ABOCAIN SPINAL (Bupivacaine HCl)

   ABOCAIN SPINAL (Bupivacaine HCl)

ABOCAIN SPINAL  (Bupivacaine HCl)

ABOCAIN SPINAL  (Bupivacaine HCl)

DESCRIPTION

ABOCAIN SPINAL is Abbott's brand name for Bupivacaine Spinal (Bupivacaine in Dextrose injection. USP) 

available m sterile, hyperbaric solution tor subarachnoid injection (spinal block). Each 1ml. of Bupivacaine Spinal contains 7.5 mg bupivacaine hydrochloride. anhydrous and 82 5mg dextrose, anhydrous. The pH of this 

solution is adjusted to 5.5 (4.0 to 65) with sodium hydroxide and/or hydrochloric acid The specific gravity of Bupivacaine Spinal is between 1.030 and 1.035 at 25°C and 1 03 at 37°C. Bupivacaine hydrochloride is 1 -Butyl 2' 6' Pipecotoxylidide monochloride. monohydrate. a white crystalline 

powder that is freely soluble in chloroform or acetone. It has following structural formula:

Dextrose is D-glucopyranose monohydrate and has the following structural formula.

CLINICAL PHARMACOLOGYC

Local anaesthetics 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 anaesthesia 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 anaesthetics produce effects on the cardiovascular and central nervous system (CNS). At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, 

excitability, refractoriness, contractility, and peripheral vascular resistance are minimal.

PHARMACOKINETICS

The rate of systemic absorption of local anaesthetics 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 anaesthetic solution. A dilute concentration of epinephrine (1 : 200,000 or 5 µ/g/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 actionThe onset of action with bupivacaine is rapid and anaesthesia is long lasting. The duration of anaesthesia is significantly longer with bupivacaine than with any other commonly used local anaesthetic. 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 strong analgesics is reduced.

The onset of sensory blockade following spinal block with Bupivacaine Spinal (bupivacaine in dextrose injection) is very rapid (Within one minute), maximum motor blockade and maximumdermatome level are achieved within 15 minutes in most cases. Duration of sensory blockage (time to return of complete sensation 

in the operative site or regression of two dermatomes) following a 12mg dose averages 2 hour with or without 

0.2mg epinephrine. The time to return of complete motor ability with 12mg Bupivacaine Spinal (bupivacaine 

in dextrose injection) averages 3 1/2 hours without the addition of epinephrine and 4 1/2 hours if 0.2 mg epinephrine is added. When compared to equal milligram doses of hyperbaric tetracaine, the duration of 

sensory blockade was the same but time to complete motor recovery was significantly longer for tetracaine.

Local anaesthetics appear to cross the placenta by passive diffusion. The rate and degree of diffusion is governed by (1) degree of plasma protein binding, (2) degree of ionization, and (3) the degree of lipid solubility. 

Fetal / maternal ratios of focal anaesthetics appear to be inversely related to the degree of plasma protein 

binding, because only the free, unbound drug is available for placenta! transfer. Bupivacaine has a high protein 

binding capacity (95%) and a low fetal/maternal ratio (0.2 to 0.4).

Depending upon the route of administration, focal anaesthetics 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 profiles 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 tissue, such as muscle and fat. The elimination of drug from 

tissue distribution depends largely upon the ability of binding sites in the circulation to carry it to the liver 

where it is metabolized.

Various pharmacokinetic parameters of the local anaesthetics 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 3.5+2 hours and in neonates 81 hours.

Amide type local anaesthetics such as bupivacaine are metabolized primarily in the liver via conjugation with 

glucronic acid. Patients with hepatic disease, especially those with severe hepatic disease, may be more 

susceptible to the potential toxicities of the amide-type focal anaesthetics. Pipecotoxylidine is the major 

metabolite of bupivacaine.

The kidney is the main excretory organ for most local anaesthetic and their metabolites. Urinary excretion is 

affected by renal perfusion and factors affecting urinary pH. Only 5% of bupivacaine is excreted unchanged in 

the urine.

When administered in recommended doses and concentrations, bupivacaine does not ordinarily, produces 

irritation or tissue damage and dose not cause methemogiobinemia.

