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Journal ArticleDOI

Suxamethonium Is Dangerous in Polyneuropathy

01 Dec 1981-Survey of Anesthesiology-Vol. 25, Iss: 6, pp 360

TL;DR: A 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy and neuropathy relapsed over the next five years until she presented with deteriorating pulmonary function and an inability to cough due to muscle weakness, for which she required artificial ventilation.

AbstractCase 1?A 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy. On examination she had a mild peripheral sensory disturbance, definite distal muscle weakness, and absent tendon reflexes. Cerebrospinal fluid (CSF) protein was 20 g/1. The neuropathy relapsed over the next five years until she presented with deteriorating pulmonary function and an inability to cough due to muscle weakness, for which she required artificial ventilation. She was given atropine and thiopentone to induce anaesthesia and then paralysed with suxamethonium (succinylcholine) before in? tubation. During this procedure she developed a ventricular tachycardia, which returned promptly to sinus rhythm with intravenous lignocaine and DC cardioversion. Case 2?A 42-year-old man presented with paraesthesia in the hands and feet and left-sided facial weakness. Over the next seven months his arms and legs became progressively weak, extending proximally. He was almost completely paralysed in the arms, legs, and trunk and had a peripheral sensory dis? turbance and absent reflexes. CSF protein concentration was raised at 2-84 g/1. Because he could not cough effectively and his respiratory function was deteriorating he required artificial ventilation. He was given atropine 0-3 mg, thiopentone 200 mg, and suxamethonium 75 mg intravenously before intubation. His pulse was lost immediately, and ECG monitoring showed ventricular tachycardia, which progressed to ventricular fibrillation. He was given intravenous lignocaine and cardio verted on four occasions before returning to sinus rhythm. No further arrhythmias were noted. Case 3?A 75-year-old man was admitted with a five-month history of progressive weakness of the legs. On examination he had flaccid paralysis of all muscle groups with absent tendon reflexes. CSF protein concentration was 3-2 g/1. He developed purulent sputum and a chest radiograph showed consolidation in the right lower lobe. Because he was unable to cough and blood gas concentrations were falling he was intubated, artificial

Topics: Respiratory function (53%), Facial weakness (52%), Muscle weakness (50%)

Summary (1 min read)

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Summary

  • Case 1-A 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy.
  • On examination she had a mild peripheral sensory disturbance, definite distal muscle weakness, and absent tendon reflexes.
  • Cerebrospinal fluid (CSF) protein was 2-0 g/l.
  • The neuropathy relapsed over the next five years until she presented with deteriorating pulmonary function and an inability to cough due to muscle weakness, for which she required artificial ventilation.
  • She was given atropine and thiopentone to induce anaesthesia and then paralysed with suxamethonium before intubation.
  • During this procedure she developed a ventricular tachycardia, which returned promptly to sinus rhythm with intravenous lignocaine and DC cardioversion.
  • Case 2-A 42-year-old man presented with paraesthesia in the hands and feet and left-sided facial weakness.
  • Over the next seven months his arms and legs became progressively weak, extending proximally.
  • He was almost completely paralysed in the arms, legs, and trunk and had a peripheral sensory disturbance and absent reflexes.
  • His pulse was lost immediately, and ECG monitoring showed ventricular tachycardia, which progressed to ventricular fibrillation.
  • Hp developed purulent sputum and a chest radiograph showed consolidation in the right lower lobe.
  • Because he was unable to cough and blood gas concentrations were falling he was intubated, artificial.

