Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1508
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Carbocaine (Injection, Solution)
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The dose of any local anesthetic administered
varies with the anesthetic procedure, the area to be anesthetized, the vascularity
of the tissues, the number of neuronal segments to be blocked, the depth of
anesthesia and degree of muscle relaxation required, the duration of anesthesia
desired, individual tolerance and the physical condition of the patient. The
smallest dose and concentration required to produce the desired result should
be administered. Dosages of CARBOCAINE should be reduced for elderly and debilitated
patients and patients with cardiac and/or liver disease. The rapid injection
of a largevolume of local anesthetic solution should be avoided and fractional
doses should be used when feasible. For specific techniques
and procedures, refer to standard textbooks. The recommended
single adult dose (or the total
of a series of doses given in one procedure) of CARBOCAINE for unsedated,
healthy, normal-sized individuals should not usually exceed 400 mg. The recommended
dosage is based on requirements for the average adult and should be reduced
for elderly or debilitated patients. While maximum doses
of 7 mg/kg (550 mg) have been administered without adverse effect, these are
not recommended, except in exceptional circumstances and under no circumstances
should the administration be repeated at intervals of less than 1 1/2 hours.
The total dose for any 24-hour period should not exceed 1,000 mg because of
a slow accumulation of the anesthetic or its derivatives or slower than normal
metabolic degradation or detoxification with repeat administration (see CLINICAL
PHARMACOLOGY and PRECAUTIONS). Pediatric
patients tolerate the local anesthetic as well as adults. However,
the pediatric dose should be carefully measured as a percentage of the total adult dose based
on weight, and should not exceed 5 mg/kg to 6 mg/kg (2.5 mg/lb to
3 mg/lb) in pediatric patients, especially those weighing less than 30 lb.
In pediatric patients under 3 years of age
or weighing less than 30 lb concentrations less than 2% (e.g.,
0.5% to 1.5%) should be employed. Unused
portions of solutions not containing preservatives, i.e., those supplied in
single-dose vials, should be discarded following initial use. This
product should be inspected visually for particulate matter and discoloration
prior to administration whenever solution and container permit. Solutions
which are discolored or which contain particulate matter should not be administered.
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Mepivacaine hydrochloride is 2-Piperidinecarboxamide, N-(2,6-dimethylphenyl)-1-methyl, monohydrochloride
and has the following structural formula: It is a white crystalline odorless powder, soluble in water,
but very resistant to both acid and alkaline hydrolysis. CARBOCAINE
is a local anesthetic available as sterile isotonic solutions (clear, colorless)
in concentrations of 1%, 1.5%, and 2% for injection via local infiltration,
peripheral nerve block, and caudal and lumbar epidural blocks. Mepivacaine
hydrochloride is related chemically and pharmacologically to the amide-type
local anesthetics. It contains an amide linkage between the aromatic nucleus
and the amino group. *In Water for Injection. The pH of
the solution is adjusted between 4.5 and 6.8 with sodium hydroxide or hydrochloric
acid.
