Sensorcaine

SENSORCAINE- bupivacaine hydrochloride injection, solution
Henry Schein, Inc.

DESCRIPTION

Sensorcaine® (bupivacaine HCl) injections are sterile isotonic solutions that contain a local anesthetic agent with and without

epinephrine (as bitartrate) 1:200,000 and are administered parenterally by injection. See INDICATIONS AND USAGE for specific
uses. Solutions of bupivacaine HCl may be autoclaved if they do not contain epinephrine.

Sensorcaine injections contain bupivacaine HCl which is chemically designated as 2-piperidinecarboxamide, 1-butyl-N-(2, 6-dimethylphenyl)-, monohydrochloride, monohydrate and has the following structure:

Formula1
(click image for full-size original)

Epinephrine is (-)-3, 4-Dihydroxy-a [(methylamino)methyl] benzyl alcohol. It has the following structural formula:

Formula2
(click image for full-size original)

The pKa of bupivacaine (8.1) is similar to that of lidocaine (7.86). However, bupivacaine possesses a greater degree of lipid solubility

and is protein bound to a greater extent than lidocaine.
Bupivacaine is related chemically and pharmacologically to the aminoacyl local anesthetics. It is a homologue of mepivacaine and is
chemically related to lidocaine. All three of these anesthetics contain an amide linkage between the aromatic nucleus and the amino or
piperidine group. They differ in this respect from the procaine-type local anesthetics, which have an ester linkage.

Dosage forms listed as Sensorcaine-MPF indicates single dose solutions that are Methyl Paraben Free (MPF).

Sensorcaine-MPF is a sterile isotonic solution containing sodium chloride. Sensorcaine in multiple dose vials, each mL also contains
1 mg methylparaben as antiseptic preservative. The pH of these solutions is adjusted to between 4.0 and 6.5 with sodium hydroxide
and/or hydrochloric acid.

Sensorcaine-MPF with Epinephrine 1:200,000 (as bitartrate) is a sterile isotonic solution containing sodium chloride. Each mL
contains bupivacaine hydrochloride and 0.005 mg epinephrine, with 0.5 mg sodium metabisulfite as an antioxidant and 0.2 mg citric
acid (anhydrous) as stabilizer. Sensorcaine with Epinephrine 1:200,000 (as bitartrate) in multiple dose vials, each mL also contains 1
mg methylparaben as antiseptic preservative. The pH of these solutions is adjusted to between 3.3 to 5.5 with sodium hydroxide and/
or hydrochloric acid. Filled under nitrogen.

Note: The user should have an appreciation and awareness of the formulations and their intended uses (see DOSAGE AND
ADMINISTRATION).

CLINICAL PHARMACOLOGY

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: (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 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, ventricular arrhythmias and cardiac arrest, sometimes resulting in fatalities. In addition, myocardial
contractility is depressed and peripheral vasodilation occurs, leading to decreased cardiac output and arterial blood pressure. Recent

clinical reports and animal research suggest that these cardiovascular changes are more likely to occur after unintended intravascular
injection of bupivacaine. Therefore, incremental dosing is necessary.
Following systemic absorption, local anesthetics can produce central nervous system stimulation, depression or both. Apparent
central stimulation is usually 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 without a prior excited stage.
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 peak plasma concentration of
bupivacaine, permitting the use of moderately larger total doses and sometimes prolonging the duration of action.
The onset of action with bupivacaine is rapid and anesthesia is long-lasting. The duration of anesthesia is significantly longer with
bupivacaine than with any other commonly used local anesthetic. It has also been noted that there is a period of analgesia that persists
after the return of sensation, during which time the need for potent analgesics is reduced.
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 proteins.
Local anesthetics appear to cross the placenta by passive diffusion. The rate and degree of diffusion is 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, because only the free, unbound drug is available for placental
transfer. Bupivacaine, with a high protein binding capacity (95%), has a low fetal/maternal ratio (0.2 to 0.4). 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.
Pharmacokinetic studies on the plasma profile of bupivacaine after direct intravenous injection suggest a three-compartment open
model. The first compartment is represented by the rapid intravascular distribution of the drug. The second compartment represents
the equilibration of the drug throughout the highly perfused organs such as the brain, myocardium, lungs, kidneys, and liver. The third
compartment represents an equilibration of the drug with poorly perfused tissues, such as muscle and fat. The elimination of drug
from tissue depends largely upon the ability of binding sites in the circulation to carry it to the liver where it is metabolized.
After injection of Sensorcaine (bupivacaine HCl) for caudal, epidural or peripheral nerve block in man, peak levels of bupivacaine in
the blood are reached in 30 to 45 minutes, followed by a decline to insignificant levels during the next 3 to 6 hours.
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 bupivacaine in adults is 2.7 hours and in neonates 8.1 hours.
In clinical studies, elderly patients reached the maximal spread of analgesia and maximal motor blockade more rapidly than younger
patients. Elderly patients also exhibited higher peak plasma concentrations following administration of this product. The total plasma
clearance was decreased in these patients.
Amide-type local anesthetics such as bupivacaine are metabolized primarily in the liver via conjugation with glucuronic acid.
Patients with hepatic disease, especially those with severe hepatic disease, may be more susceptible to the potential toxicities of the
amide-type local anesthetics. Pipecoloxylidine is the major metabolite of bupivacaine.
The kidney is the main excretory organ for most local anesthetics and their metabolites. Urinary excretion is affected by renal
perfusion and factors affecting urinary pH. Only 6% of bupivacaine is excreted unchanged in the urine.
When administered in recommended doses and concentrations, Sensorcaine (bupivacaine HCl) does not ordinarily produce irritation
or tissue damage and does not cause methemoglobinemia.

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