiovascular toxicity, as well as for signs of unintended intrathecal administration, before proceeding (see Dosage). When clinical conditions permit, consideration should be given to employing local anesthetic solutions that contain epinephrine for the test dose because circulatory changes compatible with epinephrine may also serve as a warning sign of unintended intravascular injection. An intravascular injection is still possible even if aspirations for blood are negative. Syringe aspirations should also be performed before and during each supplemental injection when using indwelling catheter techniques.

Repeated doses of Xylocaine CO2 may cause significant increases in blood levels with each repeated dose because of slow accumulation of the drug or its metabolites. Tolerance to elevated blood levels varies with the status of the patient. Debilitated, elderly patients, acutely ill patients and children should be given reduced doses commensurate with their age and physical condition. Xylocaine CO2 should also be used with extreme caution in patients with epilepsy, impaired cardiac conduction, bradycardia, impaired hepatic or renal function, and in severe shock.

Because amide-type local anesthetics such as lidocaine are metabolized by the liver, these drugs, especially repeat doses, should be used cautiously in patients with hepatic disease. Patients with severe hepatic disease, because of their inability to metabolize local anesthetics normally, are at greater risk of developing toxic plasma concentrations.

Lidocaine should also be used with caution in patients with impaired cardiovascular function since they may be less able to compensate for functional changes associated with the prolongation of AV conduction produced by these drugs.

Xylocaine CO2 is not intended for spinal or subarachnoid administration, i.e., it should not enter the cerebrospinal fluid.

Lumbar and caudal epidural anesthesia should be used with extreme caution in persons with the following conditions: existing neurological disease, spinal deformities, septicemia, and severe hypertension.

Central nerve blocks may cause cardiovascular depression, especially in the presence of hypovolemia. Epidural anesthesia should be used with caution in patients with impaired cardiovascular function.

Paracervical block can sometimes cause fetal bradycardia/tachycardia, and careful monitoring of the fetal heart rate is necessary.

Epidural anesthesia may lead to hypotension and bradycardia. This risk can be reduced either by preloading the circulation with crystalloidal or colloidal solutions, or by injecting a vasopressor such as ephedrine 20 to 40 mg i.m., or by treating promptly with e.g., ephedrine 5 to 10 mg i.v. and repeating as necessary.

Local anesthetic procedures should not be used when there is inflammation and/or sepsis in the region of the proposed injection.

Solutions containing epinephrine should be used with caution in patients whose medical history and physical evaluation suggest the existence of untreated hypertension, poorly controlled thyrotoxicosis, diabetes, ischemic heart disease, heart block, cerebral vascular insufficiency and peripheral vascular disorder. These solutions should also be used cautiously in areas of the body supplied by end arteries, such as digits, or otherwise having a compromised blood supply (see also Drug Interactions).

Careful and constant monitoring of cardiovascular and respiratory (adequacy of ventilation) vital signs and the patient’s state of consciousness should be performed after each local anesthetic injection. It should be kept in mind at such times that restlessness, anxiety, incoherent speech, lightheadedness, numbness and tingling of the mouth and lips, metallic taste, tinnitus, dizziness, blurred vision, tremors, twitching, depression or drowsiness may be early warning signs of central nervous system toxicity.

Many drugs used during the conduct of anesthesia are considered potential triggering agents for familial malignant hyperthermia. It has been shown that the use of amide local anesthetics in malignant hyperthermia is safe. However, there is no guarantee that neural blockade will prevent the development of malignant hyperthermia during surgery. It is also difficult to predict the need for supplemental general anesthesia. Therefore, a standard protocol for the management of malignant hyperthermia should be available.

Lidocaine should be used with caution in persons with known drug sensitivities. Patients allergic to para-aminobenzoic acid derivatives (procaine, tetracaine, benzocaine, etc.) have not shown cross sensitivity to lidocaine.

Use in Brachial Plexus Block: The supraclavicular or axillary approach to the brachial plexus is usually preferred. If the supraclavicular route is chosen, great care is necessary to prevent pneumothorax or inadvertent phrenic block, (therefore bilateral supraclavicular block should be avoided). Using a short needle, 1/2 inch (13 mm), 24 gauge, greatly reduces these risks.

Use in the Head and Neck Area: Small doses of local anesthetics injected into the head and neck area, including retrobulbar, dental and stellate ganglion blocks, may produce adverse reactions caused by inadvertent injection to an artery. These reactions may be similar to systemic toxicity seen with unintentional intravascular injections of larger doses. Inadvertent injections into an artery can cause cerebral symptoms even at low doses. Confusion, convulsions, respiratory depression and/or respiratory arrest, and cardiovascular stimulation or depression leading to cardiac arrest have been reported. Patients receiving these blocks should have their circulation and respiration monitored and be constantly observed.