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Local anesthetics block the generation and the conduction
of nerve impulses, presumably by increasing the threshold for electrical excitation
in the nerve, by slowing the propagation of the nerve impulse and by reducing
the rate of rise of the action potential. In general, the progression of anesthesia
is related to the diameter, myelination, and conduction velocity of affected
nerve fibers. Clinically, the order of loss of nerve function is as follows:
pain, temperature, touch, proprioception, and skeletal muscle tone. Systemic
absorption of local anesthetics produces effects on the cardiovascular and
central nervous systems. At blood concentrations achieved with normal therapeutic
doses, changes in cardiac conduction, excitability, refractoriness, contractility,
and peripheral vascular resistance are minimal. However, toxic blood concentrations
depress cardiac conduction and excitability, which may lead to atrioventricular
block and ultimately to cardiac arrest. In addition, myocardial contractility
is depressed and peripheral vasodilation occurs, leading to decreased cardiac
output and arterial blood pressure. Following systemic
absorption, local anesthetics can produce central nervous system stimulation,
depression, or both. Apparent central stimulation is manifested as restlessness,
tremors, and shivering, progressing to convulsions, followed by depression
and coma progressing ultimately to respiratory arrest. However, the local
anesthetics have a primary depressant effect on the medulla and on higher
centers. The depressed stage may occur withouta prior excited stage. A
clinical study using 15 mL of 2% epidural mepivacaine at the T 9-10 interspace
in 62 patients, 20-79 years of age, demonstrated a 40% decrease in the
amount of mepivacaine required to block a given number of dermatomes in the
elderly (60-79 years, N=13) as compared to young adults 20-39 years). Another
study using 10 mL of 2% lumbar epidural mepivacaine in 161 patients, 19-75
years of age, demonstrated a strong inverse relationship between patient age
and the number of dermatomes blocked per cc of mepivacaine injected. Pharmacokinetics The
rate of systemic absorption of local anesthetics is dependent upon the total
dose and concentration of drug administered, the route of administration,
the vascularity of the administration site, and the presence or absence of
epinephrine in the anesthetic solution. A dilute concentration of epinephrine
(1:200,000 or 5 mcg/mL) usually reduces the rate of absorption and plasma
concentration of CARBOCAINE, however, it has been reported that vasoconstrictors
do not significantly prolong anesthesia with CARBOCAINE. Onset
of anesthesia with CARBOCAINE is rapid, the time of onset for sensory block
ranging from about 3 to 20 minutes depending upon such factors as the anesthetic
technique, the type of block, the concentration of the solution, and the individual
patient. The degree of motor blockade produced is dependent on the concentration
of the solution. A 0.5% solution will be effective in small superficial nerve
blocks while the 1% concentration will block sensory and sympathetic conduction
without loss of motor function. The 1.5% solution will provide extensive and
often complete motor block and the 2% concentration of CARBOCAINE will produce
complete sensory and motor block of any nerve group. The
duration of anesthesia also varies depending upon the technique and type of
block, the concentration, and the individual. Mepivacaine will normally provide
anesthesia which is adequate for 2 to 2 1/2 hours of surgery. Local
anesthetics are bound to plasma proteins in varying degrees. Generally, the
lower the plasma concentration of drug, the higher the percentage of drug
bound to plasma. Local anesthetics appear to cross the
placenta by passive diffusion. The rate and degree of diffusion is governed
by the degree of plasma protein binding, the degree of ionization, and the
degree of lipid solubility. Fetal/maternal ratios of local anesthetics appear
to be inversely related to the degree of plasma protein binding, because only
the free, unbound drug is available for placental transfer. CARBOCAINE is
approximately 75% bound to plasma proteins. The extent of placental transfer
is also determined by the degree of ionization and lipid solubility of the
drug. Lipid soluble, nonionized drugs readily enter the fetal blood from the
maternal circulation. Depending upon the route of administration,
local anesthetics are distributed to some extent to all body tissues, with
high concentrations found in highly perfused organs such as the liver, lungs,
heart, and brain. Various pharmacokinetic parameters
of the local anesthetics can be significantly altered by the presence of hepatic
or renal disease, addition of epinephrine, factors affecting urinary pH, renal
blood flow, the route of drug administration, and the age of the patient.
The half-life of CARBOCAINE inadults is 1.9 to 3.2 hours and in neonates
8.7 to 9 hours. Mepivacaine, because of its amide structure,
is not detoxified by the circulating plasma esterases. It is rapidly metabolized,
with only a small percentage of the anesthetic (5 percent to 10 percent)
being excreted unchanged in the urine. The liver is the principal site of
metabolism, with over 50% of the administered dose being excreted into the
bile as metabolites. Most of the metabolized mepivacaine is probably resorbed
in the intestine and then excreted into the urine since only a small percentage
is found in the feces. The principal route of excretion is via the kidney.
Most of the anesthetic and its metabolites are eliminated within 30 hours.
It has been shown that hydroxylation and N-demethylation, which are detoxification
reactions, play important roles in the metabolism of the anesthetic. Three
metabolites of mepivacaine have been identified from human adults: two phenols,
which are excreted almost exclusively as their glucuronide conjugates, and
the N-demethylated compound (2���6���-pipecoloxylidide). Mepivacaine
does not ordinarily produce irritation or tissue damage, and does not cause
methemoglobinemia when administered in recommended doses and concentrations.