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BRITISH
MEDICAL
JOURNAL
VOLUME
282
24
JANUARY
1981
Lesson
of
the
Week
Suxamethonium
is
dangerous
in
polyneuropathy
R
J
FERGUSSON,
D
J
WRIGHT,
R
F
WILLEY,
G
K
CROMPTON,
I
W
B
GRANT
Artificial
ventilation,
tracheostomy,
and
bronchoscopy
are
often
essential
procedures
in
patients
with
polyneuropathy
who
develop
respiratory
failure.
We
report
on
four
patients
who
had
life-threatening
ventricular
arrhythmias
during
induction
of
general
anaesthesia
for
these
procedures.
Case
reports
Case
1-A
23-year-old
woman
developed
weak
arms
and
legs
and
diplopia
during
her
second
pregnancy.
On
examination
she
had
a
mild
peripheral
sensory
disturbance,
definite
distal
muscle
weakness,
and
absent
tendon
reflexes.
Cerebrospinal
fluid
(CSF)
protein
was
2-0
g/l.
The
neuropathy
relapsed
over
the
next
five
years
until
she
presented
with
deteriorating
pulmonary
function
and
an
inability
to
cough
due
to
muscle
weakness,
for
which
she
required
artificial
ventilation.
She
was
given
atropine
and
thiopentone
to
induce
anaesthesia
and
then
paralysed
with
suxamethonium
(succinylcholine)
before
in-
tubation.
During
this
procedure
she
developed
a
ventricular
tachycardia,
which
returned
promptly
to
sinus
rhythm
with
intravenous
lignocaine
and
DC
cardioversion.
Case
2-A
42-year-old
man
presented
with
paraesthesia
in
the
hands
and
feet
and
left-sided
facial
weakness.
Over
the
next
seven
months
his
arms
and
legs
became
progressively
weak,
extending
proximally.
He
was
almost
completely
paralysed
in
the
arms,
legs,
and
trunk
and
had
a
peripheral
sensory
dis-
turbance
and
absent
reflexes.
CSF
protein
concentration
was
raised
at
2-84
g/l.
Because
he
could
not
cough
effectively
and
his
respiratory
function
was
deteriorating
he
required
artificial
ventilation.
He
was
given
atropine
0
3
mg,
thiopentone
200
mg,
and
suxamethonium
75
mg
intravenously
before
intubation.
His
pulse
was
lost
immediately,
and
ECG
monitoring
showed
ventricular
tachycardia,
which
progressed
to
ventricular
fibrillation.
He
was
given
intravenous
lignocaine
and
cardio-
verted
on
four
occasions
before
returning
to
sinus
rhythm.
No
further
arrhythmias
were
noted.
Case
3-A
75-year-old
man
was
admitted
with
a
five-month
history
of
progressive
weakness
of
the
legs.
On
examination
he
had
flaccid
paralysis
of
all
muscle
groups
with
absent
tendon
reflexes.
CSF
protein
concentration
was
3-2
g/l.
Hp
developed
purulent
sputum
and
a
chest
radiograph
showed
consolidation
in
the
right
lower
lobe.
Because
he
was
unable
to
cough
and
blood
gas
concentrations
were
falling
he
was
intubated,
artificial
Respiratory
Unit,
Northern
General
Hospital
and
Departments
of
Medicine
and
Anaesthetics,
Western
General
Hospital,
Edinburgh
R
J
FERGUSSON,
MB,
cHs,
research
assistant
and
honorary
registrar
D
J
WRIGHT,
FFARCS,
consultant
anaesthetist
R
F
WILLEY,
MRCP,
senior
registrar
G
K
CROMPTON,
FRCP,
consultant
physician
I
W
B
GRANT,
FRCP,
consultant
physician
Suxamethonium
is
likely
to
cause
ventricular
arrhythmias
in
patients
with
polyneuropathy
ventilation
was
started,
and
five
days
later
a
tracheostomy
was
performed.
There
were
no
recorded
dysrhythmias
during
anaesthesia
with
thiopentone
and
suxamethonium
for
either
of
these
procedures,
but
six
days
later
the
tracheostomy
had
to
be
refashioned
and
he
was
given
a
further
anaesthetic
(thiopentone
300
mg
and
suxamethonium
50
mg).
During
this
procedure
he
developed
ventricular
tachycardia
and
then
ventricular
fibrilla-
tion.
Sinus
rhythm
was
restored
with
external
cardiac
massage
and
intravenous
lignocaine.
Case
4-A
53-year-old
woman
presented
with
a
six-month
history
of
progressive
weakness
of
the
arms
preceded
by
sensory
symptoms
in
the
hands
and
face.
On
examination
she
had
appreciable
proximal
weakness
of
the
arms
and
legs
with
absent
reflexes.
CSF
protein
concentration
was
normal.
She
had
difficulty
in
coughing
and
developed
purulent
sputum.
Chest
radiographs
showed
collapse
of
the
left
lower
lobe
and
it
was
necessary
to
remove
secretions
using
rigid
bronchoscopy.
Intravenous
anaesthesia
was
induced
with
atropine
0
4
mg,
thiopentone
250
mg,
and
suxamethonium
50
mg.
Immediately
after
the
bronchoscope
was
inserted
her
pulse
was
lost.
ECG
monitoring
showed
ventricular
tachycardia,
which
reverted
spontaneously
to
sinus
rhythm.
Subsequent
investigations
showed
that
she
had
a
relapsing
polyneuropathy
associated
with
paraproteinaemia.
Comment
Three
possible
causes
of
the
ventricular
arrhythmias
in
our
patients
were
autonomic
dysfunction,
hypoxaemia,
and
hyper-
kalaemia
after
giving
suxamethonium.
Autonomic
dysfunction
in
the
Guillain-Barre
syndrome
has
been
severe
enough
to
cause
sudden
death,'
but
ventricular
arrhythmias
have
not
been
reported
in
these
patients.
Autonomic
reflexes
related
to
endotracheal
intubation
may
have
caused
the
arrhythmias.
If
this
was
the
mechanism,
however,
we
might
have
expected
to
see
similar
arrhythmia
during
the
manipulation
associated
with
subsequent
tracheal
aspiration,
but
this
did
not
happen.
All
four
patients
had
normal
arterial
partial
pressures
of
oxygen
(case
3
breathing
40%
oxygen
and
the
others
breathing
air)
on
the
day
that
the
anaesthetic
was
given
and
all
were
given
oxygen
before
anaesthesia,
which
makes
hypoxaemia
an
improbable
cause
of
the
arrhythmias.
We
think
that
the
most
likely
reason
for
the
ventricular
arrhythmias
was
transient
hyperkalaemia
after
intravenous
suxamethonium
although,
unfortunately,
no
measurements
of
serum
potassium
concentra-
tions
were
made
at
the
time
the
arrhythmias
occurred.
Suxamethonium-induced
hyperkalaemia
has
been
well
298
copyright.
on 9 August 2022 at India:BMJ-PG Sponsored. Protected byhttp://www.bmj.com/Br Med J (Clin Res Ed): first published as 10.1136/bmj.282.6260.298 on 24 January 1981. Downloaded from