ABOCAIN SPINAL  (Bupivacaine HCl)

INDICATION AND USAGE

Abocain Spinal is indicated for the production of subarachnoid block (spinal anaesthesia) 

CONTRAINDICATIONS

Abocain Spinal (Bupivacaine in Dextrose Injection) is contraindicated in patients with a known hyper-

sensitivity to it or to any local anaesthetic agent of the amide-type.

The following conditions preclude the use of spinal anaesthesia:

1. Severe haemorrhage, severe hypotension or shock and arrhythmias, such as complete heart block, which 

severely restrict cardiac output.

2. Local infection at the site of proposed lumbar puncture.

3. Septicaemia

WARNINGS

LOCAL ANAESTHETICS SHOULD ONLY BE EMPLOYED BY CLINICIANS WHO AREWELL VERSED IN DIAGNOSIS AND MANAGEMENT OF DOSE-RELATEDTOXICITY AND OTHER 

ACUTE EMERGENCIES WHICH MIGHT ARISE FROM THE BLOCK TO BEEMPLOYED, 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, PRECAUTIONS, and

OVERDOSAGE). 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.

Spinal anaesthetics should not be injected during uterine contractions, because spinal fluid current may carry 

the drug further cephalad then desired.

A free flow of cerebrospinal fluid during the performance of spinal anaesthesia is indicative of entry into the subarachnoid space. However, aspiration should be performed before the anaesthetic solution is injected to confirm entry into the subarachnoid space and to avoid intravascular injection.

Bupivacaine solutions containing epinephrine or other vasopressors should, not be used concomitantly with 

ergot-type oxytocic drugs, because a severe persistent hypertension may occur. Likewise, solutions of bupivacaine containing a vasoconstrictor, such as epinephrine, should be used with extreme caution in patients receiving monoamine oxidase inhibitors (MAOI) or antidepressant of the triptyline or pramine types, because severe prolonged hypertension may result.

Mixing or the prior or intercurrent use of any other local anaesthetic with bupivacaine cannot be recom-

mended because of insufficient data on the clinical use of such mixtures

PRECAUTIONS

General: The safety and effectiveness of spinal anaesthetic depend on proper dosage, correct technique, 

adequate precautions and readiness for emergencies. Resuscitative equipment, oxygen and other resucitative 

drugs should be available for immediate use. (See WARNINGS, ADVERSEREACTIONS and 

OVERDOSAGE.) The patient should have I.V. fluids running via an indwelling catheter to assure a 

functioning intravenous pathway. The lowest dosage of local anaesthetic that results in effective anaesthesia 

should be used. Aspiration for blood should be performed before injection and should be made slowly. 

Tolerance varies with the status of the patients. Debilitated, elderly patients and acutely ill patients may 

require reduced doses. Reduced doses may also be indicated in patients with increased intra-abdominal 

pressure (including obstetrical patients), if otherwise suitable for spinal anaesthesia.

There should be careful and constant monitoring of cardiovascular and respiratory (adequacy of ventilation) 

vital signs and the patient's state of consciousness after local anaesthetic injection. Restless- ness, anxiety, 

incoherent speech, light-headedness. numbness and tingling of the mouth and lips, metallic taste, tinnitus, 

dizziness, blurred vision, tremors, depression or drowsiness may be early warn-ing sign of central nervous 

system toxicity.

Spinal anaesthetics should be used with caution in patients with severe disturbances of cardiac rhythm, shock, 

or heart block.

Sympathetic blockade occurring during spinal anaesthesia may result in peripheral vasodilation and 

hypotension, the extent depending on the number of dermatomes blocked. Blood pressure should, therefore, 

be carefully monitored especially in the early phases of anaesthesia. Hypotension may be controlled by 

vasoconstrictors in dosages depending on the severity of hypotension and response of treatment. The level of 

anaesthesia should be carefully monitored because it is not always controllable in spinal techniques.

