2011-07-30_155517.mp4
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This can happen….
First Case Reports
What they recommended…1920’s
Pathogenesis and Etiology
Calcium in normal VS MH muscle
Calcium
Triggers for MH
Convincing Stats
Ambulatory Surgery Center (ASC) Key Actions…
Communication is KEY
Bibliography
Bibliography
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This
can
happen…. Use
media
converter
to
get
a
you
tube
video
into
a
PPThttp://www.youtube.com/watch?v=DDmlG63NuhA 3
First
Case
Reports 4
What
they
recommended…1920’s Dr.
Jones
wrote
a
letter
to
the
“sister
of
the
house”Dear
Miss….”
in
view
of
what
occurred
in
the
case
of
mother
and
brother….Family
member
should
never
have
chloroform
for
an
operation,
but
rather
any
operation
should
be
with
either
gas
and
oxygen
or
ether
by
open
method
preceded
by
morphine
gr
1/6
and
atropine
gr
1/20
….and
the
risks
should
be
practically
negligible….Yours
truly” #1
reference
same
as
abovePicture
from:
http://www.aasc-norwalk.com/types_Intro.php 5
Pathogenesis
and
Etiology Syndrome
genetically
transmitted-heterogenic
(more
than
one
gene)
Mutation
in
Ryanodine
receptor–abnormal
Ca
releaseIncreased
Ca
release
greater
than
Ca
removalHypermetabolic
state-no
compensatory
mechanismsDepletes
ATP
and
glycogen
storesAccelerated
metabolism
no
muscle
relaxationincreased
O2
consumption
excess
CO2
production The
increased
rate
of
CO2
and
respiratory
acidosis
leads
to
release
of
catecholamines
which
in
turn
cause
vasoconstriction
and
tachycardia.
The
peripheral
vasoconstriction
leads
to
a
powerful
and
overwhelming
hyperthermic
syndrome
and
rapid
deterioration
in
overall
cellular
metabolism
and
eventual
death
of
cells
and
demise
of
patient.
#2 10
Calcium
in
normal
VS
MH
muscle Induction
of
MH
caused
by
abnormalities
in
the
Ca
release
of
the
SR.LEFT
is
Normal
function
of
Ca:
remember
that
muscle
contraction,
glycolysis
and
mitochondrial
function
are
regulated
by
cytoplasmic
Ca.
In
the
normal
relaxation/contraction
cycle
(left)
Ca
is
pumped
into
the
ST
by
Ca
ATPase
to
initiate
relaxation,
stored
in
the
lumen
in
association
with
calsequestrin
and
released
thru
a
Ca
release
channel
to
initiate
contraction.
Glycolytic
and
metabolism
proceed
only
rapidly
enough
to
maintaine
the
energy
balance
of
the
cell.
The
Ca
release
can
be
regulated
by
Ca
itself,
ATP,
Mg
and
calmodulin
and
even
when
stimulated
has
a
short
open
time.RIGHT:
The
abnormal
malignant
hyperthermia
Ca
release
channel
is
sensitive
to
lower
concentrations
of
stimulator
for
opening,
releases
Ca
at
enhanced
rates,
and
does
NOT
close
rapidly.
The
abnormal
channel
floods
the
cell
with
Ca
and
overpowers
the
Ca
pump
that
ordinarily
lowers
cytoplasmic
Ca.
Sustained
muscle
contraciton
account
the
rigidity
and
sustained
glycoytic
and
metabolism
.
This
causes
a
build
up
of
lactic
acid,
Co2
and
heat
with
enhanced
O2
consumption
and
ultimate
depletion
of
energy
stores.
This
leads
to
systemic
manifestations
and
ultimately
cell
death.
Reference:
#4
Malignant
Hyperthermia
by
David
MacLennan
and
Michael
S
Phillips.
Science,
vol
256
may
8
1992,
p.
789-794 11
Calcium http://www.youtube.com/watch?v=CepeYFvqmk4 12
Triggers
for
MH SuccinylcholineAnesthetic
GasesHalothaneIsofluraneEnfluraneSevofluraneDesfluraneMethoxyfluraneCyclopropaneOthers
arepotassium
salts,
curare
and
phenothiazines
Clinical
Anesthesia,
Barash
#3.
pg
598-621Succs
pic:
http://products.hospira.com/search/productDetails?listNumber=SUCCINYLCHOLINE_CHLORIDE_20&page=Drugs&sort=ndc&order=ascSevo
pic:
http://www.baxter.com/healthcare_professionals/products/sevoflurane.html 13
Convincing
Stats Mortality:
Hospital
vs.
Ambulatory
Settings
January
2006-May
2008
MHAUS
MH
Hotline503
calls
from
hospitals28
determined
MH-2
deaths
-
(7%
mortality)
44
calls
from
ambulatory
settings13
determined
MH-3
deaths-(21%
mortality)
Fulminant
MH
episode
occurring
outside
of
the
hospital
setting
is
more
likely
to
lead
to
a
bad
outcome 30
Ambulatory
Surgery
Center
(ASC)Key
Actions… Recognition
of
suspected
MHD/C
of
trigger
agentsInitiation
of
treatmentInitiation
of
emergent
MH
transfer
planTransfer
considerations/capabilitiesImplementation
of
transfer
decisionNotification
of
receiving
health
care
facility-communication
32
Communication
is
KEY Patient
DataEnd
Tidal
CO2
declining
or
normalHeart
rate
stable
or
decreasing-no
dysrhythmiasIV
Dantrolene-point
of
administrationTemperature
decliningGeneralized
muscle
tone
statusDirect
Personal
CommunicationASC
anesthesia
care
provider
and
Critical
care,
primary
or
ER
physician 34
Bibliography Allen,
G.