BRITISH
MEDICAL
JOURNAL
VOLUME
282
24
JANUARY
1981
299
documented
in
patients
with
upper
motor
neurone
paralysis
secondary
to
spinal
cord
injury,
tumour,
or
cerebrovascular
accidents.1
Nicholson3
described
a
child
suffering
from
diffuse
lower
motor
neurone
disease
who
had
a
cardiac
arrest
three
minutes
after
receiving
intravenous
suxamethonium.
Sinus
rhythm
returned
after
external
cardiac
massage
and
the
serum
potassium
concentration
15
seconds
after
the
arrest
was
7
9
mmol
(mEg)/l.
Experimental
studies4
suggest
that
denervation
appears
to
sensitise
the
muscle
cell
membrane
to
suxamethonium,
leading
to
the
release
of
substantial
amounts
of
potassium.
This
hyperkalaemia
is
a
transient
phenomenon
lasting
for
only
three
to
seven
minutes
and
many
of
the
dysrhythmias
it
causes
resolve
spontaneously.
It
may
be
relevant
that
our
four
patients
had
all
had
severe
muscle
weakness
for
a
long
time.
We
have
not
found
such
arrhythmias
in
patients
with
acute
polyneuritis
in
whom
bronchoscopy,
tracheal
intubation,
or
tracheostomy
was
performed
at
an
early
stage
in
the
illness
under
anaesthesia
with
thiopentone
and
suxamethonium.
This
observation
is
in
keeping
with
the
laboratory
findings
of
Stone,5
who
showed
that
suxamethonium-induced
hyperkalaemia
in
dogs
with
transected
sciatic
nerves
and
spinal
cords
was
a
time-related
effect,
maximal
at
28
days.
Clinical
reports
on
patients
with
upper
motor
neurone
lesions
also
suggest
that
suxamethonium-induced
hyperkalaemia
does
not
occur
during
the
first
three
to
four
weeks
of
paralysis.'
6
7
Apart
from
these
four
patients
we
have
ventilated
only
one
other
patient
with
relapsing
polyneuropathy,
a
34-year-old
woman
in
whom
two
separate
tracheostomies
were
performed
two
years
apart
under
general
anaesthesia.
No
arrhythmias
occurred
with
these
procedures
but
on
neither
occasion
was
the
patient
given
suxamethonium.
Our
case
reports
provide
circumstantial
evidence
that
suxamethonium
may
produce
life-threatening,
though
fortunately
easily
treated,
ventricular
arrhythmias
in
patients
with
chronic
or
relapsing
polyneuropathies.
Although
this
effect
may
not
occur
when
suxamethonium
is
given
soon
after
the
onset
of
muscle
weakness
in
acute
cases,
it
seems
wise
to
avoid
suxamethonium
and
consider
using
a
non-depolarising
agent
in
all
patients
with
polyneuropathy
who
require
muscle
relaxation
during
general
anaesthesia.
We
thank
Dr
C
Mawdsley,
Dr
E
H
Jellinek,
and
Dr
B
Ashworth
for
permission
to
publish
the
case
reports
on
their
patients,
and
Drs
Slawson,
Davies,
Donnelly,
and
Barrie
for
help
with
anaesthesia
and
resuscitation.
We
are
also
grateful to
Miss
Allison
Gillespie
for
secretarial
assistance.
RJF
is
supported
by
a
research
grant
funded
by
Astra
Pharmaceuticals
and
Glaxo
Group
Research.
References
Lichtenfield
P.
Autonomic
dysfunction
in
the
Guillain-Barr6
syndrome.
Am
J
Med
1971;50:772-80.
2
Cooperman
LH.
Succinylcholine-induced
hyperkalemia
in
neuromuscular
disease.
JAMA
1970;213:1867-71.
3Nicholson
MJ.
Circulatory
