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

consumed in the conversion of water to vapor

• Example: sweating and respiration

• Accounts for approximately 22% of heat loss (combined with convection)

• How to counteract this:

• Humidified circuits • Run lower gas

flows

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 transported in blood to subcutaneous vessels, where heat is lost to the environment through radiation.

• Accounts for approximately 60% of heat loss

• Major form of heat loss in surgical patients

• Ways to counteract this:• Keep patient covered• Warming blankets• Keep room temperature

elevated

•

The research says….• Best to use a warmer

ambient room temperature and warming blankets

• Pre-warming proved beneficial in studies

• Esophagus, nasopharynx or rectum (highly perfused tissues, the temperature of which is uniform and high in 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 rate increases• Vasoconstriction (in un-

anesthetized child)

• Cellular hypoxia and metabolic acidosis

• Pulmonary vasoconstriction= right to left shunting if PFO or ductus present

• 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)• Inhalation induction with N2O

and sevo • Intubation with ETT • Rectal temp placed• 22g, 24g, and 20g IV placed• A-line placed (took quite a

long time)• Infant on under body blanket,

heated circuit used, and room temperature increased

• Remi and precedex gtts used

• 0.9% NS and LR infusing • Maintained on Sevoflurane • Upper body blanket placed

on infant, in addition to under body blanket

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• Call for help!!!!• Sevo stopped, flows increased• CO2 absorber and circuit

changed• Ice applied to infant, warming

blankets turned off, and room temp decreased

• Dantrolene 2.5 mg/kg initial dose• Insulin R • Dextrose • Gtts changed to plasma-lyte

• Remi and precedex gtts ran as anesthetic agents

• Calcium chloride given• MHAUS called and assisted in

treatment plan• Emergency algorithm guide

used • Versed given • Subsequent doses of

Dantrolene 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

the youngest age group (0-24 months), 163 in the middle age group (25 months- 12 years), and 66 in the oldest group (13-18 years).

• Sinus tachycardia, hypercarbia, and rapid temperature increase were more common in the oldest age cohort. Higher maximum temperatures and higher peak potassium values were seen in the oldest age cohort.

• Masseter spasm was more common in the middle age cohort.

• The youngest age cohort was more likely to develop skin mottling and was approximately half as likely to develop muscle rigidity. The youngest age group also demonstrated significantly higher peak lactic acid levels and lower peak CK values. The youngest subjects had greater levels of metabolic acidosis.

(Nelson, 2013)

A Published Case ReportThe 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.

• No family history of MH or muscle disease

• A minor rise of end tidal CO2 • Increased rectal temperature• Rhabdomyolysis and his father’s

positive IVCT results

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 concentration in muscles and any number of physiological variables that dictate the efficacy of Ca2+ homeostatic processes in each patient.

(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 post-op 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.1460-9592.2009.03204.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 YouQuestions?