SUCCINYLCHOLINE
Drugs in Pregnancy and Lactation.
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Name: SUCCINYLCHOLINE
Class: Skeletal Muscle Relaxant
Risk Factor: CM
Fetal Risk Summary
Succinylcholine is a depolarizing neuromuscular blocking agent that is used as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Approximately 90% of the drug is rapidly hydrolyzed by plasma cholinesterase to succinylmonocholine, a metabolite that is clinically inactive, and then more slowly to succinic acid and choline. The remaining 10% is excreted unchanged in the urine (1).
According to the manufacturer, reproduction studies in animals with succinylcholine have not been conducted (1). A 1984 source, however, stated that studies conducted in the 1950s in rabbits and dogs did not observe embryo or fetal toxicity or teratogenicity (2). Succinylcholine has no direct action on the uterus or other smooth muscles and, because it is highly ionized and has low lipid solubility, does not readily cross the placenta (1).
A study published in 1961 noted the lack of quantitative data on the placental transfer of succinylcholine in animals and humans (3). Although published reports involving more than 1,800 deliveries had shown the drug to be safe for the fetus and newborn, there were anecdotal reports of flaccid, apneic infants whose condition was attributed to succinylcholine (3). The authors cited two studies in which doses less than 100 mg in pregnant rabbits had no adverse effect on the newborns, but in dogs, paralysis was demonstrated in pups when a 400-mg dose was administered to the mother immediately before delivery (3). They then studied 14 patients delivered by cesarean section under general anesthesia, in whom a single 100-mg IV dose of succinylcholine was followed by a continuous infusion of a 0.2% succinylcholine solution (3). The patients received a total dose (IV plus infusion) of 100600 mg. Three of the newborn infants had Apgar scores less than 7 (time when determined not specified). In an additional eight patients undergoing vaginal delivery, a single 100-mg IV dose was given within 4 minutes of birth. None of these infants had a depressed Apgar score. Of the total 22 newborns, no paralysis was observed. Placental transfer of succinylcholine as determined by a biologic test, however, could not be demonstrated in any of the cases.
In a second study by these same authors, pregnant rabbits at term were treated with a single IV dose of succinylcholine (0.25570 mg/kg) with delivery of the fetuses 36 minutes later (4). A difference in vigor compared with that in controls was observed when the mother had received 340 mg/kg, about 600 times the human clinical dose based on weight. [The human clinical dose to facilitate tracheal intubation is 0.6 mg/kg IV, range 0.31.1 mg/kg (1)]. At 540 mg/kg, all rabbit fetuses were alive but paralyzed. In the human part of this study, 13 women at term who were about to undergo vaginal delivery were given a single 200- to 500-mg rapid IV dose, 15.25 minutes before delivery (4). Maternal blood levels varied from 0 to 11.6 ΅g/mL, whereas cord blood concentrations varied from 0 to 2.0 ΅g/mL. Cord blood levels of 1.12.0 ΅g/mL occurred in six of eight fetuses whose mothers had received doses of 300 mg/kg or more. No drug was found in the cord blood of five newborns after a 200-mg/kg maternal dose. None of the newborns appeared to be affected by succinylcholine, but all of the mothers were apneic at delivery and for periods up to 16 minutes.
The placental transfer of succinylcholine using radioactive tracers was studied in near-term Macaca mulatta monkeys, using IV doses of 23 mg/kg followed by repeated doses of 1.2 and 2 mg/kg (5). Rapid placental transfer occurred, reaching a peak fetal plasma concentration approximately 30% of the maternal plasma level 510 minutes after the dose. Fetal metabolism of succinylcholine to inactive succinylmonocholine was demonstrated, albeit at a slower rate than that which occurred in the mother, an indication that fetal cholinesterase (pseudocholinesterase) activity was lower than that in the mother (5). The authors concluded that the amount of active drug transferred to the fetus produced a slight effect on skeletal muscle activity and was unlikely to depress respiration in the newborn (5).
Atypical cholinesterase is an autosomal dominant inherited condition with a prevalence, for the dibucaine-resistant form, of 1:2000 to 1:4000 in various populations (6). The homozygote state is diagnosed by the onset of prolonged apnea (>10 minutes), in the absence of excessive amounts of other depressants, after succinylcholine (13 mg/kg) administration (6). Some of the anecdotal reports, mentioned in Reference #3, of flaccid, apneic infants after succinylcholine administration may represent cases of this genetic trait. Four maternal cases of atypical cholinesterase with probable atypical homozygote infants in three are discussed below.