Retrobulbar injections may very occasionally reach the cranial subarachnoid space causing temporary blindness, cardiovascular collapse, apnea, convulsions, etc. These reactions, which may be due to intraarterial injection or direct injection into the CNS via the sheaths of the optic nerve, must be diagnosed and treated promptly.

Drug Interactions: Lidocaine should be used with caution in patients receiving other local anesthetics or agents structurally related to the amide-type local anesthetics, since the toxic effects are additive.

Xylocaine solutions containing epinephrine or other vasopressors should not be used concomitantly with ergot-type oxytocic drugs, because a severe persistent hypertension may occur and cerebrovascular and cardiac accidents are possible. Likewise, Xylocaine solutions containing epinephrine or another vasoconstrictor should be used with extreme caution in patients receiving monoamine oxidase (MAO) inhibitors or antidepressants of the triptyline or imipramine types, because severe prolonged hypertension may result. In situations when concurrent therapy is necessary, careful patient monitoring is essential. Phenothiazines and butyrophenones may reduce or reverse the pressor effect of epinephrine.

If sedatives are employed to reduce patient apprehension, they should be used in reduced doses, since local anesthetic agents, like sedatives, are CNS depressants which in combination may have an additive effect.

Solutions containing epinephrine should be used with caution in patients undergoing general anesthesia with inhalation agents such as halothane, due to the risk of serious cardiac arrhythmias.

Drug/Laboratory Test Interactions : The i.m. injection of lidocaine may result in an increase in creatine phosphokinase levels. Thus, the use of this enzyme determination, without isoenzyme separation, as a diagnostic test for the presence of acute myocardial infarction may be compromised by the i.m. injection of lidocaine.

Information for the Patient: When appropriate, patients should be informed in advance that they may experience temporary loss of sensation and motor activity, usually in the lower half of the body, following proper administration of epidural anesthesia.

Pregnancy : It is reasonable to assume that a large number of pregnant women and women of child-bearing age have been given lidocaine. No specific disturbances to the reproductive process have so far been reported, e.g., no increased incidence of malformations. However, care should be given during early pregnancy when maximum organogenesis takes place.

There are no adequate and well-controlled studies in pregnant women, on the effect of lidocaine on the developing fetus.

Labor and Delivery: Local anesthetics rapidly cross the placenta and when used for epidural, paracervical, pudendal or caudal block anesthesia, can cause varying degrees of maternal, fetal and neonatal toxicity. The potential for toxicity depends upon the procedure performed, the type and amount of drug used, and the technique of drug administration. Adverse reactions in the parturient, fetus and neonate involve alterations of the CNS, peripheral vascular tone and cardiac function.

Maternal hypotension has resulted from regional anesthesia. Local anesthetics produce vasodilation by blocking sympathetic nerves. Elevating the patient’s legs and positioning her on her left side will help prevent decreases in blood pressure. A vasopressor, such as ephedrine, may be indicated (see Precautions). The fetal heart rate also should be monitored continuously, and electronic fetal monitoring is highly advisable.

Epidural, spinal, paracervical, or pudendal anesthesia may alter the forces of parturition through changes in uterine contractility or maternal expulsive efforts. In one study, paracervical block anesthesia was associated with a decrease in the mean duration of first stage labor and facilitation of cervical dilation. However, spinal and epidural anesthesia have also been reported to prolong the second stage of labor by removing the parturient’s reflex urge to bear down or by interfering with motor function. The use of obstetrical anesthesia may increase the need for forceps assistance.

Fetal bradycardia may occur in 20 to 30% of patients receiving paracervical nerve block anesthesia with the amide-type local anesthetics and may be associated with fetal acidosis. Fetal heart rate should always be monitored during paracervical anesthesia. The physician should weigh the possible advantages against risks when considering paracervical block in prematurity, toxemia of pregnancy, and fetal distress. Careful adherence to recommended dosage is of the utmost importance in obstetrical paracervical block. Failure to achieve adequate analgesia with recommended doses should arouse suspicion of intravascular or fetal intracranial injection. Cases compatible with unintended fetal intracranial injection of local anesthetic solution have been reported following intended paracervical or pudendal block or both. Babies so affected, present with unexplained neonatal depression at birth, which correlates with high local anesthetic serum levels, and often manifest seizures within 6 hours. Prompt use of supportive measures combined with forced urinary excretion of the local anesthetic has been used successfully to manage this complication.