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CARBOCAINE is contraindicated in patients with a known hypersensitivity
to it or to any local anesthetic agent of the amide-type or to other components
of solutions of CARBOCAINE.
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Single-dose vials and multiple-dose vials of CARBOCAINE may
be sterilized by autoclaving at 15 pound pressure, 121��C (250��F)
for 15 minutes. Solutions of CARBOCAINE may be reautoclaved when necessary.
Do not administer solutions which are discolored or which contain particulate
matter. THESE SOLUTIONS ARE NOT INTENDED FOR SPINAL
ANESTHESIA OR DENTAL USE 1%-Single-dose vials of 30
mL, List 1036 1%-Multiple-dose vials of 50 mL, List
1038 1.5%-Single-dose vials of 30 mL, List 1041 2%-Single-dose
vials of 20 mL, List 1067 2%-Multiple-dose vials of
50 mL, List 2047 Store at 20 to 25��C (68 to 77��F).
[See USP Controlled Room Temperature.] Revised: February
2005 HOSPIRA, INC., LAKE FOREST,
IL 60045 USA
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General: The safety and effectiveness of local anesthetics depend
on proper dosage, correct technique, adequate precautions, and readiness for
emergencies. Resuscitative equipment, oxygen, and other resuscitative drugs
should be available for immediate use. (See WARNINGS and ADVERSE REACTIONS.)
During major regional nerve blocks, the patient should have IV fluids running
via an indwelling catheter to assure a functioning intravenous pathway. The
lowest dosage of local anesthetic 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. Current opinion favors fractional administration
with constant attention to the patient, rather than rapid bolus injection.
Syringe aspirations should also be performed before and during each supplemental
injection in continuous (intermittent) catheter techniques. An intravascular
injection is still possible even if aspirations for blood are negative. During
the administration of epidural anesthesia, it is recommended that a test dose
be administered initially and the effects monitored before the full dose is
given. When using a���continuous���catheter technique, test doses
should be given prior to both the original and all reinforcing doses, because
plastic tubing in the epidural space can migrate into a blood vessel or through
the dura. When clinical conditions permit, an effective test dose should contain
epinephrine (10 mcg to 15 mcg have been suggested) to serve as a warning of
unintended intravascular injection. If injected into a blood vessel, this
amount of epinephrine is likely to produce an���epinephrine response���within 45 seconds, consisting of an increase of pulse and 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. Therefore, following the test dose, the
heart rate should be monitored for a heart rate increase. The test dose should
also contain 45 mg to 50 mg of CARBOCAINE to detect an unintended intrathecal
administration. This will be evidenced within a few minutes by signs of spinal
block (e.g., decreased sensation of the buttocks, paresis of the leg, or,
in the sedated patient, absent knee jerk). Injection
of repeated doses of local anesthetics may cause significant increases in
plasma levels with each repeated dose due to slow accumulation of the drug
or its metabolites or to slow metabolic degradation. Tolerance to elevated
blood levels varies with the status of the patient. Debilitated, elderly patients,
and acutely ill patients should be given reduced doses commensurate with their
age and physical status. Local anesthetics should also be used with caution
in patients with severe disturbances of cardiac rhythm, shock, heart block,
or hypotension. 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. Local
anesthetic solutions containing a vasoconstrictor should be used cautiously
and in carefully restricted quantities in areas of the body supplied by end
arteries or having otherwise compromised blood supply such as digits, nose,
external ear, penis. Patients with hypertensive vascular disease may exhibit
exaggerated vasoconstrictor response. Ischemic injury or necrosis may result. Mepivacaine
should be used with caution in patients with known allergies and sensitivities. Because
amide-type local anesthetics such as CARBOCAINE are metabolized by the liver
and excreted by the kidneys, these drugs, especially repeat doses, should
be used cautiously in patients with hepatic and renal disease. Patients with
severe hepatic disease, because of their inability to metabolize local anesthetics
normally, are at a greater risk of developing, toxic plasma concentrations.