A study published in 1975 described respiratory depression and decreased muscular activity in a newborn whose mother had received succinylcholine, 80 mg IV followed by an IV infusion that delivered an additional 60 mg of drug, for cesarean section at term (7). Newborn ventilation support was required for 10 minutes after birth. Neuromuscular block in the mother continued for approximately 5.5 hours. Because the cholinesterase activity in the mother and that in the 2-day-old infant were 10% of normal, neither was able to rapidly metabolize the succinylcholine (7).
Low concentrations of plasma cholinesterase were thought to be responsible for transient respiratory depression in a newborn following the use of succinylcholine for cesarean section (8). The mother had received 200 mg thiamylal (a barbiturate similar to thiopental that is not currently available) and 100 mg succinylcholine IV for induction of general anesthesia 3 minutes prior to delivery. The onset of respiration and the development of an acceptable respiratory pattern in the newborn were slightly delayed with Apgar scores of 5 and 8 at 1 and 5 minutes, respectively. After recovery, the newborn did well. The mother required mechanical ventilation for 4 hours before return of spontaneous muscular activity and respiration (8). Cholinesterase activity in the mother was below the level of test sensitivity. Enzyme activity in the newborn was 410 U/L (normal 24364872 U/L) (8). Three months later, the infant's pseudocholinesterase activity had risen to 910 U/L. Enzyme concentrations in the father (2420 U/L) were slightly low, normal in one sibling (2480 U/L), and markedly depressed in five other siblings (range 150760 U/L).
A description of two mothers at term with atypical cholinesterase who were administered succinylcholine prior to elective cesarean section was reported in 1975 (9). The first mother received 100 mg IV succinylcholine 5 minutes before delivery of a male baby. Apnea in the mother persisted for 2.5 hours after delivery before return of spontaneous respirations. Her infant was flaccid, apneic, and unresponsive to stimulation. Respiratory assistance was required for 6 hours before occurrence of full recovery. In the second mother, who also received succinylcholine 100 mg IV, recovery from paralysis required 2 hours. Her infant, delivered 10 minutes after the dose, cried immediately and had Apgar scores of 8 and 10 at 1 and 5 minutes, respectively. Analysis of serum cholinesterase activity and dibucaine numbers in the mothers and infants revealed that the mothers and the affected infant were atypical homozygotes, whereas the unaffected infant was a heterozygote (9).
The Collaborative Perinatal Project monitored 50,282 mother-child pairs, 26 of whom had 1st-trimester exposure to succinylcholine (10). No congenital malformations were observed in any of the newborns.
In summary, succinylcholine is not embryotoxic or teratogenic in two animal species or, although the data are very limited, in humans. Succinylcholine has been routinely used in obstetrical patients prior to delivery since the 1950s and no reports of fetal toxicity have been located. Partial or complete newborn paralysis with resulting respiratory depression have been reported, however, when the drug was administered to women with the genetic trait for atypical cholinesterase. Prolonged newborn respiratory depression may occur when this trait has been inherited by the infant. The level of cholinesterase activity in the infant will determine the duration of paralysis. Women without the genetic trait for atypical cholinesterase rapidly metabolize the drug and, because clinically significant placental transfer is concentration dependent, prevent toxicity in the newborn.
Breast Feeding Summary
The passage of succinylcholine into breast milk has not been studied. Because the drug is rapidly hydrolyzed by plasma cholinesterase (pseudocholinesterase) to an inactive metabolite, it is doubtful that clinically significant amounts of active drug are transferred into milk (11). Women with the genetic trait for atypical cholinesterase will have high concentrations of succinylcholine, but the effects of the drug on the mother will preclude breast feeding.
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References
- Product information. Anectine. Glaxo Wellcome, 1998.
- Onnis A, Grella P. The Biochemical Effects of Drugs in Pregnancy. Vol 1. West Sussex, England: Ellis Horwood Limited, 1984:2301.
- Moya F, Kvisselgaard N. The placental transmission of succinylcholine. Anesthesiology 1961;22:16.
- Kvisselgaard N, Moya F. Investigation of placental thresholds to succinylcholine. Anesthesiology 1961;22:710.
