Suxamethonium Chloride
A white or almost white, odourless, hygroscopic, crystalline
powder. Suxamethonium I mg is equivalent to 1.37mg of
suxamethonium chloride dihydrate and to 1.24 mg of anhy-
drous suxamethonium chloride. Soluble I in I of water and I
in 350 of alcohol: slightly soluble in chloroform; practically
insoluble in ether. A 0.5% solution in water has a pH of 4,0 to
5.0. Store in airtight containers. Protect from light.
Incompatibility. Incompatibilities of neuromuscular block-
crs are discussed under Atracurium.
Stability. A study of the loss of potency of suxamethonium
chloride 20 mg per mL in water indicated that decomposition
occurred at a considerably higher rate at 40Β° than at 25Β° and
that the pH range of maximum stability was 3.75 to 4.50 for
unbuffered solutions. Assuming the usual conditions of man-
ufacturing, transit, and storage the total loss of potency was
estimated to be 7% and 9% respectively for injections kept at
room temperature for 4 and 6 weeks. If unbuffered suxame-
thonium chloride injection complying with USP pH limits
(3.0 to 4.5) must be stored at room temperature, it should not
be kept for longer than 4 weeks.
Adverse Effects
The neuromuscular blocking action of suxametho-
nium chloride is terminated by the enzyme plasma
cholinesterase and prolonged apnoea may occur in
patients with an atypical enzyme or with low en-
zyme activity. Apnoea may also occur following de-
velopment of phase II block (see Uses and
Administration, below) after high or repeated doses
of suxamethonium chloride, although tachyphylaxis
may also occur with repeated doses.
Administration of suxamethonium chloride results
in transient fasciculations during the onset of depo-
larising block. Rhabdomyolysis, myoglobinaemia,__
and myoglobinuria have been reported and may be
associated with muscle damage following fascicula-
tions. Postoperative muscle pain occurs in some pa-
tients but is not directly related to the degree of
fasciculation. A transient rise in intra-gastric prs-
sure may occur secondary to fasciculation of ab-
dominal muscles. A transient increase in intra-
ocular pressure often occurs. Depolarization of skel-
etal muscle produces an immediate increase in plas-
ma-potassium concentration and this can have
serious consequences in some patients (see below).
Stimulation of the vagus nerve and parasympathetic
ganglia by suxamethonium chloride may be fol-
lowed by bradycardia. other arrhythmias, and hypo-
tension and may be exacerbated by the raised
plasma-potassium concentration; cardiac arrest has
been reported. Tachycardia and an increase in blood
pressure due to stimulation of sympathetic ganglia
have also been reported.
Suxamethonium chloride may cause an increase in
salivary, bronchial, and gastric secretion and other
muscarinic effects. Salivary gland enlargement has
occurred.
Direct release of histamine from mast cells occurs
but this is not the main mechanism of hypersensitiv-
ity reactions (see Hypersensitivity, below). Flush-
ing. skin rash. bronchospasm, and shock have been
reported.
Other reported effects include prolonged respiratory
depression and apnoea.
Administration of suxamethonium chloride is impli-
cated in the development of malignant hyperthermia
in those patients with a genetic predisposition to the
syndrome.
Effects on intra-ocular pressure. Administration of sux-
amethonium is often followed 20 to 30 seconds later by a
transient increase in intra-ocular pressure which may be due
in part to contracture of extra-ocular muscles. If suxametho-
nium is administered during eye surgery after incision of the
eyeball or to patients with penetrating eye injury there is a
theoretical risk that any increase in intra-ocular pressure may
result in extrusion of ocular contents and loss of sight. How-
ever, there appear to be few reports of vitreous extrusion as-
sociated with suxamethonium and a large retrospective
studv2 has failed to find any evidence that suxamethonium
caused additional eye damage in patients with penetrating eye
injuries. Furthermore the procedure of intubation is associat-
ed with a greater increase in intra-ocular pressure than that
seen with suxamethonium. Nonetheless, opinion on the safety
of suxamethonium in eye surgery vanes. While some suggest
that a rapid competitive neuromuscular blocker would be
preferable to aid intubation in patients with penetrating eye
injuries, after incision of the eyeball, and in glaucoma others
advocate that the risk of a transient rise of intra-ocular
press-
ure in these situations should be weighed against the need for
rapid intubation.