Local anesthetics should also be used with caution in patients with impaired
cardiovascular function because they may be lessable to compensate for functional
changes associated with the prolongation of AV conduction produced by these
drugs. Serious dose-related cardiac arrhythmias may
occur if preparations containing a vasoconstrictor such as epinephrine are
employed in patients during or following the administration of potent inhalation
anesthetics. In deciding whether to use these products concurrently in the
same patient, the combined action of both agents upon the myocardium, the
concentration and volume of vasoconstrictor used, and the time since injection,
when applicable, should be taken into account. Many
drugs used during the conduct of anesthesia are considered potential triggering
agents for familial malignant hyperthermia. Because it is not known whether
amide-type local anesthetics may trigger this reaction and because the need
for supplemental general anesthesia cannot be predicted in advance, it is
suggested that a standard protocol for management should be available. Early
unexplained signs of tachycardia, tachypnea, labile blood pressure, and metabolic
acidosis may precede temperature elevation. Successful outcome is dependent
on early diagnosis, prompt discontinuance of the suspect triggering agent(s),
and institution of treatment, including oxygen therapy, indicated supportive
measures, and dantrolene. (Consult dantrolene sodium intravenous package insert
before using.) Use
In Head and Neck Area Small doses of local
anesthetics injected into the head and neck area may produce adverse reactions
similar to systemic toxicity seen with unintentional intravascular injections
of larger doses. The injection procedures require the utmost care. Confusion,
convulsions, respiratory depression, and/or respiratory arrest, and cardiovascular
stimulation or depression have been reported. These reactions may be due to
intra-arterial injection of the local anesthetic with retrograde flow to the
cerebral circulation. Patients receiving these blocks should have their circulation
and respiration monitored and be constantly observed. Resuscitative equipment
and personnel for treating adverse reactions should be immediately available.
Dosage recommendations should not be exceeded.<br/>Information for Patients: 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 caudal or
epidural anesthesia. Also, when appropriate, the physician should discuss
other information including adverse reactions listed in the package insert
on CARBOCAINE.<br/>Clinically Significant Drug Interactions: The administration of local anesthetic solutions containing
epinephrine or norepinephrine to patients receiving monoamine oxidase inhibitors
or tricyclic antidepressants may produce severe, prolonged hypertension. Concurrent
use of these agents should generally be avoided. In situations when concurrent
therapy is necessary, careful patient monitoring is essential. Concurrent
administration of vasopressor drugs and of ergot-type oxytocic drugs may cause
severe, persistent hypertension or cerebrovascular accidents. Phenothiazines
and butyrophenones may reduce or reverse the pressor effect of epinephrine.<br/>Carcinogenesis, Mutagenesis, and Impairment of Fertility: Long-term studies in animals of most local anesthetics including
mepivacaine to evaluate the carcinogenic potential have not been conducted.
Mutagenic potential or the effect on fertility have not been determined. There
is no evidence from human data that CARBOCAINE may be carcinogenic or mutagenic
or that it impairs fertility.<br/>Pregnancy Category C: Animal reproduction studies have not been conducted with
mepivacaine. There are no adequate and well-controlled studies in pregnant
women of the effect of mepivacaine on the developing fetus. Mepivacaine hydrochloride
should be used during pregnancy only if the potential benefit justifies the
potential risk to the fetus. This does not preclude the use of CARBOCAINE
at term for obstetrical anesthesia or analgesia. (See Laborand Delivery.) CARBOCAINE has been used for
obstetrical analgesia by the epidural, caudal, and paracervical routes without
evidence of adverse effects on the fetus when no more than the maximum safe
dosages are used and strict adherence to technique is followed.<br/>Labor and Delivery: Local anesthetics rapidly cross the placenta, and when used
for epidural, paracervical, caudal, or pudendal block anesthesia, can cause
varying degrees of maternal, fetal, and neonatal toxicity. (See Pharmacokinetics - CLINICAL PHARMACOLOGY.) The
incidence and degree of toxicity depend 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
central nervous system, 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. The fetal heart rate also should be monitored continuously and electronic
fetal monitoring is highly advisable. Epidural, paracervical,
caudal, 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. Epidural anesthesia
has been reported to prolong the second stage of labor by removing the parturient's
reflex urge to bear down or byinterfering with motor function. The use of
obstetrical anesthesia may increase the need for forceps assistance. The
use of some local anesthetic drug products during labor and delivery may be
followed by diminished muscle strength and tone for the first day or two of
life. The long-term significance of these observations is unknown. Fetal
bradycardia may occur in 20 to 30 percent of patients receiving paracervical
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. Added risk appears to be present in prematurity, postmaturity,
toxemia of pregnancy, and fetal distress. The physician should weigh the possible
advantages against dangers when considering paracervical block in these conditions.