collapse
following
succinylcholine:
report
of
a
patient
with
diffuse
lower
motor
neurone
disease.
Anesth
Analg
1971
;50:431-7.
4Gronert
GA,
Lambert
EH,
Theye
RA.
The
response
of
denervated
skeletal
muscle
to
succinylcholine.
Anesthesiology
1973;39:13-22.
5
Stone
WA,
Beach
TP,
Hamelberg
W.
Succinylcholine-induced
hyper-
kalaemia
in
dogs
with
transected
sciatic
nerves
or
spinal
cords.
Anaesthesiology
1970
;32
:515-20.
6
Stone
WA,
Beach
TF,
Hamelberg
W.
Succinylcholine
danger
in
the
spinal
cord
injured
patient.
Anaesthesiology
1970;32:168-9.
7Cooperman
LH,
Strobel
GE,
Kennell
EM.
Massive
hyperkalaemia
after
administration
of
succlinylcholine.
Anesthesiology
1970:32:161-4.
(Accepted
22
October
1980)
Reading
for
Pleasure
Grandfather's
footsteps
R
C
HUMPHREYS
Sometimes
between
the
pages
I
still
smell
frangipani,
Between
others,
damp
bamboo.
When,
as
a
boy,
I
read
my
grandfather's
diary
and
letters
I
had
never
heard
of
Andre
Gide
but
consciously
felt,
as
he
did,
that
one
read
a
writer
not
merely
to
get
an
idea
of
what
he
said
but
to
go
off
with
him
and
travel
in
his
company.
My
grandfather
was
a
Victorian
and
long
dead
in
the
1930s
when,
through
his
diary,
I
joined
him
in
Singapore
on
28
May
1889
to
"seek
what
riches
might
be
hidden
in
the
form
of
gold
or
other
precious
metals
among
the
rocky
highlands
of
Pahang."
The
journey
started
on
the
coasting
steamer
Sappho,
which
took
us
up
the
Straits
of
Malacca
and
picked
its
way
into
the
jungle-hidden
mouth
of
the
Klang
river.
We
disembarked
at
the
village
of
Klang
and
travelled
Crickhowell,
Powys
R
C
HUMPHREYS,
MD,
FRCGP,
general
practitioner
the
19
miles
to
Kuala
Lumpur
by
train.
KL
looks
different
now.
In
1889
there
was
no
hotel,
and
the
resthouse
was
dirty
and
dilapidated.
My
grandfather
and
I
were
fortunate
in
that
the
Punjom
Mining
Company's
agent
invited
us
to
stay
with
him
and
he
helped
us
to
enlist
coolies
and
obtain
provisions
before
we
set
out
on
foot
into
the
interior.
When
we
left
Kuala
Lumpur
by
road,
walking
was
easy,
but
this
soon
became
a
jungle
track
with
rivers
to
be
waded
and
baggage
to
be
dragged
by
ropes
up
precipitous
rocks,
while
leeches
and
violent
thunderstorms
compounded
the
dis-
comforts
of
a
journey
which
lasted
many
days
and
eventually
finished
in
a
dug-out
canoe.
I
had
to
hide
my
head
under
the
bedclothes
when
I
heard
his
dog
whine
and
tremble
when
we
were
being
tracked
by
a
tiger.
I
was
fascinated
by
his
letters
to
Messrs
John
Little
and
Co
of
Singapore.
"Please
send:
Claret
(St
Julien)
1
doz
pints;
Whisky
(Old
Glenlivet)
1
case;
1
keg
corned
beef;
2
doz
table
napkins;
1
butter
dish;
1
sugar
bowl."
This
and
similar
orders
were
being
sent
while
a
letter
home
records
that
"Jolly
and
Jones
have
been
away
in
the
jungle
for
eleven
days
but
Jolly
says
they
copyright.
on 9 August 2022 at India:BMJ-PG Sponsored. Protected byhttp://www.bmj.com/Br Med J (Clin Res Ed): first published as 10.1136/bmj.282.6260.298 on 24 January 1981. Downloaded from
Citations
More filters