Because amide-type local anaesthetics such as bupivacaine are metabolized by the liver, these drugs, 

especially repeat doses, should be used cautiously in patients with hepatic disease. Patients-with se- vere 

hepatic disease, because of their inability to metabolize local anaesthetics normally, are at a greater risk of 

developing toxic plasma concentrations. Local anaesthetics should also be used with caution in patients with 

impaired cardiovascular function because they may be less able to compensate tor functional changes 

associated with the prolongation of AV conduction produced by these drugs. However, dosage 

recommendations for spinal anaesthesia are much lower than dosage recommendations for other major blocks 

and most experience regarding hepatic and cardiovascular disease dose-related toxicity is derived from these 

other major blocks.

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 agents. 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 anaesthesia are considered potential triggering agents for familial 

malignant hyperthermia. Because it is not known whether amide-type local anaesthetics may trigger this 

reaction and because the need for supplemental general anaesthesia cannot be predicted in advance, it is 

suggested that 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 

prompt institution of treatment, including oxygen therapy, indicated supportive measures, and dantrolene. 

(Consult dantrolene sodium intravenous package insert before using).

The following conditions may preclude the use of spinal anaesthesia, depending upon the physician's 

evaluation of the situation and ability to deal with the complications or complaints which may occur:

l Per-existing disease of the central nervous system, such as those attributable to pernicious anaemia, 

poliomyelitis, syphilis, or tumour

l Haematological disorders predisposing to coagulopathies or on anticoagulant therapy.

l Trauma to a blood vessel during conduct of patients on spinal anaesthesia may, in some instances, result 

in uncontrollable central nervous system haemorrhage or soft tissue haemorrhage.

l Chronic backache and preoperative headache.

l Hypotension and hypertension.

l Technical problems (persistent paresthesias, persistent body tap).

l Arthritis or spinal deformity.

l Extremes of age.

l Psychosis or other causes of poor co-operation by the patient.

CLINICALLY SIGNIFICANT DRUG INTERACTIONS

The administration of local anaesthetic solutions containing epinephrine or norepinephrine to patient 

receiving monoamine oxidase inhibitors or tricycilc antidepressants may produce severe, prolonged 

hypertension. 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.

CARCINOGENESIS, MUTAGENESIS AND IMPAIRMENT OF FERTILITY

Long term studies, in animals of most local anaesthetics including bupivacaine 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 Bupivacaine Spinal (Bupivacaine in Dextrose Injection) may be 

carcinogenic or mutagenic or that it impairs fertility.

PREGNANCY CATEGORY C

Decreased pup survival in rats and an embryocidal effect in rabbits have been observed when bupivacaine 

hydrochloride was administered to these species in doses comparable to 230 and 130 times respectively the 

maximum recommended human spinal dose. There are no adequate and well controlled studies in pregnant 

women of the effect of bupivacaine on the developing fetus.

Bupivacaine hydrochloride should be used during pregnancy only if the potential benefit justifies the potential 

risk to the fetus, this does not exclude the use of Bupivacaine Spinal at term for obstetrical anaesthesia. (See 

Labor and Delivery)

LABOUR AND DELIVERY

Spinal anaesthesia has a recognized use during labor and delivery. Bupivacaine hydrochloride, when 

administered properly via the epidural route in doses 10 to 12 times the amount used in Spinal anaesthesia has 

been used for obstetrical analgesia and anaesthesia without evdience of adverse effects on the fetus.

Maternal hypotension has resulted from regional anaesthesia. Local anaesthetics produce vasodilation by 

blocking sympathetic nerves. Elevating the patients legs and positioning her on her left side will help prevent 

decreases in blood pressure. The fetal heart rate should also be monitored continuously and electronic fetal 

monitoring is highly advisable.

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 dis-placed to the left.

Spinal anaesthesia may alter the forces of parturition through changes in uterine contractility or maternal 

expulsive effort. Spinal anaesthesia 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 

anaesthesia may increase the need for forceps assistance.

The use of some local anaesthetic drug products during labor and delivery may be followed by diminished 

muscle strength arid tone for the first day or two of life. This has not been reported with bupivacaine.