Case reports of maternal convulsions and cardiovascular collapse following use of some local anesthetics for paracervical block in early pregnancy (as anesthesia for elective abortion) suggest that systemic absorption under these circumstances may be rapid. The recommended maximum dose of each drug should not be exceeded. Injection should be made slowly and with frequent aspiration. Allow a 5-minute interval between sides.

Lactation: Lidocaine is excreted in the breast milk, but in such small quantities that there is generally no risk of affecting the infant at therapeutic dose levels. It is not known whether epinephrine enters breast milk, but it is unlikely to affect the breast-fed infant.

Adverse Reactions: Adverse experiences following the administration of lidocaine are similar in nature to those observed with other amide local anesthetic agents. These adverse experiences are, in general, dose-related and may result from high plasma levels caused by overdosage or rapid absorption, or inadvertent intravascular injection, or may result from a hypersensitivity, idiosyncrasy or diminished tolerance on the part of the patient.

Serious adverse experiences are generally systemic in nature. The following types are those most commonly reported: CNS: CNS manifestations are excitatory and/or depressant and may be characterized by circumoral paresthesia, light-headedness, nervousness, apprehension, euphoria, confusion, dizziness, drowsiness, hyperacusis, tinnitus, blurred vision, vomiting, sensations of heat, cold or numbness, twitching, tremors, convulsions, unconsciousness, respiratory depression and arrest. The excitatory manifestations may be very brief or may not occur at all, in which case the first manifestation of toxicity may be drowsiness merging into unconsciousness and respiratory arrest.

Drowsiness following the administration of lidocaine is usually an early sign of a high plasma level of the drug and may occur as a consequence of rapid absorption.

Cardiovascular: Cardiovascular manifestations are usually depressant and are characterized by bradycardia, hypotension, arrhythmia, and cardiovascular collapse, which may lead to cardiac arrest.

Allergic: Allergic reactions are characterized by cutaneous lesions, urticaria, edema or in the most severe instances, anaphylactic shock. Allergic reactions of the amide type are rare and, may occur as a result of sensitivity either to the local anesthetic agent or to other components in the formulation.

Neurologic: The incidence of adverse reactions may be related to the total dose of local anesthetic administered but is also dependent upon the particular drug used, the route of administration and the physical status of the patient. Neuropathy and spinal cord dysfunction (e.g., anterior spinal artery syndrome, arachnoiditis, cauda equina syndrome), have been associated with regional anesthesia. Neurological effects may be related to local anesthetic techniques, with or without a contribution from the drug.

In the practice of lumbar epidural block, occasional unintentional penetration of the subarachnoid space by the catheter or needle may occur. For example, a high spinal is characterized by paralysis of the legs, loss of consciousness, respiratory paralysis and bradycardia.

Neurologic effects following unintentional subarachnoid administration during epidural anesthesia may include spinal block by varying magnitude (including total or high spinal block), hypotension secondary to spinal block, urinary retention, fecal and urinary incontinence, loss of perineal sensation and sexual function, persistent anesthesia, paresthesia, weakness, paralysis of the lower extremities and loss of sphincter control, all of which may have slow, incomplete or no recovery; headache, backache, septic meningitis, meningismus, slowing of labor, increased incidence of forceps delivery, or cranial nerve palsies due to traction on nerves from loss of cerebrospinal fluid.

Symptoms And Treatment Of Overdose: Acute systemic toxicity from local anesthetics is generally related to high plasma levels encountered during therapeutic use of local anesthetics and originates mainly in the central nervous and the cardiovascular systems (see Adverse Effects, Warnings, and Precautions).Symptoms: With accidental intravascular injections, the toxic effect will be obvious within 1 to 3 minutes, while with overdosage, peak plasma concentrations may not be reached for 20 to 30 minutes depending on the site of injection, with signs of toxicity thus being delayed.

CNS toxicity is a graded response, with symptoms and signs of escalating severity. The first symptoms are circumoral paresthesia, numbness of the tongue, lightheadedness, hyperacusis and tinnitus. Visual disturbance and muscular tremors are more serious and precede the onset of generalized convulsions. Unconsciousness and grand mal convulsions may follow, which may last from a few seconds to several minutes. Hypoxia and hypercarbia occur rapidly following convulsions due to the increased muscular activity, together with the interference with normal respiration. In severe cases apnea may occur. Acidosis increases the toxic effects of local anesthetics.