- Drabkova J, Crul JF, van der Kleijn E. Placental transfer of 14C labelled succinylcholine in near-term Macaca mulatta monkeys. Br J Anaesthesia 1973;45:108796.
- Donnell GN. Cholinesterase, atypical. In Buyse ML. Editor-in Chief. Birth Defects Encyclopedia. Vol 1. Cambridge, MA: Blackwell Scientific Publications, 1990:3167.
- Owens WD, Zeitlin GL. Hypoventilation in a newborn following administration of succinylcholine to the mother: a case report. Anesth Analg 1975;54:3840.
- Cherala SR, Eddoe DN, Sechzer PH. Placental transfer of succinylcholine causing transient respiratory depression in the newborn. Anaesthesia Intensive Care 1989;17:2024.
- Baraka A, Haroun S, Bassili M, Abu-Haider G. Response of the newborn to succinylcholine injection in homozygotic atypical mothers. Anesthesiology 1975;43:1156.
- Heinonen OP, Slone D, Shapiro S. Birth Defects and Drugs in Pregnancy. Littleton, MA: Publishing Sciences Group, 1977:35860.
- Spigset O. Anaesthetic agents and excretion in breast milk. Acta Anaesthesiol Scand 1994;38:94103.
Q&A about Succinylcholine
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Mississippi tried it for a short period back in 1973 as an answer to reduce the number of wounded Deer during Archery Bow Season. In fact, the was a study done that showed that the wounded Deer "problem" did not truly exist to begin with, and the existing "problem" greatly exaggerated.The results were the use of Succinylcholine, was a DISMAL failure.The fact that the poison left no harmful residue that would harm humans or other animals was also questioned. In fact within days of being made available, it began to be abused. Poor shots attempted on Deer resulted in death each and every time. Deer that normally would have survived the wounds were dying. The majority of the legitimate hunting community felt it a violation of basic sportsmanship.Mississippi's "Poaching" percentages using this drug went up 822% in just one year!
Personally with the technology of today the term "Primitive" in terms of a style of hunting is a falsehood within itself. Historically, Bowhunting goes back hundreds of years to when it was in fact "primitive", but that tag hardly applies now as the equipment, and techniques have totally evolved past any such stage. The whole idea was dropped like a hot potato. In years since the hunting community hasn't had to deal with the issues any more.
Curiously, the drug Succinylcholine is the drug of choice for drug induced homicide's now, as it leaves no traces in the human body after being injected, and is virtually impossible for Forensic Pathologists to trace. If we allow ourselves to go backward, the results will just be additional abuses.It would not be a good thing.
Based on this research I vote a heartfelt NO........
Neostigmine is an anti-acetylcholinesterase. It blocks the enzyme that breaks down acetylcholine in the body. As the acetylcholine builds up, it can displace the muscle relaxant at the motor end plate and the person can once again move. All of the various muscle relaxants are metabolized by the body, with or without the introduction of neostigmine as a reversal agent.
In general, Succ wears off so fast it does not need reversal. In fact the half life of the neostigmine is considerably greater than the Succ. Since neostigmine is a weak "nerve agent" and can cause paralysis itself the view is, if you do not need it, do not give it.
There are people out there who can not break down Succ, so the proper treatment is to give fresh frozen plasma which contains the enzyme needed to break it down. (If you give neostigmine you might see a very temporary improvement but if you do not get the Succ metabolized, when the neo wears off, you will be right back where you started.)
There is only one instance where neostigmine is indicated after the use of Succ. As Succ gets broken down, one of the products of the break down is succ MONO choline. That is a very weak non-depolarizer muscle relaxant. In cases where a person got a lot of Succ, such as in the "olden days" when a constant drip of Succ was used, or when the anesthesia provider gives repeated doses, the build up of succ MONO choline could cause prolonged paralysis. And for THAT you could use neostigmine, but the provider had better make sure he is correct in his assessment.
Acetylcholine is a neurotransmitter that transmits a signal from a nerve cell to a muscle cell, causing the muscle to contract. How is the neurotransmitter inactivated so that the muscle can relax?
a. acid
b. it diffuses away
c. it is hydrolyzed by pepsin
d. it is hydrolyzed by acetylcholinesterase
e. it is replaced by succinylcholine
