Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/4001
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Chloroprocaine Hydrochloride (Injection, Solution)
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Chloroprocaine may be administered as a single injection
or continuously through an indwelling catheter. As with all local anesthetics,
the dose administered varies with the anesthetic procedure, the vascularity
of the tissues, the depth of anesthesia and degree of muscle relaxation required,
the duration of anesthesia desired, and the physical condition of the patient.
The smallest dose and concentration required to produce the desired result
should be used. Dosage should be reduced for children, elderly and debilitated
patients and patients with cardiac and/or liver disease. The maximum single
recommended doses of chloroprocaine in adults are: without epinephrine, 11 mg/kg,
not to exceed a maximum total dose of 800 mg; with epinephrine (1:200,000),
14 mg/kg, not to exceed a maximum total dose of 1000 mg. For specific techniques
and procedures, refer to standard textbooks. Caudal and Lumbar Epidural Block: In
order to guard against adverse experiences sometimes noted following unintended
penetration of the subarachnoid space, the following procedure modifications
are recommended: 1. Use an adequate test dose (3 mL of 3% or 5 mL of 2% Chloroprocaine
Hydrochloride Injection) prior to induction of complete block. This test dose
should be repeated if the patient is moved in such a fashion as to have displaced
the epidural catheter. Allow adequate time for onset of anesthesia following
administration of each test dose. 2. Avoid the rapid injection of a large
volume of local anesthetic injection through the catheter. Consider fractional
doses, when feasible. 3. In the event of the known injection of a large volume
of local anesthetic injection 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. As a guide for some routine
procedures, suggested doses are given below: 1.
Infiltration and Peripheral Nerve Block: Chloroprocaine Hydrochloride Injection 2. Caudal and Lumbar Epidural Block: For caudal anesthesia,
the initial dose is 15 to 25 mL of a 2% or 3% solution. Repeated doses
may be given at 40 to 60 minute intervals. For lumbar
epidural anesthesia, 2 to 2.5 mL per segment of a 2% or 3% solution can be
used. The usual total volume of Chloroprocaine Hydrochloride Injection is
from 15 to 25 mL. Repeated doses 2 to 6 mL less than the original dose may
be given at 40 to 50 minute intervals. The above dosages
are recommended as a guide for use in the average adult. Maximum dosages of
all local anesthetics must be individualized after evaluating the size and
physical condition of the patient and the rate of systemic absorption from
a particular injection site. Pediatric
Dosage: It is difficult to recommend a maximum
dose of any drug for children, since this varies as a function of age and
weight. For children over 3 years of age who have a normal lean body mass
and normal body development, the maximum dose is determined by the child's
age and weight and should not exceed 11 mg/kg (5 mg/lb). For example, in a
child of 5 years weighing 50 lbs (23 kg), the dose of chloroprocaine HCl without
epinephrine would be 250 mg. Concentrations of 0.5���1% are suggested
for infiltration and 1���1.5% for nerve block. In order to guard against
systemic toxicity, the lowest effective concentration and lowest effective
dose should be used at all times. Some of the lower concentrations for use
in infants and smaller children are not available in pre-packaged containers;
it will be necessary to dilute available concentrations with the amount of
0.9% sodium chloride injection necessary to obtain the required final concentration
of chloroprocaine injection. Preparation
of Epinephrine Injections: To prepare a 1:200,000
epinephrine-chloroprocaine HCl injection, add 0.15 mL of 1 to 1000 Epinephrine
Injection to 30 mL of Chloroprocaine Hydrochloride Injection. Chloroprocaine
is incompatible with caustic alkalis and their carbonates, soaps, silver salts,
iodine and iodides. Parenteral drug products should
be inspected visually for particulate matter and discoloration prior to administration,
whenever injection and container permit. As with other anesthetics having
a free aromatic amino group, Chloroprocaine Hydrochloride Injection is slightly
photosensitive and may become discolored after prolonged exposure to light.
It is recommended that this product be stored in the original outer containers,
protected from direct sunlight. Discolored injection should not be administered.
If exposed to low temperatures, Chloroprocaine Hydrochloride Injection may
deposit crystals of chloroprocaine HCl which will redissolve with shaking
when returned to room temperature. The product should not be used if it contains
undissolved (e.g., particulate) material.