Effects on the muscles. Muscle fasciculations and postop-
erative muscle pain commonly follow administration of sux-
amethonium. Fasciculations (generalised and desynchronised
contractions of skeletal muscle fibres) occur during the onset
of depolarizing block in almost all patients given suxametho-
nium and may cause muscle damage. They are seen especial-
ly in the 'fine' muscles of the hands and face and can be useful
as an indication that suxamethonium is working. Attempts
have been made to prevent their development with the aim of
reducing postoperative muscle pain. However, there appears
to be no direct correlation between the extent of visible fas-
ciculations and muscle pain. Slow infusion of suxamethonium
or administration in divided doses reduces
fasciculations but not muscle pain.
Postoperative muscle pain is one of the most common side-
effects of suxamethonium and has been noted in about 50%
of patients, although the reported incidence varies widely
from near zero to almost 100%. It usually occurs on the first
postoperative day and most commonly affects muscles of the
neck. shoulders, and upper abdomen. The incidence and se-
verity of muscle pain is increased in patients who are mobile
soon after surgery and in females, but it occurs less often in
children and pregnant women. The mechanism of suxame-
thonium-induced muscle pain is not fully understood; there
have been many attempts to prevent it. Most commonly, pre-
treatment with a small dose of a competitive neuromuscular
blocker has reduced both visible fasciculations and the inci-
dence and severity of muscle pain, but has the disadvan-
tage that it may delay the onset and reduce the intensity of
subsequent suxamethonium block and impair conditions for
intubation (see under Interactions in Atracurium).
Pretreatment with a small dose ( 10 mg) of suxamethonium in
a 'self-taming' technique appears to offer no protection
against muscle pain. There have been reports that thiopen-
tone can reduce the incidence of myalgia and muscle
fasciculations and prevent increases in serum concentra-
tions of myoglobin and creatinine kinase induced by suxam-
ethonium. Treatment with benzodiazepines has
produced conflicting results. Pretreatment with the prostag-
landin synthetase inhibitors aspirin. lysine aspirin or di-
clofenac but not ketorolac has been reported to reduce
postoperative muscle pain without abolishing visible fascicu-
lations or diminishing the intensity of neuromuscular block.
Not all methods have concentrated on drug treatment. A sim-
ple regimen of stretching exercises before premedication has
reduced the incidence of both fasciculations and postopera-
tive muscle pain.
Suxamethonium may also produce an increase in jaw tension
(masseter spasm or trismus) in both adults and
children during the onset of neuromuscular blockade.
Tracheal intubation is greatly hindered in affected patients. It
is not possible to predict which patients will show this re-
sponse and the mechanism is unknown, although in about
50% of patients it may indicate the onset of malignant hyper-
thermia. Pretreatment with a paralysing dose of a competitive
neuromuscular blocker prevents the response but it is not
known whether this is clinically useful.
Effects on plasma potassium concentration. Suxame-
thomum administration is followed by depolarization of mo-
tor end-plates in skeletal muscle resulting in an immediate
increase in plasma-potassium concentration. The rise is usu-
ally small, being about 0.5 mmol or less per litre, but suxam-
ethonium is best avoided in patients whose plasma-potassium
concentration is already high. such as those with renal impair-
ment. An exaggerated response, with severe hyperkalaemia
resulting in ventricular fibrillation and cardiac arrest, has
been
reported in patients with burns, massive trauma, neuromus-
cular disease (see under Neuromuscular Disorders in Precau-
tions. below), and severe long-lasting Sepsis. See also
Children in Precautions, below for reference to fatal cardiac
arrest associated with hyperkalaemia in children. With bums
or trauma the period of greatest risk is from about 10 to 90
days after the injury, but may be further prolonged if there is
delayed healing or persistent infection. These patients may
still react abnormally to suxamethonium 2 years after the in-
jury. In neuromuscular disease the greatest risk period is usu-
ally from 3 weeks to 6 months after onset, but severe
hyperkalaemia may occur after 24 to 48 hours or later than 6
months. Patients with severe sepsis for more than a week
should be considered at risk of hyperkalaemia and no suxam-
ethonium should be given until the infection has cleared. The
mechanism of this hyperkalaemic response appears to be a
supersensitivity of acetylcholine receptors in which the entire
muscle fibre membrane, rather than discrete motor end-plate
sites, becomes directly excitable by depolarising drugs. De-
polarisation by suxamethonium thus results in release of po-
tassium over the entire muscle fibre membrane and
hyperkalaemia results.
