Anesthesia and Austism Spectrum Disorders

[Guest guest]

The two abstracts below are offered, with permission, from the files of the CK2

group

files. You may want to show this email to and discuss with DENTISTS, SURGEONS,

ANESTHETISTS, & DOCTORS who are going to work with your children.

Please note that under the more extreme article Dr Erbe is quoted as saying, " I

don't

think these results should cause panic among the general public, "

The important lessons are that B-12 and methionine can be dangerously depleted

by

Nitrous Oxide and it looks like a good idea to be aware of the patient's levels.

Many

parents are finding methylcobalamin injections and other supplementation to

support

methionine metabolism are important therapies in their ASD child precisely

because

there seems to be some metabolic (even genetic) fragility or dependance which

needs

to be taken into account.. For families who already know their MTHFr status this

should

be a wake-up call.

HTH - someone's child get painless - and safe - help.

...

> I have been reading a lot of post about anesthesia problems. I am a

> nurse anesthetist. Hopefully I can explain a few things to everyone.

>

> Our children are deficient in B12. When we start the B12 shots, most

> of us see great improvement in our children. Do a Google search on

> B12 and nitrous oxide. Inhaling nitrous can deplete B12. It seems to

> start to cause problems after 30 minutes of exposure and with multiple

> exposures.

>

> Where I practice, this is how we take care of children. Usually for a

> pre-op we give them Versad in some grape juice. (Versad is a

> valium-type drug that relaxes you and makes you forget.) Then the

> children are brought to the operating room and a mask is placed on

> their face. High flow of nitrous, O2 and Sevoflourane ( Halothane is

> not used anymore) are used to get the child asleep and then an IV is

> started. Nitrous is usually given for the whole case. When an adult

> is given a general anesthetic, they have an IV. Diprivan( a

> pentothal-type drug) is used for induction of anesthesia, and Versad

> and a narcotic are usually given. Anesthesia is maintained with either

> of the gases Sevoflourane or Suprane. If the case is short we can use

> just Diprivan given IV as the anesthetic. There are many ways to do an

> anesthetic but this is just the basics.

>

> My advice if your child has to have an anesthetic is to ask to speak to

> the anesthesia personnel before you go to the hospital. Stress to them

> that your child has a B12 deficiency and to limit the use of nitrous.

> Tell them there are reports of serious regressions after anesthetics.

> If they cannot start an IV on your child, they can give nitrous for

> just a few minutes and then turn it off, or not use it at all and just

> give oxygen with the gas. In my practice I have stopped giving

> nitrous to my adults because of the link to nausea.

>

> About the MTHFR gene...well, we all cannot go out and get genetic

> testing, but we can assume we have a defect in folate metabolism. Last

> year I started having numbness in my hands and face. The MRI was

> negative and no one could tell me what was wrong. From my own research

> I thought it was from being exposed to the nitrous for over 20 years.

> I found that I got numbness when I would be in a room doing children

> all day. Since then I avoid doing children. My doctor also put me on

> folic acid for a high homocystine level. I am now also on B12.

> Unfortunately mainstream medicine does not link autism and B12. They

> still think it is a deficiency of Ritallin or Resperidal.

> I hope this helps.

>

Arch Dis Child 2001;85:510 ( December )

Letters to the editor

Nitrous oxide and vitamin B12

EDITOR,

----------

The paper by Kanagasundaram et al1 on the use of nitrous oxide to

alleviate pain and anxiety during painful procedures fails to mention

the effect of this gas on cobalamin metabolism. Nitrous oxide

inactivates cobalamin (1), the active derivative of vitamin B12 and

essential cofactor for the transfer of the methyl group from

methyltetrahydrofolate to homocysteine to form methionine. For subjects

with good body stores of cobalamin this effect is unimportant, but

no-one using this agent should remain unaware of the potentially

devastating complications in the nervous system of using nitrous oxide

in subjects who are of borderline or deficient vitamin B12 status.

Onset of subacute combined degeneration affecting the brain and spinal

cord is a well documented event when individuals with low body stores

of cobalamin are exposed to nitrous oxide.(2)

There is a long list of situations which put children at special risk

of cobalamin deficiency

----------

for example, diets low in animal products, synthetic feeding of any

description, small bowel malfunction, any prolonged illness with

disturbance of feeding behaviour, especially if combined with increased

metabolic demands

----------

for example, systemic malignancy or chemotherapy. Children with chronic

conditions often need painful procedures, and depleted cobalamin stores

may not be apparent unless measurements of serum B12 are made

routinely. What is more, repeated use of nitrous oxide depletes the

body stores of cobalamin even in well people.