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Chloroprocaine Hydrochloride Injection, USP is a sterile,
nonpyrogenic, isotonic, isobaric solution. Each milliliter of 2% solution
contains 20 mg of chloroprocaine hydrochloride; 4 mg sodium chloride; with
1.8 mg sodium metabisulfite added in water for injection. Each milliliter
of 3% solution contains 30 mg of chloroprocaine hydrochloride; 2.1 mg sodium
chloride; with 1.8 mg sodium metabisulfite added in water for injection. May
contain hydrochloric acid and/or sodium hydroxide for pH adjustment. It contains
no bacteriostat, antimicrobial agent or added buffer. Discard unused portion. It
is intended for production of local anesthesia by nerve block, infiltration,
caudal or other epidural blocks. Chloroprocaine Hydrochloride
Injection has a pH of 3.1 (2.7 to 4.0). Sodium Chloride,
USP is chemically designated NaCl, a white crystalline compound freely soluble
in water. Chloroprocaine Hydrochloride Injection is
identified chemically as 2-(diethylamino) ethyl 4-amino-2 chlorobenzoate monohydrochloride.
Its molecular Formula is: CHClNO���HCl
and the molecular weight is 307.22. It has the following structural formula:
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Chloroprocaine, like other local anesthetics, blocks 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: (1) pain, (2) temperature, (3)
touch, (4) proprioception, and (5) 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, with toxic blood concentrations
myocardial contractilitymay be depressed and peripheral vasodilation may
occur, leading to decreased cardiac output and arterial blood pressure. Following
systemic absorption, toxic blood concentrations of local anesthetics can produce
central nervous system stimulation, depression, or both. Apparent central
stimulation may be manifested as restlessness, tremors and shivering, which
may progress to convulsions. Depression and coma may occur, possibly 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 without a prior stage of central nervous
system stimulation. Pharmacokinetics The rate of systemic absorption of local
anesthetic drugs 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 injection.
Epinephrine usually reduces the rate of absorption and plasma concentration
of local anesthetics and is sometimes added to local anesthetic injections
in order to prolong the duration of action. The onset
of action with chloroprocaine is rapid (usually within 6 to 12 minutes), and
the duration of anesthesia, depending upon the amount used and the route of
administration, may be up to 60 minutes. Local anesthetics
appear to cross the placenta by passive diffusion. However, the rate and degree
of diffusion varies considerably among the different drugs as governed by:
(1) the degree of plasma protein binding, (2) the degree of ionization, and
(3) the degree of lipid solubility. Fetal/maternal ratios of local anesthetics
appear to be inversely related to the degree of plasma protein binding, since
only the free, unbound drug is available for placental transfer. Thus, drugs
with the highest protein binding capacity may have the lowest fetal/maternal
ratios. 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 administration, and the
age of the patient. The in vitro plasma
half-life of chloroprocaine in adults is 21��2 seconds for males and
25��1 seconds for females. The in vitro plasma half-life in neonates is 43��2 seconds. Chloroprocaine
is rapidly metabolized in plasma by hydrolysis of the ester linkage by pseudocholinesterase.
The hydrolysis of chloroprocaine results in the production of��-diethyl-aminoethanol
and 2-chloro-4-aminobenzoic acid, which inhibits the action of the sulfonamides
(see PRECAUTIONS). The kidney is the main excretory
organ for most local anesthetics and their metabolites. Urinary excretion
is affected by urinary perfusion and factors affecting urinary pH.
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Chloroprocaine Hydrochloride Injection is contraindicated
in patients hypersensitive (allergic) to drugs of the PABA ester group. 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.
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Chloroprocaine Hydrochloride Injection, USP is supplied in
single-dose containers as follows: Store at 20 to 25��C (68 to 77��F). [See USP Controlled
Room Temperature.] HOSPIRA, INC., LAKE FOREST,
IL 60045 USA
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General:: The safety and effective use of chloroprocaine 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). 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.
Syringe aspirations should also be performed before and during each supplemental
injection in continuous (intermittent) catheter techniques. During the administration
of epidural anesthesia, it is recommended that a test dose be administered
(3 mL of 3% or 5 mL of 2% Chloroprocaine Hydrochloride Injection) initially
and that the patient be monitored for central nervous system toxicity and
cardiovascular toxicity, as well as for signs of unintended intrathecal administration,
before proceeding. When clinical conditions permit, consideration should be
given to employing a chloroprocaine solution that contains epinephrine for
the test dose because circulatory changes characteristic of 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. With
the use of continuous catheter techniques, it is recommended that a fraction
of each supplemental dose be administered as a test dose in order to verify
proper location of the catheter. 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.
Tolerance to elevated blood levels varies with the physical condition of the
patient. Debilitated, elderly patients, acutely ill patients, and children
should be given reduced doses commensurate with their age and physical status.