Various methods have been tried to attenuate the hyperkalae-
mia. including pretreatment with a small dose of a competi-
tive neuromuscular blocker or with suxamethonium
itself. No method is sufficiently reliable to be used clinical-
ly.
Anaesthetics such as thiopentone and halothane can increase
the hyperkalaemic response.
Hypersensitivity. Hypersensitivity reactions to neuromus-
cular blockers occur more commonly in women than in
men, in atopic patients and those who have a history of
asthma or allergy, and in patients who have had a previous
reaction to anaesthetic drugs, Circulatory collapse, flushing,
skin rash, urticaria, and bronchospasm have occurred in hv-
persensitivity reactions associated with suxamethonium:
deaths have been reported. The exact mechanism by which
neuromuscular blockers produce hypersensitivity reactions is
still uncertain; they all have a direct effect on mast cells,
re-
leasing histamine without immunological involvement and
could cause anaphylactoid reactions. Histamine release asso-
ciated with use of aminosteroidal blockers is rare compared
with the benzylisoquinolinium blockers. Tubocurarine is
considered to be the most potent releaser of histamine. with
pancuronium and vecuronium having only very weak activity.
Suxamethonium is considered to have only 1% of the hista-
mine-releasing activity of tubocurarine but is more likely to
produce serious hypersensitivity reactions. A type I immedi-
ate hypersensitivity reaction involving IgE antibodies is con-
sidered to be the mechanism of most hypersensitivity
reactions associated with neuromuscular blockers. Anti-
bodies reacting with neuromuscular blockers. including sux-
amethonium, have been demonstrated. The antibodies
appear to be directed against quaternary or tertiary ammoni-
um-ion groups which are present in neuromuscular blockers;
such groups arc also found in other drugs, cosmetics, disin-
fectants, and foods. This may help explain the cross-reactivity
renorted between different neuromuscular blockers and
how sensitization occurs without prior exposure to any neu-
romuscular blocker. At least 50% of patients, sensitive to
one neuromuscular blocker will react to one or more others
with some patients sensitive to most. Intradermal skin tests
are used to investigate and predict sensitivity to neuromuscu-
lar blockers, but their interpretation is controversial and it
cannot be concluded that all patients with positive skin tests
will have clinical sensitivity. Although radioallergosorbent
tests can detect antibodies to suxamethonium, alcuronium,
and thiopentone some consider that their routine use is not
justified as reactions could be avoided by taking an adequate
patient history.
Treatment of Adverse Effects
Following administration of suxamethonium chio-
ride assisted respiration should be maintained until
spontaneous respiration has been fully restored.
Transfusion of fresh whole blood, frozen plasma, or
other source of plasma cholinesterase will help the
destruction of the suxamethonium when prolonged
paralysis is a result of atypical or low serum concen-
trations of plasma cholinesterase. Anticholineste-
rases should not usually be used since they
potentiate the usual phase I block (see under Uses
and Administration, below). If the neuromuscular
block ceases to be depolarising in type and acquires
some features of a competitive block (phase II
block) the cautious use of an anticholinesterase may
be considered. A short-acting anticholinesterase
such as edrophonium may be given intravenously
and if an obvious improvement is maintained for
several minutes, neostigmine may be given with at-
ropine.
Severe hypersensitivity reactions should be treated
promptly with supportive and symptomatic meas-
ures.
If malignant hyperthermia develops, it may be treat-
ed as described under Dantrolene Sodium, p. 1314.