Careful adherence to recommended dosage is of the utmost importance in obstetrical
paracervical block. Failure to achieve adequate analgesia with recommendeddoses 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 usually
manifest seizures within six hours. Prompt use of supportive measures combined
with forced urinaryexcretion 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 the local anesthetic should not be exceeded. Injection
should be made slowly and with frequent aspiration. Allow a five-minute interval
between sides. It is extremely important to avoid aortocaval
compression by the gravid uterus during administration of regional block to
parturients. To do this, the patient must be maintained in the left lateral
decubitus position or a blanket roll or sandbag may be placed beneath the
right hip and the gravid uterus displaced to the left.<br/>Nursing Mothers: It is not known whether local anesthetic drugs are excreted
in human milk. Because many drugs are excreted in human milk, caution should
be exercised when local anesthetics are administered to a nursing woman.<br/>Pediatric Use: Guidelines for the administration of mepivacaine to pediatric
patients are presented in DOSAGE AND ADMINISTRATION.<br/>Geriatric Use: Clinical studies and other reported clinical experience indicates
that use of the drug in elderly patients requires a decreased dosage, (see
CLINICAL PHARMACOLOGY, PRECAUTIONS, General, and DOSAGE AND ADMINISTRATION). Mepivacaine
and mepivacaine metabolites are known to be substantially excreted by the
kidney, and the risk of toxic reactions to this drug may be greater in patients
with impaired renal function. Because elderly patients are more likely to
have decreased renal function, care should be taken in dose selection, and
it may be useful to monitor renal function.
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Acute emergencies from local anesthetics are generally related
to high plasma levels encountered during therapeutic use of local anesthetics
or to unintended subarachnoid injection of local anesthetic solution. (See
ADVERSE REACTIONS, WARNINGS, and PRECAUTIONS.) Management of Local Anesthetic Emergencies 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 injection. At the first
sign of change, oxygen should be administered. The first step in the management of systemic toxic reactions,
as well as underventilation or apnea due to unintentional subarachnoid injection
of drug solution, consists of immediate attention to the establishment and maintenance
of a patent airway and effective assisted or controlled ventilation with 100%
oxygen with 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
the convulsions. A 50 mg to 100 mg bolus IV injection of succinylcholine will
paralyze the patient without depressing the central nervous or cardiovascular
systems and facilitate ventilation. A bolus IV dose of 5 mg to 10 mg of diazepam
or 50 mg to 100 mg of thiopental will permit ventilation and counteract
central nervous system stimulation, but these drugs also depress central nervous
system, respiratory, and cardiac function, add to postictal depression and
may result in apnea. Intravenous barbiturates, anticonvulsant agents, or muscle
relaxants should only be administered by those familiar with their use. Immediately
after the institution of these ventilatory measures, the adequacy of the circulation
should be evaluated. Supportive treatment of circulatory depression may require
administration of intravenous fluids, and when appropriate, a vasopressor
dictated by the clinical situation (such as ephedrine or epinephrine to enhance
myocardial contractile force). Endotracheal intubation,
employing drugs and techniques familiar to the clinician may be indicated
after initial administration of oxygen by mask, if difficulty is encountered
in the maintenance of a patent airway or if prolonged ventilatory support
(assisted or controlled) is indicated. Recent clinical
data from patients experiencing local anesthetic induced convulsions demonstrated
rapid development of hypoxia, hypercarbia, and acidosis within a minute of
the onset of convulsions. These observations suggest that oxygen consumption
and carbon dioxide production are greatly increased during local anesthetic
convulsionsand emphasize the importance of immediate and effective ventilation
with oxygen which may avoid cardiac arrest. If not treated
immediately, convulsions with simultaneous hypoxia, hypercarbia, and acidosis,
plus myocardial depression from the direct effects of the local anesthetic
may result in cardiac arrhythmias, bradycardia, asystole, ventricular fibrillation,
or cardiac arrest. Respiratory abnormalities, including apnea, may occur.