Journal ArticleDOI
TL;DR: The present case report investigates the neuromuscular block of vecuronium in an adolescent with CMT syndrome and introduces concerns regarding altered response to anesthetics such as thiopental and nondepolarizing muscle relaxants.
Abstract: C harcot-Marie-Tooth (CMT) syndrome (peroneal muscular atrophy) is a rare degenerative disease of the peripheral nerves that is transmitted as an autosomal dominant trait. Dyck and Lambert (1) found genetic, clinical, electrophysiologic, and pathologic evidence for heterogeneity among patients with CMT. Onset of CMT is typically in the second decade of life, which makes the disease the most common cause of chronic peripheral neuropathy in adolescents. The disease usually starts with motor impairment of the lower extremities. Later, mild distal sensory impairment develops, and, eventually, the process spreads to involve the upper extremities. Autonomic disturbances such as orthostatic hypotension, hypohidrosis, and decreased skin temperature are occasional complications. Management of anesthesia in patients with CMT syndrome introduces concerns regarding altered response to anesthetics such as thiopental(2) and to both depolarizing or nondepolarizing muscle relaxants (3,4). The present case report investigates the neuromuscular block of vecuronium in an adolescent with CMT syndrome.

25 citations


Journal ArticleDOI
TL;DR: It is proposed that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.
Abstract: Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 mm after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3–4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5–1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mglkg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = ±19 pg/ml, P < 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 ± 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.