The muscarinic effects of suxamethonium chloride.
such as bradycardia and excessive salivary secre-
tion, may be reduced by giving an antimuscarinic
such as atropine before suxamethonium. A small
dose of a competitive neuromuscular blocker given
before suxamethonium has been used to reduce
and some of the adverse effects of suxamethonium on
the muscles (see Effects on the Muscles, above).
Precautions
Doses of neuromuscular blockers need to be careful-
ly titrated for individual patients according to re-
sponse: monitoring of the degree of block is
recommended in order to reduce the risk of overdos-
age. Patients who have received a neuromuscular
blocker should always have their respiration assist-
ed or controlled until the drug has been inactivated
or antagonized.
Suxamethonium chloride is contra-indicated in pa-
tients with atypical plasma cholinesterase and
should be used with caution in patients with reduced
plasma cholinesterase activity (see below) which
may occur in certain disease states and following ex-
posure to certain drugs. Plasma cholinesterase con-
centrations fall during pregnancy and the
puerperium and therefore maternal paralysis may be
mildly prolonged. Suxamethonium is contra-indi-
cated in patients with burns, massive trauma, renal
Impairment with a raised plasma-potassium concen-
tration, severe long-lasting sepsis, and severe hyper-
kalaenia since suxamethonium-induced rises in
plasma-potassium concentration can have serious
consequences in such patients. It is contra-indicated
in patients with a history of hypersensitivity to the
drug and, because of the possibility of cross-sensi-
tivity (see above), should be used with caution when
hypersensitivity to any neuromuscular blocker has
previously occurred. Suxamethonium should be
avoided in patients with a penetrating eye injury or
glaucoma or those about to undergo incision of the
eyeball in eye surgery because of the risks from in-
creased intra-ocular pressure. Suxamethonium chlo-
ride produces muscle contractions before relaxation
and should therefore be used with caution in patients
with bone fractures. It is contra-indicated in patients
with a family history of malignant hyperthermia.
The response to suxamethonium chloride is often
unpredictable in patients with neuromuscular disor-
ders and it should be used with great caution in these
patients (see below). Caution is also needed if it is
given to a patient with cardiac or respiratory disease.
Children may be at special risk from cardiac arrest
associated with hyperkalaemia, see below.
Hypothermia may enhance the. neuromuscular
blocking effects of suxamethonium chloride and an
increase in body temperature may reduce them.
Children. Reports of fatal cardiac arrests in apparently
healthy children and adolescents, who were subsequently
the found to have had undiagnosed myopathies. led in the USA to
restrictions on the use of suxamethonium in this age group
centra-indicating it except for emergency tracheal intubation
or where an immediate securing of an ail-way is essential.
Many anaesthetists disagreed with this contra-indication and
an FDA Committee advised that the contra-indication should
be replaced by a warning about the possibility of cardiac ar-
rcst associated with hyperkalaemia with special attention be-
ing paid lo male children who are considered to be at the
highest risk. One British anaesthetist who questioned the
rationale behind restricting the elective use of suxamethoni-
um pointed out that alternatives to suxamethonium had not
been demonstrated to be as safe or effective for airway man-
agment. The rare occurrence of cardiac arrest in children
might be further reduced by taking a careful family history to
exclude undiagnosed myopathies and by using an intravenous
as opposed to inhalation induction when suxamethonium is to
be used. A survey had found that most cases of cardiac arrest
in children in the UK associated with the use of suxamethoni-
um had been caused by vagal over activity in non-atropinized
patients.
Neuromuscular disorders. Caution is needed if suxame-
thonium is to be given to patients with neuromuscular disease
since severe complications have been reported. Hyperkalae-
mia and cardiac arrhythmias or cardiac arrest have been re-
ported following administration of suxamethonium to
patients with hemiplegia. diffuse intracranial lesions (head in-
jury, encephalitis, ruptured cerebral aneurysm). tetanus, para-
plegia, acute anterior horn cell disease, and muscular
dystrophies. An exaggerated response to suxamethonium has
been reported in the myasthenic syndrome but resistance mav
occur in patients with neurofibromatosis. Resistance may also
occur in patients with myasthenia gravis. but uneventful ad-
ministration has also been reported although early onset of
phase II block is possible in these patients. Muscle contrac-
tures and hyperkalaemia may be expected in amyotrophic lat-
eral sclerosis and muscular denervation. The response to
suxamethonium is unpredictable in patients with myotonias
and it should be avoided in those patients. It is recommended
that suxamethonium is also avoided in hemiplegia, paraple-
gia, muscular denervation, and muscular dystrophies.