Underventilation or apnea due to unintentional subarachnoid injection of local
anesthetic solution may produce these same signs and also lead to cardiac
arrest if ventilatory support is not instituted. If cardiac arrest should
occur, standard cardiopulmonary resuscitative measures should be instituted
and maintained for a prolonged period if necessary. Recovery has been reported
after prolonged resuscitative efforts. The supine position
is dangerous in pregnant women at term because of aortocaval compression by
the gravid uterus. Therefore during treatment of systemic toxicity, maternal
hypotension, or fetal bradycardia following regional block, the parturient
should be maintained in the left lateral decubitus position if possible, or
manual displacement of the uterus off the great vessels be accomplished. The
mean seizure dosage of mepivacaine in rhesus monkeys was found to be 18.8
mg/kg with mean arterial plasma concentration of 24.4 mcg/mL. The intravenous
and subcutaneous LDin mice is 23 mg/kg to 35 mg/kg and 280 mg/kg
respectively.
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Mepivacaine Hydrochloride
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Carbocaine (Injection, Solution)
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Reactions to CARBOCAINE are characteristic of those associated
with other amide-type local anesthetics. A major cause of adverse reactions
to this group of drugs is excessive plasma levels, which may be due to overdosage,
inadvertent intravascular injection, or slow metabolic degradation. Systemic The most
commonly encountered acute adverse experiences which demand immediate counter-measures
are related to the central nervous system and the cardiovascular system. These
adverse experiences are generally dose related and due to high plasma levels
which may result from overdosage, rapid absorption from the injection site,
diminished tolerance, or from unintentional intravascular injection of the
local anesthetic solution. In addition to systemic dose-related toxicity,
unintentional subarachnoid injection of drug during the intended performance
of caudal or lumbar epidural block or nerve blocks near the vertebral column
(especially in the head and neck region) may result in underventilation or
apnea (���Total or High Spinal���). Also, hypotension due to loss
of sympathetic tone and respiratory paralysis or underventilation due to cephalad
extension of the motor level of anesthesia may occur. This may lead to secondary
cardiac arrest if untreated. Factors influencing plasma protein binding, such
as acidosis, systemic diseases which alter protein production, or competition
of other drugs for protein binding sites, may diminish individual tolerance. Central Nervous System Reactions These
are characterized by excitation and/or depression. Restlessness, anxiety,
dizziness, tinnitus, blurred vision, or tremors may occur, possibly proceeding
to convulsions. However, excitement may be transient or absent, with depression
being the first manifestation of an adverse reaction. This may quickly be
followed by drowsiness merging into unconsciousness and respiratory arrest.
Other central nervous system effects may be nausea, vomiting, chills, and
constriction of the pupils. The incidence of convulsions
associated with the use of local anesthetics varies with the procedure used
and the total dose administered. In a survey of studies of epidural anesthesia,
overt toxicity progressing to convulsions occurred in approximately 0.1% of
local anesthetic administrations. Cardiovascular
Reactions High doses or, inadvertent intravascular
injection, may lead to high plasma levels and related depression of the myocardium,
decreased cardiac output, heart block, hypotension (or sometimes hypertension),
bradycardia, ventricular arrhythmias, and possibly cardiac arrest. (See WARNINGS,
PRECAUTIONS, and OVERDOSAGE sections.) Allergic Allergic-type reactions are rare and may
occur as a result of sensitivity to the local anesthetic or to other formulation
ingredients, such as the antimicrobial preservative methylparaben, contained
in multiple-dose vials. These reactions are characterized by signs such as
urticaria, pruritus, erythema, angioneurotic edema (including laryngeal edema),
tachycardia, sneezing, nausea, vomiting, dizziness, syncope, excessive sweating,
elevated temperature, and possibly, anaphylactoid-like symptomatology (including
severe hypotension). Cross sensitivity among members of the amide-type local
anesthetic group has been reported. The usefulness of screening for sensitivity
has not been definitely established. Neurologic The incidences of adverse neurologic reactions
associated with the use of local anesthetics may be related to the total dose
of local anesthetic administered and are also dependent upon the particular
drug used, the route of administration, and the physical status of the patient.
