Transcript Pediatric Anesthesia and Malignant Hyperthermia

Pediatric Anesthesia and
Malignant Hyperthermia
By: Ashley Evick, BSN, SRNA
Objectives
• To identify the mechanism of thermoregulation for
children of various ages
• To identify risks of hypothermia
• To define and be able to quickly identify a malignant
hyperthermia emergency in the operating room
• To be able to discuss the differences in malignant
hyperthermia presentation in children versus the adult
Our patients…
 Children are NOT little
adults
 They are a unique patient
population
 Age groups:
•
Neonate: less than 30 days
•
Infant: 1-12 months
•
Toddler: 13-23 months
•
Preschool: 2-5 years
•
School age: 6-11 years
•
Adolescent: 12-18 years
Thinking about
our care…
• You must consider a child’s
developmental stage and
the unique features of each
stage
• Care must be appropriate to
each developmental age
• Unique physiological aspects
of each age group and
patient must also be
considered
What are our major anesthesia
differences?
Airway
•
Children have larger tongues
•
Larger heads and shorter
necks, larger occiput
•
Larynx is at C 3-4 level
•
Larger epiglottis, that is
narrower and elongated
•
Infant’s vocal cords slanted
posterior and cephalad
•
Anterior airway more prone to
injury
•
Narrowest part is cricoid
cartilage (until 5 years old)
Major Lung Differences
•
Rapid breathing rate and increased alveolar
ventilation
•
Prone to rapid desaturation due to high oxygen
consumption
•
Small FRC, fast inhalation induction
•
Prone to atelectasis closing capacity may exceed
FRC
•
Lung matures at 8 years old
•
Increased chest compliance
•
Herring-Breuer reflex- deep breath and kids stop
breathing and vagal negative feedback loop via
vagus nerve
Major Cardiac Differences
• High CO
• HR dependent
• Non-compliant heart
• Avoid air bubbles due to
possible PFO
• Vagal dominant and
unopposed
Thermoregulation
Hypothermia
• Defined as a core
temperature below 35
degrees centigrade
• Asystole occurs at 30
degrees centigrade
Pediatric Thermoregulation
• Adults use shivering to
increase heat production
(increases O2
consumption, CO2
production, and CO)
• Shivering is inefficient in
young children
• Non-shivering
thermogenesis
Non-shivering thermogenesis
•
Cold induced O2
consumption and heat
production
• Primary means in infants to
produce heat
• Utilize brown fat- rich in
mitochondria, dense capillary
network, and innervated by
SNS nerve endings
• Brown fat is 6% of neonates
total body weight
How it works…..
• When norepinephrine is
stimulated by SNS,
triglycerides are
hydrolyzed to fatty acids
and glycerol with heat
being released from
enhanced oxygen
consumption
Other Differences
• Body surface area
(BSA) to body mass is
very high
• Infant’s head is 20% of
BSA and contributes to
40% of heat loss
• Rapid heat loss
Mechanisms of Heat Loss
• Evaporation
• Conduction
• Convection
• Radiation
Evaporation
• The energy of heat is
• How to counteract this:
consumed in the conversion
• Humidified circuits
of water to vapor
• Run lower gas flows
• Example: sweating and
respiration
• Accounts for approximately
22% of heat loss (combined
with convection)
Conduction
• The transfer of heat energy
due to a temperature gradient
• Example: skin touching metal
OR table
• Accounts for approximately
15% of heat loss (combined
with convection)
• Pediatric patients have a
thinner layer of subQ fat so
more heat is lost though
conduction
• Ways to counteract this loss:
• No skin to metal contact
• Irrigation solution warmed
• Warm IV fluids
Convection
• The warmed air or water
must be moved away from
the skin surface by currents
• Example: laminar air flow in
OR
• Accounts for approximately
15% of heat loss (combined
with conduction)
• Ways to counteract this:
• Limit air flow across patient
• Warming blankets above
and below patient
Radiation
• Heat from core body tissues is
• Ways to counteract this:
transported in blood to
• Keep patient covered
subcutaneous vessels, where
• Warming blankets
heat is lost to the environment
• Keep room temperature
through radiation.
elevated
• Accounts for approximately 60%
of heat loss
• Major form of heat loss in
surgical patients
•
The research says….