18 citations


Cites background from "Suxamethonium Is Dangerous in Polyn..."

  • ...Occasionally, fatal hemodynamic crises have been observed in, but not limited to, patients with burns (l), tetanus (2), spinal cord or lower motor neuron injuries (3), polyneuropathy (4), or previous irradiation (5)....

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Journal ArticleDOI
TL;DR: It is suggested that ischaemia resulting from arterial spasm may play a role in the visual failure associated with anterior communicating artery aneurysms as well as direct compression of the visual pathways.
Abstract: failure.2 Previous reports ofpermanent visual deterioration have all concerned large aneurysms of at least 12 x 15 mm.23 The mechanism of visual loss has always been attributed to compression of the optic pathways either by aneurysm or by an associated haematoma with the pattern of loss being determined by the position of the aneurysm in relation to the optic nerves and chiasm.4 In this case, almost complete and permanent visual failure occurred six days after the primary haemorrhage. There was no evidence of further haemorrhage or clot on CT scans and the aneurysm was of moderate size with no signs of compression being seen at the time of surgery. The visual failure could have been produced by ischaemic damage to the anterior visual pathways secondary to vasospasm. A reduction in the cerebral blood flow over the period ofonset of the visual failure was evident both clinically and by measurement. Vasospasm has been postulated as a cause for transient ischaemic amaurosis before,5 but this is the first time that such an ischaemic event has lead to permanent blindness and the vasospasm has been measured quantitatively during the evolution of the symptoms. We suggest that ischaemia resulting from arterial spasm may play a role in the visual failure associated with anterior communicating artery aneurysms as well as direct compression of the visual pathways. SIMON RUBEN FARHAD AFSHAR Department ofNeurosurgery, St Bartholomew's Hospital, West Smithfield, London, UK

13 citations


Journal ArticleDOI
18 Jun 1983-BMJ
TL;DR: The most frequent complication was bronchopulmonary infection which occurred in almost every patient, Staphylococcus pyogenes, Pseudomonas pyocyanea, and coliforms being the organisms most commonly isolated.
Abstract: During the 10 year period 1972-81, 39 patients with neurological disorders referred to a respiratory unit required artificial ventilation, seven on two occasions. The decision to undertake ventilation was usually made on clinical grounds because of deteriorating respiratory effort, ineffective cough, or inability to swallow. Arterial blood gas studies were of limited value in assessing the need for ventilation. The most frequent complication was bronchopulmonary infection which occurred in almost every patient, Staphylococcus pyogenes, Pseudomonas pyocyanea, and coliforms being the organisms most commonly isolated. In contrast, serious complications of tracheostomy and pulmonary thromboembolism occurred infrequently. There were 10 deaths among the 39 patients ventilated on 46 occasions; six were directly attributable to the neurological disease itself but four resulted from complications of artificial ventilation.