Local anesthetics should also be used with caution in patients with hypotension
or heart block. Careful and constant monitoring of cardiovascular
and respiratory (adequacy of ventilation) vital signs and the patient's
state of consciousness should be accomplished after each local anesthetic
injection. It should be kept in mind at such times that restlessness, anxiety,
tinnitus, dizziness, blurred vision, tremors, depression or drowsiness may
be early warning signs of central nervous system toxicity. Local
anesthetic injections containing a vasoconstrictor should be used cautiously
and in carefully circumscribed quantities in areas of the body supplied by
end arteries or having otherwise compromised blood supply. Patients with peripheral
vascular disease and those with hypertensive vascular disease may exhibit
exaggerated vasoconstrictor response. Ischemic injury or necrosis may result. Since
ester-type local anesthetics are hydrolyzed by plasma cholinesterase produced
by the liver, chloroprocaine should be used cautiously in patients with hepatic
disease. Local anesthetics 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 A-V conduction produced by these drugs. Use in Ophthalmic Surgery: When
local anesthetic injections are employed for retrobulbar block, lack of corneal
sensation should not be relied upon to determine whether or not the patient
is ready for surgery. This is because complete lack of corneal sensation usually
precedes clinically acceptable external ocular muscle akinesia.<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 epidural
anesthesia.<br/>Clinically Significant Drug Interactions:: The administration of local anesthetic solutions containing
epinephrine or norepinephrine to patients receiving monoamine oxidase inhibitors,
tricyclic antidepressants or phenothiazines may produce severe prolonged hypotension
or 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 (for the treatment of hypotension related to obstetric blocks) and ergot-type
oxytocic drugs may cause severe, persistent hypertension or cerebrovascular
accidents. The para-aminobenzoic acid metabolite of
chloroprocaine inhibits the action of sulfonamides. Therefore, chloroprocaine
should not be used in any condition in which a sulfonamide drug is being employed.<br/>Carcinogenesis, Mutagenesis, and Impairment of Fertility:: Long-term studies in animals to evaluate carcinogenic potential
and reproduction studies to evaluate mutagenesis or impairment of fertility
have not been conducted with chloroprocaine.<br/>Pregnancy Category C:: Animal reproduction studies have not been conducted with
chloroprocaine. It is also not known whether chloroprocaine can cause fetal
harm when administered to a pregnant woman or can affect reproduction capacity.
Chloroprocaine should be given to a pregnant woman only if clearly needed.
This does not preclude the use of chloroprocaine at term for the production
of obstetrical anesthesia.<br/>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. (See
CLINICAL PHARMACOLOGY���Pharmacokinetics). 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, 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, epidural anesthesia
has 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. 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. 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 injection 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 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. There are no data concerning
use of chloroprocaine for obstetrical paracervical block when toxemia of pregnancy
is present or when fetal distress or prematurity is anticipated in advance
of the block; such use is, therefore, not recommended. The following information
should be considered by clinicians who select chloroprocaine for obstetrical
paracervical block anesthesia: 1) Fetal bradycardia (generally a heart
rate of less than 120 per minute for more than 2 minutes) has been noted by
electronic monitoring in about 5 to 10 percent of the cases (various
studies) where initial total doses of 120 mg to 400 mg of chloroprocaine were
employed. The incidence of bradycardia, within this dose range, might not
be dose related. 2) Fetal acidosis has not been demonstrated by blood gas
monitoring around the time of bradycardia or afterwards. These data are limited
and generally restricted to nontoxemic cases where fetal distress or prematurity
was not anticipated in advanceof the block. 3) No intact chloroprocaine and
only trace quantities of a hydrolysis product, 2-chloro-4-aminobenzoic acid,
have been demonstrated in umbilical cord arterial or venous plasma following
properly administered paracervical block with chloroprocaine. 4) The role
of drug factors and non-drug factors associated with fetal bradycardia following
paracervical block are unexplained at this time.<br/>Nursing Mothers:: It is not known whether this drug is excreted in human milk.
Because many drugs are excreted in human milk, caution should be exercised
when chloroprocaine is administered to a nursing woman.<br/>Pediatric Use:: Guidelines for the administration of Chloroprocaine Hydrochloride
Injection to children are presented in DOSAGE AND ADMINISTRATION.<br/>Geriatric Use:: Clinical studies of Chloroprocaine Hydrochloride Injection
did not include sufficient number of subjects 65 and over to determine whether
they respond differently from younger subjects. Other reported clinical experience
has not identified differences in responses between the elderly and younger
patients. In general, dose selection for an elderly patient should be cautious
usually starting at the low end of the dosing range, reflecting the greater
frequency of decreased hepatic, renal, or cardiac function, and of concomitant
disease or other drug therapy. This drug and its
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). In mice,
the intravenous LDof chloroprocaine HCl is 97 mg/kg and the
subcutaneous LDof chloroprocaine HCl is 950 mg/kg. 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 convulsions, as well as underventilation or apnea
due to unintentional subarachnoid injection of drug solution, consists of
immediate attention to the 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. Immediately after the institution
of these ventilatory measures, the adequacy of the circulation should be evaluated,
keeping in mind that drugs used to treat convulsions sometimes depress the
circulation when administered intravenously. Should convulsions persist despite
adequate respiratory support, and if the status of the circulation permits,
small increments of an ultra-short acting barbiturate (such as thiopental
or thiamylal) or a benzodiazepine (such as diazepam) may be administered intravenously;
the clinician should be familiar, prior to the use of local anesthetics, with
these anticonvulsant drugs. Supportive treatment of circulatory depression
may require administration of intravenous fluids and, when appropriate, a
vasopressor dictated by the clinical situation (such as ephedrine to enhance
myocardial contractile force). If not treated immediately,
both convulsions and cardiovascular depression can result in hypoxia, acidosis,
bradycardia, arrhythmias and cardiac arrest. 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. Recovery has been reported after prolonged
resuscitative efforts. 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.