Recovery is due to redistribution and metabolism of the local anesthetic drug. Recovery may be rapid unless large amounts of the drug have been administered.

Cardiovascular effects may be seen in cases with high systemic concentrations. Severe hypotension, bradycardia, arrhythmia and cardiovascular collapse may be the result in such cases.

Cardiovascular toxic effects are generally preceded by signs of toxicity in the CNS, unless the patient is receiving a general anesthetic or is heavily sedated with drugs such as a benzodiazepine or barbiturate.

Treatment: The first consideration is prevention, best accomplished by careful and constant monitoring of cardiovascular and respiratory vital signs and the patient’s state of consciousness after each local anesthetic administration. At the first sign of change, oxygen should be administered. If signs of acute systemic toxicity appear, injection of the local anesthetic should be immediately stopped.

The first step in the management of systemic toxic reactions, as well as underventilation or apnea due to unintentional subarachnoid injection consists of immediate attention to the establishment and maintenance of a patent airway and assisted or controlled ventilation with oxygen and a delivery system capable of permitting immediate positive airway pressure by mask. This may prevent convulsions if they have not already occurred.

If necessary, use drugs to control convulsions. An anticonvulsant should be given i.v. if the convulsions do not stop spontaneously in 15 to 20 seconds. Thiopental 100 to 150 mg i.v. will abort the convulsions rapidly. Alternatively, diazepam 5 to 10 mg i.v. may be used, although its action is slower. Succinylcholine will stop the muscle convulsions rapidly, but will require tracheal intubation and controlled ventilation, and should only be used by those familiar with these procedures.

If cardiovascular depression is evident (hypotension, bradycardia), ephedrine 5 to 10 mg i.v. should be given and may be repeated, if necessary, after 2 to 3 minutes.

Should circulatory arrest occur, immediate cardiopulmonary resuscitation should be instituted. Optimal oxygenation and ventilation and circulatory support as well as treatment of acidosis are of vital importance, since hypoxia and acidosis will increase the systemic toxicity of local anesthetics. Epinephrine (0.1 to 0.2 mg as i.v. or intracardial injections) should be given as soon as possible and repeated, if necessary.

Children should be given doses commensurate with their age and weight.

Dosage And Administration: Table I summarizes the recommended doses and total doses of Xylocaine CO2 for various types of anesthetic procedures. The dosages suggested in Table I are for normal healthy adults and refer to the use of epinephrine-free solutions.

When larger volumes are required, only solutions containing epinephrine should be used except in those cases where vasopressor drugs may be contraindicated. To make a solution of Xylocaine CO2 with 1:200 000 epinephrine, it is recommended that 0.1 mL of an epinephrine solution 1:1 000 be added to 20 mL of Xylocaine CO2. No clinical trials have been used with Xylocaine CO2 with epinephrine for caudal anesthesia.

These recommended doses serve only as a guide to the amount of anesthetic required for most routine procedures. The actual volumes and concentrations to be used depend on a number of factors such as type and extent of surgical procedure, depth of anesthesia and degree of muscular relaxation required, duration of anesthesia required, and the physical condition of the patient. In all cases the lowest concentration and smallest dose that will produce the desired result should be given. Dosages should be reduced for elderly and debilitated patients and patients with cardiac and/or liver disease. No pediatric dose has been established.

The onset of anesthesia, the duration of anesthesia and the degree of muscular relaxation are proportional to the volume and concentration (i.e., total dose) of local anesthetic used. Thus, an increase in volume and concentration of Xylocaine CO2 will decrease the onset of anesthesia, prolong the duration of anesthesia, provide a greater degree of muscular relaxation and increase the segmental spread of anesthesia. However, increasing the volume and concentration of Xylocaine CO2 may result in a more profound fall in blood pressure when used in epidural anesthesia. Although the incidence of side effects with lidocaine is quite low, caution should be exercised when employing large doses since the incidence of side effects is directly proportional to the total dose of local anesthetic agent injected. The risk of reaching a toxic plasma concentration or inducing a local neural injury must be considered when prolonged blocks and/or repeated administration are employed.

In general, complete block of all nerve fibres in large nerves requires the higher concentrations of drug. In smaller nerves, or when a less intense block is required (e.g., in the relief of labor pain), the lower concentrations are indicated. The volume of drug used will affect the extent of spread of anesthesia.