There have been reports of cardiac arrest during use of bupivacaine hydrochloride 0.75% solution for epidural 

anaesthesia in obstetrical patients. The package insert for bupivacane hydrochloride for epidural nerve block, 

etc, has a more complete discussion of preparation for and management of this problem. These cases are 

compatible with systemic toxicity following unintended intravascular injection of the much larger dose 

recommended for epidural anaesthesia and have not occurred for spinal anaesthesia in obstetrics. The 0.75% 

concentration of bupivacaine hydrochloride is therefore not recommended for obstetrical epidural 

anaesthesia

NURSING MOTHERS

It is not known whether local anaesthetic drugs are excreted in human milk. Because many drugs are excreted 

in human milk, caution should be exercised when local anaesthetic drugs are administered to a nursing woman.

PEDIATRIC USE

Until further experience is gained in patients younger than 18 years, administration of Bupivacaine Spinal in 

this age group is not recommended.

ADVERSE REACTIONS

Reactions to bupivacaine are characteristic of those associated with other amide type local anaesthetics

The most commonly encountered acute of those adverse experiences which demand immediate 

countermeasures following the administration of spinal anaesthesia are hypertension due to loss of sympa-

thetic tone and respiratory paralysis or underventilation due to cephalad extension of the motor level of 

anaesthesia. These may lead to cardiac arrest if untreated. In addition, dose related convulsions and 

cardiovascular collapse may result from diminished tolerance, rapid absorption from the injection site or from 

unintentional intravascular injection of a local anaesthetic solution Factors influencing plasma protein binding, 

such as acidosis, systemic disease which alter protein production, or competition of other drugs for protein 

binding sites, may diminish individual tolerance.

RESPIRATORY SYSTEM

Respiratory paralysis or underventilation may be noted as a result of upward extension of the level of spinal 

anaesthesia and may lead to secondary hypoxic cardiac arrest if untreated. Preanaesthetic medication, intra-

operative analgesics and sedatives, as well as surgical manipulation, may contribute to underventilation. This 

will usually be noted within minutes of the injection of spinal anaesthetic solution, but because of differing 

surgical maximal onset times, differing intercurrent drug usage and differing manipulation, it may occur any 

time during surgery or the immediate recovery period.

CARDIOVASCULAR SYSTEM

Hypotension due to loss of sympathetic tone is a commonly encountered extension of the clinical phar-

macology of spinal anaesthesia. This is more commonly observed in patients with decreased blood volume, 

decreased interstitial fluid volume, cephalad spread of the local anaesthetic, and / or mechanical obstruction of 

venous return. Nausea and vomiting are frequently associated with hypotensive episodes following the 

administration of spinal anaesthesia. High doses, or inadvertent intravascular injection, may lead to high 

plasma levels and related depression of the myocardium, decreased cardiac output, bradycardia, heart block, 

ventricular arrhythmias, and possibly, cardiac arrest. (See WARNINGS PRECAUTIONS and

OVERDOSAGEsection)

CENTRAL NERVOUS SYSTEM

Respiratory paralysis or underventilation secondary to cephalad spread of the level of spinal anaesthesia (See 

Respiratory System) and hypotension for the same reason (see Cardiovascular System) are the two most 

common encountered central nervous system related adverse observations which demand immediate 

countermeasures.

High dose or inadvertent intravascular injection may leads to high plasma levels and related central nervous 

system toxicity characterized by excitement 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.

NEUROLOGIC

The incidence of adverse neurologic reactions associated with the use of local anaesthetics may be related to 

the total dose of local anaesthetic 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 

anaesthetic techniques, with or without contribution from the drug.

Neurologic effects following spinal anaesthesia may include loss of perineal sensation and sexual function, 

persistent anaesthesia, paresthesia weakness and paralysis of the lower extremities and loss of sphincter 

control all of which may have slow, incomplete or no recovery, hypotension, high or total spinal block, urinary 

retention, headache, backache, septic meningitis, meningismus, arachnoiditis, slowing of labor, increased 

incidence of forceps delivery, shivering, cranial nerve palsies due to traction of nerves from loss of 

cerebrospinal fluid and feacal and urinary incontinence.

Allergic : Allergic-type reactions are rare and may occur as a result of sensitivity to the local anaesthetic These 

reactions are characterized by signs as urticaria, pruritus, erythema, angioneurotic edema (including laryngeal 

edema) tachycardia, sneezing, nausea, vomiting, dizziness, syncope, sweating, elevated temperature and 

possibly, anaphylactoid like symptomatology (including severe hypotension). Cross sensitivity among 

members of the amide type local anaesthetic group has been reported. The usefulness of screening to 

sensitivity has not been definitely established.