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Chloroprocaine Hydrochloride
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Chloroprocaine Hydrochloride (Injection, Solution)
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Systemic: The
most commonly encountered acute adverse experiences that demand immediate
countermeasures are related to the central nervous system and the cardiovascular
system. These adverse experiences are generally dose-related and may result
from 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 subarachnoidinjection
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 Spinal���).
Factors influencing plasma protein binding, such as acidosis, systemic diseases
that alter protein production, or competition of other drugs for protein binding
sites, may diminish individual tolerance. Plasma cholinesterase deficiency
may also account for diminished tolerance to ester-type local anesthetics. 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. 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 percent of local anesthetic administrations. Cardiovascular System Reactions: High
doses, or unintended intravascular injection, may lead to high plasma levels
and related depression of the myocardium, hypotension, bradycardia, ventricular
arrhythmias and, possibly, cardiac arrest. Allergic: Allergic-type reactions
are rare and may occur as a result of sensitivity to the local anesthetic.
These reactions are characterized by signs such as urticaria, pruritis, erythema,
angioneurotic edema (including laryngeal edema), tachycardia, sneezing, nausea,
vomiting, dizziness, syncope, excessive sweating, elevated temperature, and
possibly, anaphylactoid-type symptomatology (including severe hypotension).
Cross sensitivity among members of the ester-type local anesthetic group has
been reported. The usefulness of screening for sensitivity has not been definitely
established. Neurologic: In
the practice of caudal or lumbar epidural block, occasional unintentional
penetration of the subarachnoid space by the catheter may occur (see PRECAUTIONS).
Subsequent adverse observations may depend partially on the amount of drug
administered intrathecally. These observations may include spinal block of
varying magnitude (including total spinal block), hypotension secondary to
spinal block, loss of bladder and bowel control, and loss of perineal sensation
and sexual function. Arachnoiditis, persistent motor, sensory and/or autonomic
(sphincter control) deficit of some lower spinal segments with slow recovery
(several months) or incomplete recovery have been reported in rare instances.
(See DOSAGE AND ADMINISTRATION discussion of Caudal andLumbar Epidural Block).
Backache and headache have also been noted following lumbar epidural or caudal
block.
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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 ENSURING 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. Chloroprocaine Hydrochloride
Injection, contains no preservative; discard unused injection remaining in
vial after initial use. Vasopressors should not be used
in the presence of ergot-type oxytocic drugs, since a severe persistent hypertension
may occur. To avoid intravascular injection, aspiration
should be performed before the anesthetic solution is injected. The needle
must be repositioned until no blood return can be elicited. However, the absence
of blood in the syringe does not guarantee that intravascular injection has
been avoided. Mixtures of local anesthetics are sometimes
employed to compensate for the slower onset of one drug and the shorter duration
of action of the second drug. Experiments in primates suggest that toxicity
is probably additive when mixtures of local anesthetics are employed, but
some experiments in rodents suggest synergism. Caution regarding toxic equivalence
should be exercised when mixtures of local anesthetics are employed. Chloroprocaine
Hydrochloride Injection contains sodium metabisulfite, a sulfite that may
cause allergic-type reactions including anaphylactic symptoms and life-threatening
or less severe asthmatic episodes in certain susceptible people. The overall
prevalence of sulfite sensitivity in the general population is unknown and
probably low. Sulfite sensitivity is seen more frequently in asthmatic than
in nonasthmatic people.
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Chloroprocaine Hydrochloride Injection in single-dose containers
without preservative and without EDTA, is indicated for the production oflocal anesthesia by infiltration, peripheral and central nerve block, including
lumbar and caudal epidural blocks. Chloroprocaine Hydrochloride
Injection is not to be used for subarachnoid administration.
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Chloroprocaine Hydrochloride
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