Plasma cholinesterase deficiency. Suxamethonium is
normally rapidly hydrolysed by plasma cholinesterase and
the clinical effects usually last for only several minutes. Ac-
tivity of the enzyme varies between individuals and pro-
longed paralysis following suxamethonium is commonly due
to a hereditary or acquired reduction in plasma cholinesterase
activity. The genes involved in the control of plasma
cholinesterase production are termed usual, atypical (dibu-
caine-resistant), fluoride-resistant, and silent. About 96% of
the population are homozygous for the normal gene. The
commonest variant in western populations is the atypical
form with about 3 to 4% of the population being heterozygous
for this variant. They exhibit a slightly prolonged response to
suxamethonium. Homozygotes for the atypical variant have a
frequency of about 0.04%. They exhibit markedly prolonged
apnoea following a standard dose of suxamethonium but can
be readily identified by biochemical tests. The fluoride-resist-
ant and silent variants occur very rarely. A measure of plasma
cholinesterase activity can be obtained from the percentage
inhibition of the enzyme by the local anaesthetic cinchocaine
(commonly known in this context by its American name.
dibucaine) to give the dibucaine number. Most normal people
have a dibucaine number of about 80.
Acquired plasma cholinesterase deficiency is clinically less
important than genetically determined deficiency. The en-
zyme is synthesised in the liver and severe liver impairment
or malnutrition may cause abnormally low enzyme levels
with some prolongation of suxamethonium activity. Reduced
enzyme a cavity may also be found in severe anaemia, burns,
cancer, collagen diseases, severe dehydration, severe infec-
tions, malnutrition, myocardial infarction. myxoedema. and
renal impairment; plasmapheresis or plasma exchange re-
moves significant amounts of plasma cholinesterase.
During pregnancy there is a rapid fall in plasma cholineste-
rase concentration which persists throughout pregnancy and
for up to several weeks into the puerperium. The concentra-
tion of atypical plasma cholinesterase is also reduced in preg-
nancy and the puerperium. A number of drugs reduce plasma
cholinesterase synthesis or activity and may prolong suxame-
thonium paralysis as discussed under Interactions, below.
Renal impairment. Suxamethonium chloride may be given
in usual doses to patients with renal failure but should be
avoided if hyperkalaemia is also present (see Effects on Plas-
ma-potassium Concentration above).
Interactions
A number of drugs may interact with depolarising
neuromuscular blockers such as suxamethonium.
The mechanisms of interaction may include a direct
effect on neuromuscular transmission or an altera-
tion of enzyme activity and may result in potentia-
tion or antagonism of neuromuscular block. In
general, interactions with suxamethonium are po-
tentially more serious in patients with impaired neu-
romuscular function (see Neuromuscular Disorders,
above) and in patients with reduced activity of plas-
ma cholinesterase enzyme (see above).
Interactions common to competitive and depolaris-
ing neuromuscular blockers are covered under Atra-
curium whereas those specific for
depolarising blockers are discussed below; well es-
tablished interactions are covered as are interactions
that have only been the subject of anecdotal reports.
Antiarrhythmics. See under Atracurium
Antibacterials. See under Atracurium.