Other: Nausea and vomiting may occur during spinal anaesthesia.

OVERDOSAGE

Acute emergencies from local anaesthetics are generally related to high plasma levels encountered during 

therapeutic use to underventilation (and perhaps apnea) secondary to upward extension of spinal anaesthesia. 

Hypotension is commonly encountered during the conduct of spinal anaesthesia due to relaxation of 

sympathetic tone, and sometimes contributory mechanical obstruction of venous return.

MANAGEMENT OF LOCAL ANAESTHETIC 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 anaesthetic 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 due to a high or total 

spinal consists of immediate attention of the establishment and maintenance of patient airway and effective 

assisted or controlled ventilation with 100% oxygen with a delivery system capable of permitting immediate 

positive airway pressure.

Hypotension due to sympathetic relaxation may be managed by giving intravenous fluids (such as sodium 

chloride injection 09% or Lactated Ringer's Injection), in an attempt to relieve mechanical obstruction of 

venous return, or by using vasopressors (such as ephedrine which increases the force of myocardial 

contractions) and, if indicated, by giving plasma expanders or whole blood. 

Recent clinical data from patients experiencing local anaesthetic induced convulsions demonstrated rapid 

development of hypoxia, hypercarbia, and acidosis with bupivacaine within a minute of the onset of 

convulsions. These observations suggest that oxygen consumption and carbon dioxide production are greatly 

increased during local anaesthetic convulsions and 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 anaesthetic may result in cardiac arrhythmias, bradycardia, 

asystole, ventricular fibrillation, or cardiac arrest. Respiratory abnormalities, including ap-nea. may occur. 

Underventilation or apnea due to a high or total spinal 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.

Convulsions may be controlled, if necessary, with drugs such as succinylcholine. diazepam or thiopental 

Hypotension may be managed by giving intravenous fluids.

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 il possible, or manual 

displacement of the uterus off the great vessels be accomplished.

The mean seizure dosage of bupivacaine in rhesus monkeys was found to be 4.4 mg/kg with mean arterial 

plasma concentration of 4.5 meg/ml. The intravenous and subcutanadus LD in mice is 6 mg/ kg to 8 mg/kg 50

and 38 mg/kg to 54 mg/kg, respectively.

DOSAGE AND ADMINISTRATION

The dose of ABOCAIN SPINAL (Bupivacaine in dextrose Injection,) varies with the anaesthetic procedure, 

the area to be anaesthetized, the vascularity of the tissues, the number of neuronal segments to be blocked, 

the depth of anaesthesia and degree of muscle relaxation required, the duration of anaesthesia 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 Abocain Spinal (Bupivacaine in Dextrose 

Injection) should be reduced for elderly and debilitated patients and patients with cardiac and/or liver disease.

For specific techniques and procedures, refer to standard textbooks.

In the average adult, seven and one half mg (7.5 mg or 1.0 ml) Abocain Spinal has generally proven satisfactory 

v

for spinal anaesthesia for lower extremity and perineal procedures including TURP and vaginal hysterectomy. 

Twelve mg (12 mg or 1.6 ml) has been used for lower abdominal procedures such as abdominal hysterectomy, 

tubal ligation, and appendectomy.

Because experience with Bupivacine Spinal is limited in patients below the age 18 years, dosage 

recommendations in this age group cannot be made.

OBSTETRICAL USE

Doses as low as 6 mg bupivacaine hydrochloride have been used for vaginal delivery under spinal anaesthesia. 

The dose range of 7.5 mg to 10.5 mg (1 ml to 1.4 ml) bupivacaine hydrochloride has been used forcaesarean 

section under spinal anaesthesia.

Abocain Spinal should be inspected visually for discolouration and particulate matter prior to administration: 

solutions which are discoloured or which contain particulate matter should not be administered.

Unused portion of solutions should be discarded following initial use.

Bupivacaine Spinal may be autoclaved once at 15 pounds pressure, 121° C (250°F) for 15 minutes. However do 

not administer any solution which is discoloured or contains paniculate matter