5 citations


Journal ArticleDOI
11 Feb 1984-BMJ
TL;DR: Points Effects of perforated appendicitis in girls on subsequent fertility (W G Mills); Eld(er)ology (G Smelt); Not . . . achalasia (F W Wright); Potentiation of oral anti?
Abstract: Fetal monitoring during labour R S Sawers, mrcog. 484 Rational treatment of asthma P W Ind, mrcp. 484 Addiction to aerosol treatment I M Slessor . 485 Adrenocortical suppression in multiply injured patients: a complication of etomidate treatment H D Chee, md, and others; R W Logan, frcpath, and Josephine I McKee, mrcpath 485 Ethical dilemmas of brain failure in the elderly G S Robertson, ffarcs; P H Millard, frcp; J Kellett, frcpsych . 486 Standardisation of oral anticoagulant treatment A M H P van den Besselaar, phd, and others 486 Infection with netilmicin resistant Serrada marcescens M W Casewell, mrcpath, and Philomena Ronan, bsc . 487 Impact of audit on preventive measures R G H Bethel, mrcgp . 487 Screening for asymptomatic bowel cancer in general practice N C Armitage, frcs, and J D Hardcastle, mchir . 488 Institutional malnutrition A Burns, mrcp. 488 Arthritis in Roman Britain Juliet Rogers, MB, and P Dieppe, mrcp_488 Oxygen as a driving gas for nebulisers: safe or dangerous? S J Austin, MB, and C Chan, mrcp. 488 Development of a strategy for higher education I M Richardson, frcped; B H Taylor, bsc(econ) . 488 No man is an island J Callander, mrcgp. 489 Points Effects of perforated appendicitis in girls on subsequent fertility (W G Mills); Eld(er)ology (G Smelt); Not . . . achalasia (F W Wright); Potentiation of oral anti? coagulants by ketoconazole (T K Daneshmend); Calcium antagonists in hypertension (J J Jones); Kawasaki syn? drome (M B McEvoy and S M Hall); BMA sponsored candidates for GMC election (R G Watson) . 489

1 citations


References
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Journal ArticleDOI
TL;DR: A review of pathologic data obtained from the literature indicates that involvement of autonomic pathways in this condition is not uncommon and an approach to management that takes into account the autonomic status may lessen the mortality of this condition.
Abstract: Twenty-eight cases of the Guillain-Barre syndrome were reviewed for evidence of autonomic dysfunction. In twelve cases the patients were closely followed throughout their illness; the remaining sixteen cases were reviewed retrospectively from available data. Autonomic dysfunction occurred frequently and at times was severe. It took the form of either excessive or inadequate activity of the sympathetic and/or parasympathetic systems. Paroxysmal episodes of excessive autonomic activity bore a particularly poor prognosis. Autonomic dysfuction was closely related to the sudden deaths of two patients and probably related to the fatal outcome in two additional patients. Only one of the six fatalities could be attributed to respiratory insufficiency. Electrocardiographs abnormalities were encountered frequently and were related to alterations in autonomic and central nervous system status. These changes do not alone provide adequate evidence for a diagnosis of "myocarditis." A review of pathologic data obtained from the literature indicates that involvement of autonomic pathways in this condition is not uncommon. An approach to management that takes into account the autonomic status may lessen the mortality of this condition.

194 citations


Journal ArticleDOI
14 Sep 1970-JAMA
TL;DR: The dangerously high levels of plasma potassium known to follow succinylcholine chloride administration in patients with burns or trauma have also been noted in Patients with paraplegia or hemiplegia, muscular dystrophy, and multiple sclerosis.
Abstract: The dangerously high levels of plasma potassium known to follow succinylcholine chloride administration in patients with burns or trauma have also been noted in patients with paraplegia or hemiplegia, muscular dystrophy, and multiple sclerosis. Of 40 patients with these neuromuscular diseases, 15 had increases in potassium levels between 1 and 6 mEq/liter after receiving succinylcholine chloride, 1 mg/kg of body weight. Most increases over 1 mEq/liter occurred in those patients who had been ill for less than six months or, if longer, who had disease of a progressive nature. The degree and extent of muscle paralysis seemed directly correlated with relaxant-induced hyperkalemia.

173 citations




Journal ArticleDOI
TL;DR: The responses of denervated and normal canine gastroenemius muscle to succinylcholine (SCh) were compared and contrasted in regard to potassium (K+) flux &OV0312;O2, muscle tension, and electrical activity.
Abstract: The responses of denervated and normal canine gastroenemius muscle to succinylcholine (SCh) were compared and contrasted in regard to potassium (K+) flux O2, muscle tension, and electrical activity. K+ efflux and O2 of denervated muscle increased 20-fold and fourfold after SCh, respectively, while K

53 citations


Frequently Asked Questions (1)
Q1. What are the contributions in this paper?

In this paper, a 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy, and was given atropine and thiopentone to induce anaesthesia and then paralysed with suxamethonium ( succinylcholine ) before intubation.