Many of these effects may be related to local anesthetic techniques, with
or without a contribution from the drug. In the practice
of caudal or lumbar epidural block, occasional unintentional penetration of
the subarachnoid space by the catheter or needle may occur. Subsequent adverse
effects may depend partially on the amount of drug administered intrathecally
and the physiological and physical effects of a dural puncture. A high spinal
is characterized by paralysis of the legs, loss of consciousness, respiratory
paralysis, and bradycardia. Neurologic effects following
epidural or caudal anesthesia may include spinal block of varying magnitude
(including high or total 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; cranial nerve palsies
due to traction on nerves from loss of cerebrospinal fluid. Neurologic
effects following other procedures or routes of administration may include
persistent anesthesia, paresthesia, weakness, paralysis, all of which may
have slow, incomplete, or no recovery.
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LOCAL ANESTHETICS SHOULD ONLY BE
EMPLOYED BY CLINICIANS WHO ARE WELL VERSED IN DIAGNOSIS AND MANAGEMENT OF
DOSE-RELATED TOXICITY AND OTHER ACUTE EMERGENCIES WHICH MIGHT ARISE FROM THE
BLOCK TO BE EMPLOYED, AND THEN ONLY AFTER INSURING THE IMMEDIATE AVAILABILITY
OF OXYGEN, OTHER RESUSCITATIVE DRUGS, CARDIOPULMONARY RESUSCITATIVE EQUIPMENT,
AND THE PERSONNEL RESOURCES NEEDED FOR PROPER MANAGEMENT OF TOXIC REACTIONS
AND RELATED EMERGENCIES. (See also ADVERSE REACTIONS 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. Local anesthetic
solutions containing antimicrobial preservatives (i.e., those supplied in
multiple-dose vials) should not be used for epidural or caudal anesthesia
because safety has not been established
with regard to intrathecal injection, either intentionally or inadvertently,
of such preservatives. It is essential that aspiration
for blood or cerebrospinal fluid (where applicable) be done prior to injecting
any local anesthetic, both the original dose and all subsequent doses, to
avoid intravascular or subarachnoid injection. However, a negative aspiration
does not ensure against an intravascular or subarachnoid injection. Reactions
resulting in fatality have occurred on rare occasions with the use of local
anesthetics. CARBOCAINE with epinephrine or other vasopressors
should not be used concomitantly with ergot-type oxytocic drugs, because a
severe persistent hypertension may occur. Likewise, solutions of CARBOCAINE
containing a vasoconstrictor, such as epinephrine, should be used with extreme
caution in patients receiving monoamine oxidase inhibitors (MAOI) or antidepressants
of the triptyline or imipramine types, because severe prolonged hypertension
mayresult. Local anesthetic procedures should be used
with caution when there is inflammation and/or sepsis in the region of the
proposed injection. Mixing or the prior or intercurrent
use of any local anesthetic with CARBOCAINE cannot be recommended because
of insufficient data on the clinical use of such mixtures.
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CARBOCAINE is indicated for production of local or regional
analgesia and anesthesia by local infiltration, peripheral nerve block techniques,
and central neural techniques including epidural and caudal blocks. The
routes of administration and indicated concentrations for CARBOCAINE are: See DOSAGE AND ADMINISTRATION for additional information.
Standard textbooks should be consulted to determine the accepted procedures
and techniques for the administration of CARBOCAINE.
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| dailymed-instance:name |
Carbocaine
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