L.
(1998).
Sensitivity
and
Specificity
of
the
Caffeine-halothane
contracture
test.
Anesthesiology
,
88
(3),
579-88.ASC.
(2011).
Retrieved
June/July
2011,
Ambulatory
Surgery
Center
Association.
http://ascassociation.orgChristian,
A.
E.
(1989).
Is
there
a
relationship
between
masseteric
muscle
spasm
and
malignant
hyperpyrexia?
Bristish
Journal
of
Anesthesia
,
62,
540-44.Denborough,
M.
(1998).
Malignant
Hyperthermia.
The
Lancet
,
352,
1131-36.Deufel,
T.
G.
(1992).
Evidence
for
Genetic
Heterogeneity
of
Malignant
Hyperthermia
Susceptibility.
American
Journal
of
Human
Genetics
,
50,
1151-61.Ellis,
F.
H.
(1990).
Clinical
Presentation
of
suspected
malignant
hyperthermia
during
anesthesia
in
402
probands.
Anaesthesia
,
45,
838-41.Fletcher,
J.
R.
(1999).
Comparison
of
European
and
North
American
Malignant
Hyperthermia
Diagnostic
Protocol
Outcomes
for
Use
in
Genetic
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Anesthesiology
,
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(3),
654-61.Glahn,
K.
E.
(2010).
Recognizing
and
managing
a
malignant
hyperthermia
crisis:
guideline
from
the
European
Malignant
Hyperthermia
group.
British
Journal
of
Anaesthesia
,
105
(4),
417-410.Gronert,
G.
A.
Clinical
Management
of
Malignant
Hyperthermia.Hall,
S.
(2001).
General
Pediatric
Emergencies
Malignant
Hyperthermia
Syndrome.
Anesthesiology
Clinics
of
North
America
,
19
(2),
367-82.Harrison,
G.
I.
(1992).
Malignant
Hyperthermia.
Anaesthesia
,
47,
54-56.Hartung,
E.
K.
(1996).
Malignant
hyperthermia
(MH)
diagnostics:
a
comparison
between
the
halothane-caffeine-and
the
ryanodine-contracture-test
results
in
MH
susceptible,
normal
and
control
muscle.
ACTA
Anaesthesiologica
Scandinavica
,
40,
437-44.Hommertzheim,
R.
S.
(2006).
Malignant
Hyperthermia:
the
perioperative
nurse's
role.
AORN
Journal
,
83
(1),
149-164.Hopkins,
P.
H.
(1994).
Diagnosing
malignant
hyperthermia
susceptibility.
Anaesthesia
,
49,
373-75.Hopkins,
P.
(2000).
Malignant
Hyperthermia:
advances
in
clinical
management
and
diagnosis.
British
Journal
of
Anaesthesia
,
85,
118-28. 36
Bibliography Isaacs,
H.
B.
(1993).
False-negative
results
with
muscle
caffeine
halothane
contracture
testing
for
malignant
hyperthermia.
Anesthesiology
,
79
(1),
5-9.Jurkat-Rott,
K.
M.-H.
(2000).
Genetics
and
Pathogenesis
of
Malignant
Hyperthermia.
Muscle
and
Nerve
,
23,
4-17.Larach,
M.
L.
(1994).
A
Clinical
Grading
Scale
to
Predict
Malignant
Hyperthermia
Susceptibility.
Anesthesiology
,
80
(4),
771-79.Larach,
M.
R.
(1997).
Prediction
of
Malignant
Hyperthermia
Susceptibility
by
Clinical
Signs.
Anesthesiology
,
66
(4),
547-50.Malignant
Hyperthermia:
An
OR
Emergency.
(2000).
Plastic
Surgical
Nursing
,
20
(4),
222-26.Martin,
S.
V.
(2000).
Malignant
Hyperthermia:
A
case
study.
Seminars
in
Perioperative
Nursing
,
9
(1),
27-36.MHAUS.
(2011).
Retrieved
January
2011,
from
Malignant
Hyperthermia
Association
of
the
United
States:
www.MHAUS.orgNelson,
T.
L.
(1996).
Dantrolene
Sodium
can
Increase
or
Attenuate
Activity
of
Skeletal
Muscle
Ryanodine
Receptor
Calcium
Release
Channel.
Anesthesiology
,
84
(6),
1368-79.Ording,
H.
G.
(1997).
4-chloro-m-cresol
test-a
possible
supplementary
test
for
diagnosis
of
malignant
hyperthermia
susceptibility.
ACTA
Anaesthesiologica
Scandinavica
,
41,
967-72.Schick,
L.
Malignant
Hyperthermia.Should
We
Use
Muscle
Biopsy
to
Diagnose
Malignant
Hyperthermia
Susceptability?
(1993).
Anesthesiology
,
79
(1),
1-4.Stanton,
C.
(2010,
September).
Transferring
patients
with
malignant
hyperthermia.
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from
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C.
H.
(1998).
Malignant
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A
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in
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,
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(1),
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V.
S.
(1996).
Chlorocresol,
an
Additive
to
Commercial
Succinylcholine,
Induces
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of
Human
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Muscles
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Activation
of
the
Ryanodine
Receptor
Ca+
Channel.
Anesthesiology
,
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1380-85. 37