Anticholinesterases. The action of suxamethonium can be
markedly prolonged in patients using eye drops containing
ecothiopate. a long-acting anticholinesterase which inhibits
both acetylcholinesterase and plasma cholinesterase. Follow-
ing systemic absorption of ecothiopate. plasma cholinesterase
activity may rapidly be reduced to 5% or less of normal and
prolonged apnoea after administration of suxamethonium has
occurred. On discontinuing ecothiopate, enzyme activity re-
mains depressed for I to 2 months. If a patient has used eco-
thiopate eye drops in the previous 2 months, suxamethonium
should not be given unless normal plasma cholinesterase ac-
tivity can be demonstrated: a competitive neuromuscular
blocker is preferable. Exposure to organophosphorus insecti-
cides may also reduce plasma cholinesterase activity resulting
in prolonged paralysis following administration of suxame-
thonium: enzyme activity may be totally abolished. Anti-
cholinesterase such as neostigmine enhance the action of
suxamethonium although suxamethonium-induced phase II
block can be reversed with an anticholinesterase. Care should
be taken if there is a need to use suxamethonium for urgent
short procedures after a competitive-neuromuscular-induced
block has been antagonised with an anticholinesterase as the
resulting block may be greatly prolonged. Inhibition of plas-
ma cholinesterase with tacrine has been used clinically to po-
tentiate and prolong the action of suxamethonium, although
this is no longer widely practiced.
Antiepileptics. The mean time to recovery from suxame-
thonium-induced neuromuscular block was 14.3 minutes in 9
patients receiving chronic treatment with phenytoin and/or
carbamazepine compared with 10.0 minutes in 9 patients not
receiving antiepileptics.
Antineoplastics. Cyclophosphamide has been reported to
prolong the neuromuscular block produced by suxamethoni-
um through reduction of plasma cholinesterase activity, pos-
sibly by alkylation of the enzyme. Since enzyme activity
may be reduced by up to 70% for several days to several
weeks, it was suggested that suxamethonium should be
avoided if possible in patients receiving cyclophosphamide.
Other alkylating agents also reported to reduce plasma
cholinesterase activity include mustine. thiotepa, and treta-
mine.
Aprotinin. See under Atracurium.
Benzodiazepines. See under Atracurium.
Beta blockers. See under Atracurium.
Cardiac inotropes. See under Atracurium.
Ganglion blocker. See under Atracurium.
General anaesthetics. Tachyphylaxis and phase II block
(see below) develop earlier, and after smaller total doses of
suxamethonium. when inhalation anaesthetics are used.
Halothane may increase the incidence of arrhythmias associ-
ated with suxamethonium and may potentiate suxamethoni-
um-induced muscle damage. Suxamethonium should be
used with caution with other drugs that might produce addi-
tive cardiovascular effects. Severe bradycardia and asystole
have occurred when used in anaesthetic regimens with propo-
fol and opioids such as fentanyl.
Histamine H-2 antagonists. See under Atracurium.
Lithium. See under Atracurium.
Local anaesthetics. Procaine, cocaine, and chloroprocaine
are ester-type local anaesthetics which are hydrolysed by
plasma cholinesterase and may competitively enhance the
neuromuscular blocking activity of suxamethonium. See also
Antiarrhythmics under Atracurium.
Magnesium salts. See under Atracurium.
MAOls. Reduction of plasma cholinesterase activity by
phenelzine has been reported' to cause Significant prolonga-
tion of suxamethonium paralysis. Enzyme activity may be re-
duced to 10% of normal and recovery may take up to a month.
The dosage of suxamethonium may need to be substantially
reduced or a competitive neuromuscular blocker used.
Metoclopramide. Dose-dependent prolongation of suxam-
ethonium-induced neuromuscular blockade has been reported
in patients given metoclopramide. The potent inhibitory ef-
fect of metoclopramide on plasma cholinesterase may ac-
count for this interaction.
Neuromuscular blockers. See under Atrecurium.
Sex hormones. Oestrogens and oestrogen-containing oral
contraceptives reduce plasma cholinesterase activity possi-
bly due to suppression of hepatic synthesis of the enzyme, but
little prolongation of suxamethonium paralysis may be ex-
pected since activity is reduced by only about 20%. See also
under Atracurium.
Sympathomimetics. Bambuterol can inhibit plasma
cholinesterase activity and so prolong the activity of suxamc-
thonium. Phase II block has been reported in some patients
with abnormal plasma cholinesterase.