• Esophagus, nasopharynx
• Best to use a warmer
or rectum (highly
ambient room
perfused tissues, the
temperature and
temperature of which is
warming blankets
uniform and high in
• Pre-warming proved
beneficial in studies
comparison with the rest
of the body) best for
measurement
Effect of General Anesthesia
• With GA there is a
redistribution of heat from
core to periphery as a result
of vasodilation
• Anesthetic inhibits
vasoconstriction
• With GA heat production is
decreased by 30%
• See a rapid decrease in core
body temperature
Risk with hypothermia
•
After cold exposure infant’s metabolic
•
acidosis
rate increases
•
Vasoconstriction (in un-anesthetized
Cellular hypoxia and metabolic
•
Pulmonary vasoconstriction= right to
left shunting if PFO or ductus present
child)
•
Worsening hypoxia
Additional Risks with
Hypothermia
• Adverse cardiac events
• Prolonged stay in the recovery room and hospital
• Delayed surgical wound healing and higher infection
rates
• Cold-induced coagulation dysfunction
• Prolonged drug metabolism
Hyperthermia
• Elevated body temperature
due to failure of
thermoregulation or other
disorder
• Heat stroke
• Adverse reaction to drugs,
such as malignant
hyperthermia
Case Discussion
History
• 4 month old male
• Wt. 6.48 kg
• NKDA
• No past surgical HX
• No medications
• HX of trigonocephaly and
premature birth
• No family HX of surgery
Surgical procedure
• Craniosynostosis
• GA with ETT
• Anticipation of large blood loss
Anesthetic plan
• No premedication (child calm)
• Remi and precedex gtts used
• Inhalation induction with N2O
• 0.9% NS and LR infusing
and sevo
• Maintained on Sevoflurane
• Intubation with ETT
• Upper body blanket placed
• Rectal temp placed
on infant, in addition to
• 22g, 24g, and 20g IV placed
under body blanket
• A-line placed (took quite a long
time)
• Infant on under body blanket,
heated circuit used, and room
temperature increased
Case progression
•
90 minutes into case
•
HR increased to 150s
•
BP slight increase
•
O2 saturation decreased to 97%
•
EtCO2 gradually increasing to a
peak of 53 (unresponsive to changes
in ventilation)
•
Temp. increasing 0.1 degree Celsius
at a time (child hypothermic to
begin 33 degrees Celsius)
•
See next slide for graphic
Differential Diagnosis
• Gave fentanyl and remi
boluses to assure child
was not too light
• No change in EtCO2 in
ventilation changes
• ETT in good position
and not obstructed
• MALIGNANT
HYPERTHERMIA!!!!
Labs
time
1013
1112
1129
1200
1448
ph
7.29
7.17
7.29
7.21
7.39
CO2
48
60
39
51
38
O2
97
71
250
393
419
K
3.6
5.1
5.1
3.7
4.0
temp
33.5
38.1
37.2
35.0
Bicarb
22.3
19.4
19.3
19.3
23.6
FiO2
60
100
100
100
100
Ca
1.26
1.24
1.55
1.40
1.45
time
1130
1357
1911
0116
0500
0841
2350
0438
CK
155
192
197
245
199
202
213
83
Myoglobin in urine: negative
Treatment
• Remi and precedex gtts ran as
• Call for help!!!!
• Sevo stopped, flows increased
• CO2 absorber and circuit changed
• Ice applied to infant, warming
blankets turned off, and room
temp decreased
anesthetic agents
• Calcium chloride given
• MHAUS called and assisted in
treatment plan
• Emergency algorithm guide used
• Dantrolene 2.5 mg/kg initial dose
• Versed given
• Insulin R
• Subsequent doses of Dantrolene
• Dextrose
• Gtts changed to plasma-lyte
given at 1.5 mg/kg then 1 mg/kg
• Child transferred to PICU and
remained on ventilator
Malignant Hyperthermia
• Autosomal dominant genetic
disorder of ryanodine receptor
gene (RYR1)
• Causes uncontrolled increase in
skeletal muscle oxidative
metabolism, overwhelming
oxygen supply and removal of
carbon dioxide, this reaction
releases heat and causes acidosis
and circulatory collapse
• Triggers: volatile anesthetic
gases, succinylcholine, and stress
• Signs/symptoms: elevated
temperature, increases HR,
increased RR, acidosis, hypoxia,
rigid muscles, rhabdomyolysis,
myoglobin in urine, CK elevation
Differences in pediatrics
•
A study analyzed 264 records: 35 in
•
in the middle age cohort.