Caudal and Lumbar Epidural Block: Test Dose: As a precaution against the adverse experience sometimes observed following unintentional penetration of the subarachnoid space, a test dose such as 3 to 5 mL of 1.5% lidocaine should be administered at least 5 minutes prior to injecting the total volume required for a lumbar or caudal epidural block. During the administration of a test dose, it is recommended that constant ECG monitoring occur. The test dose should be repeated if the patient is moved in a manner that may have displaced the catheter. Epinephrine, if contained in the test dose (10 to 15 g have been suggested), may serve as a warning of unintentional intravascular injection. If injected into a blood vessel, this amount of epinephrine is likely to produce a transient epinephrine response within 45 seconds, consisting of an increase in heart rate and systolic blood pressure, circumoral pallor, palpitations and nervousness in the unsedated patient. The sedated patient may exhibit only a pulse rate increase of 20 or more beats per minute for 15 or more seconds. Patients on beta blockers may not manifest changes in heart rate, but blood pressure monitoring can detect an evanescent rise in systolic blood pressure. Adequate time should be allowed for onset of anesthesia after administration of each test dose. The rapid injection of a large volume of Xylocaine CO2 through the catheter should be avoided and when feasible, fractional doses should be administered.

The main dose should be injected slowly at a rate of 100 to 200 mg/minute, or in incremental doses, while keeping in constant verbal contact with the patient. If toxic symptoms occur, the injection should be stopped immediately.

In the event of the known injection of a large volume of local anesthetic solution into the subarachnoid space, after suitable resuscitation and if the catheter is in place, consider attempting the recovery of drug by draining a moderate amount of cerebrospinal fluid (such as 10 mL) through the epidural catheter.

Maximum Recommended Dosages: Adults: For normal healthy adults, the individual maximum recommended dose of Xylocaine CO2 should not exceed 15 mL or 330 mg (equivalent to 300 mg lidocaine HCl). When used with epinephrine the maximum individual dose should not exceed 25 mL or 550 mg (equivalent to 500 mg lidocaine HCl). For continuous epidural or caudal anesthesia, the maximum recommended dosage should not be administered at intervals of less than 90 minutes. When continuous lumbar or caudal epidural anesthesia is used for nonobstetrical procedures, more drug may be administered if required to produce adequate anesthesia.

Sterilization, Storage and Technical Procedures: Xylocaine CO2 can be autoclaved by steam sterilization at 121°C for 15 to 20 minutes. Just prior to cooling the vials to room temperature, they should be agitated briefly to dissolve any traces of lidocaine base which may have been deposited on the inner surface of the vial above the level of the solution during sterilization. This solution must not be used if a precipitate is present. Ethylene oxide sterilization is not recommended.

The 30 mL vials contain lidocaine base 1.73% (by weight) in water, equilibrated with carbon dioxide at a partial pressure of 700 mm Hg. This concentration of lidocaine base is equivalent to lidocaine HCl 2%. The pH of a freshly opened vial at 28°C is about 6.5, but after equilibration with carbon dioxide at a partial pressure of 36 mm Hg the pH rises to about 7.3.

A wide-bore cannula should be used when filling syringes, and the solution should be aspirated slowly with minimal negative pressure. Once the solution is drawn up into the syringe, the pCO2 will remain fairly constant for an hour or two provided the hub is capped and sealed (a disposable hypodermic needle with its plastic guard in place makes a suitable seal). Effort should be made, however, to use the solution as quickly as possible after aspiration into the syringe. Once opened, the unused portion should be discarded.

If a vasoconstrictor is required, epinephrine should be added carefully from a small graduated syringe in the appropriate amount (0.1 mL of 1:1 000 epinephrine added to 20 mL solution of Xylocaine CO2 provides a dilution of approximately 1:200 000).

Adequate precautions should be taken to avoid prolonged contact between local anesthetic solutions containing epinephrine (low pH) and metal surfaces (e.g., needles or metal parts of syringes), since dissolved metal ions, particularly copper ions, may cause severe local irritation (swelling, edema) at the site of injection and accelerate the degradation of epinephrine.

Availability And Storage: Each mL of solution contains: lidocaine base 17.3 mg. Nonmedicinal ingredients: carbon dioxide, sodium chloride and water for injection. The pH of the solution is 6.3 to 6.9. Preservative-free. Twenty mL of lidocaine hydrocarbonate solution 2.2% (equivalent to lidocaine HCl 2%) in single use vials of 30 mL. Discard unused portion. Store at controlled room temperature 15 to 30°C.

XYLOCAINE® CO2 Astra Lidocaine Hydrocarbonate Local Anesthetic

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