Pharmacokinetics
After injection, suxamethonium is rapidly hydro-
lysed by plasma cholinesterase in plasma. One mol-
ecule of choline is split off rapidly to form
succinylmonocholine which is then slowly hydro-
lysed to succinic acid and choline. Only a small pro-
portion of suxamethonium is excreted unchanged in
the urine. Succinylmonocholine has weak muscle-
relaxant properties mainly of a competitive nature.
The gene responsible for the expression of plasma
cholinesterase exhibits polymorphism and enzyme
activity varies between individuals (see under Pre-
cautions, above).
Small amounts of suxamethonium do cross the pla-
centa but clinical experience indicates that the ne-
onate is not adversely affected when it has been used
for caesarean section.
Uses and Administration
Suxamethonium is a depolarising neuromuscular
blocker used to produce muscle relaxation. It acts as
an acetylcholine agonist at the neuromuscular junc-
tion, combining with cholinergic receptors of the
motor end-plate to produce depolarisation which
may produce transient fasciculations. Suxamethoni-
um is resistant to breakdown by acetylcholineste-
rase, the depolarisation is prolonged, and the
refractory period of the motor end-plate extended.
This prevents repolarisation and subsequent depo-
larisation and a flaccid muscle paralysis occurs. This
initial depolarisation block is commonly known as a
phase I block. The muscles that produce fine rapid
movements such as those of the face are the first to
be affected followed by those of the limbs, abdo-
men. and chest; the diaphragm is affected last. Re-
covery occurs in reverse order. When excessive
amounts of suxamethonium accumulate at the neu-
romnscular junction, for example following high or
prolonged dosage, the nature of the block may
change to one with characteristics similar to com-
petitive block. This is commonly termed phase II
block or dual block and may be associated with
prolonged neuromuscular blockade and apnoea.
Following intravenous injection suxamethonium
chloride acts in about 30 to 60 seconds and has a
duration of action of about 2 to 6 minutes. Following
intramuscular injection it acts in 2 to 3 minutes and
has a duration of action of about 10 to 30 minutes. It
is used in surgical and other procedures in which a
rapid onset and brief duration of muscle relaxation
is needed, including intubation, endoscopies, and
electroconvulsive therapy.
It is normally given by intravenous injection, usually
as the chloride (but the bromide and iodide have also
been used). Suxamethonium has to be given after in-
duction of general anaesthesia because paralysis is
usually preceded by painful muscle fasciculations.
A competitive neuromuscular blocker may some-
times be given before suxamethonium to try to re-
duce some of the adverse effects on the muscles (sec
under Effects on the Muscles, above). Premedica-
tion with an antimuscarinic may be of value in re-
ducing bradycardia and excessive salivation.
Assisted respiration is necessary.
An initial test dose of 0.1 mg per kg of suxametho-
nium chloride may be given intravenously if in-
creased sensitivity is suspected. The response to
suxamethonium varies considerably and the usual
single dose of suxamethonium chloride for an adult
is 0.3 to I.I mg per kg body-weight by intravenous
injection with a usual range of 20 mg to a maximum
total of 100 mg. Supplementary doses of 50 to 100%
of the initial dose may be administered at 5 to 10
minute intervals if required but the total dose given
by repeated intravenous injection or continuous in-
fusion (see below) should not exceed 500 mg per
hour. Infants and children are more resistant to sux-
amethonium than adults. A recommended intrave-
nous dose for infants under one year of age is 2 mg
per kg; a dose of I mg per kg is recommended for
children I to 12 years old.
When a suitable vein is inaccessible suxamethoni-
um chloride has been given by intramuscular injec-
tion, a suggested dose being 2.5 to 4 mg per kg
body-weight to a maximum total of 150 mg. The in-
tramuscular dose for infants is up to 4 to 5 mg per kg
and for older children up to 4 mg per kg to a maxi-
mum total of 150 mg.
For prolonged procedures in adults sustained relax-
ation may be obtained by continuous intravenous in-
fusion of a 0.1 to 0.2% solution. A rate of 2 to 5 mg
per minute is usually adequate but may be adjusted
as necessary. The total dose given by repeated intra-
venous injection (see above) or continuous infusion
should not exceed 500 mg per hour.