the youngest age group (0-24
months), 163 in the middle age group
•
Masseter spasm was more common
•
The youngest age cohort was more
(25 months- 12 years), and 66 in the
likely to develop skin mottling and
oldest group (13-18 years).
was approximately half as likely to
Sinus tachycardia, hypercarbia, and
develop muscle rigidity. The
rapid temperature increase were
youngest age group also
more common in the oldest age
demonstrated significantly higher
cohort. Higher maximum
peak lactic acid levels and lower peak
temperatures and higher peak
CK values. The youngest subjects
potassium values were seen in the
had greater levels of metabolic
oldest age cohort.
acidosis.
(Nelson, 2013)
A Published Case Report
The Case:
•
7-year-old boy with cholesteatomas
underwent tympanoplasty.
•
Three previous anesthetics with
sevoflurane induction and maintenance
with propofol infusion were not associated
with MH symptoms.
Discussion:
•
MH-susceptible patient responds
differently to various agents
•
Atypical MH forms are problematic
•
It is possible that the speed of onset
reflects the rate of increase of the
intracellular Ca2+ concentration, which
depends on the particular drug used, its
•
No family history of MH or muscle disease
•
A minor rise of end tidal CO2
of physiological variables that dictate the
•
Increased rectal temperature
efficacy of Ca2+ homeostatic processes in
•
Rhabdomyolysis and his father’s positive
each patient.
IVCT results
concentration in muscles and any number
(BONCIU, 2007)
Another Case Report
•
Two cases of MH triggered by sevoflurane:
•
First Case: 6 year old girl stabismus repair 30 min after induction, etCO2 was over
60 mmHg. Muscle rigidity of legs and elevation in temperature. Maximum
esophageal temperature was noted to be 40.4 degrees Celsius. CK was 252 postop and 1690 the next day.
•
Second Case: 1 year and 9 month boy undergoing accessory ear resection.
Sevoflurane used. 40 min after induction temperature was 38.6 degrees Celsius,
HR 191, and oxygen saturation 93%. Muscle rigidity of the legs was noted.
Highest temperature was 39.3 degrees Celsius. Both parents had no history of
MH.
(Kinouchi,2001)
Take Home Message
• Kids can present with
MH differently than
adults
• If MH is suspected treat
with MH protocols
• Early interventions
have the best outcomes
References
•
CASSEY , J., KING, R., & ARMSTRONG , P. (2009). Is there thermal benefit from preoperative warming in
children?. Pediatric Anesthesia, 20(1), 63-71. Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/j.14609592.2009.03204.x/abstract
•
Díaz, M., & Becker, D.(2010). Thermoregulation: Physiological and clinical considerations during sedation and
general anesthesia. Anesthesia Progress, 57(1), 25-33. Retrieved from
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844235/
•
Pearce, B., Christensen, R., & Voepel-Lewis, T. (n.d.). Perioperative hypothermia in the pediatric population:
Prevalence, risk factors and outcomes. Journal of Anesthesia & Clinical Research, 1(1), 1-4. Retrieved from
http://www.omicsonline.org/2155-6148/2155-6148-1-102.pdf
•
Sessler, D. (2011). Temperature monitoring: Consequences and prevention of mild perioperative hypothermia.
American Society of Anesthesiologists, 109, 1-7.
References
•
BONCIU, M., DE LA CHAPELLE, A., DELPECH, H., DEPRET, T., KRIVOSIC-HORBER, R., & AIMÉ, M.
(2007). Minor increase of endtidal CO2 during sevoflurane-induced malignant hyperthermia.
Pediatric Anesthesia, 17(2), 180-182. doi:10.1111/j.1460-9592.2006.02051.
•
Kinouchi, K., Okawa, M., Fukumitsu, K., Tachibana, K., Kitamura, S., & Taniguchi, A. (2001). [Two
pediatric cases of malignant hyperthermia caused by sevoflurane]. Masui. The Japanese Journal Of
Anesthesiology, 50(11), 1232-1235.
•
Nelson, P., & Litman, R. (2013). Malignant Hyperthermia in Children: An Analysis of the North
American Malignant Hyperthermia Registry. Anesthesia And Analgesia.
Thank You
Questions?