Given the scale of use which would result from routine use of nitrous

oxide in children undergoing painful procedures, there should be real

concern about the potential for an accident in a child with occult

cobalamin deficiency. The message must be: never forget vitamin B12

when thinking of using nitrous oxide.

ISABEL SMITH

Clinical Audit Department, Great Ormond Street Hospital, Great Ormond

Street, London WC1N 3JH, smithi@g...

References

1.

Kanagasundaram SA, Lane LJ, Cavaletto BP, et al. Efficacy and safety

of nitrous oxide in alleviating pain and anxiety during painful

procedures. Arch Dis Child 2001;84:492-495[Abstract/Free Full Text].

2.

Lee P, I, Piesowicz A, et al. Spastic parapareisis after

anaesthesia. Lancet 1999;353:554[Medline].

© 2001 by Archives of Disease in Childhood

=============================================

check methionine before giving nitrous oxide anesthesia to our kids

Nitrous Oxide Anesthesia Implicated in Death of Child With MTHFR

Deficiency

By J. Brown, MD

NEW YORK (Reuters Health) Jul 02 - Nitrous oxide anesthesia

administered to a child born with an undiagnosed deficiency in a

key metabolic enzyme appears to have caused the child's death,

according to a report published in the July 3rd issue of The New

England Journal of Medicine.

The deficient enzyme, 5,10-methlyenetetrahydrofolate reductase

(MTHFR), is involved in the metabolism of folate and in the

production of methionine, which is needed for a variety of

important biochemical reactions, senior author Dr. Kirk Hogan,

from the University of Wisconsin in Madison, and colleagues

note.

In the current case, because of the enzyme deficiency, the child

probably had baseline methionine levels that, although low, were

survivable. Unfortunately, in this situation treatment with

nitrous oxide, an agent known to block methionine synthesis,

may have resulted in fatally low levels.

The case involved a male infant who appeared normal until 3 months of

age when he presented with a mass in the left leg. Excisional biopsy of

the lesion was performed under anesthesia that included nitrous oxide.

The procedure lasted 45 minutes and the pathology results indicated

fibrosarcoma.

The child was taken back to the OR four days later for complete

resection of the mass. Once again, nitrous oxide-containing anesthesia

was administered, but this time the procedure lasted 270 minutes. Still,

the patient was discharged on postoperative day 7 in seemingly good

health.

Seventeen days after discharge, the infant was admitted to the

hospital with seizures and apnea episodes. The patient was found to

be severely hypotonic and CT scan revealed generalized brain atrophy

with enlarged prepontine and medullary cisterns. In addition, plasma

methionine levels were low, while homocysteine levels were elevated-

-both findings consistent with a MTHFR deficiency.

Forty-six days after surgery, the infant died after respiratory arrest.

Postmortem examination showed extensive damage to the

central nervous system.

Although it was not known at the time of surgery, two of the child's

relatives had elevated homocysteine levels. However, none had ever

been treated with nitrous oxide.

The case was initially reported in 1987, but at that time the

technology was not available to test for MTHFR activity or for

mutations in the corresponding gene, Dr. W. Erbe, co-author

of a related editorial, told Reuters Health.

When Dr. Hogan's team went back and tested fibroblast samples from the

patient and his family, they found a novel MTHFR mutation associated

with severely decreased enzyme activity.

" I don't think these results should cause panic among the general

public, " Dr. Erbe, from the University at Buffalo, noted. " There were

clues in this particular case that suggested a problem before the

nitrous oxide was given, " he added.

Moreover, the MTHFR mutation in the current case appears to be

rather rare,

Dr. Erbe said. " There is a MTHFR mutation that is present in up to

50% of the population, but there is no evidence that nitrous oxide

is unsafe for carriers of this mutation. "

However, in children with developmental delay or altered homocysteine

metabolism, methionine levels should be determined before using

nitrous oxide-containing anesthesia, he noted.

Carcinogenesis. 2003 Jun;24(6):1097-103. Epub 2003 Apr 24.

Folate status, metabolic genotype, and biomarkers of genotoxicity in

healthy subjects.

[Guest guest]

Just wanted to say, thank you for sending this in..my daughter is scheduled to

get dental work done tomorrow..she'll be going under general anethesia for the

work.

[Guest guest]

A parent mentioned " sweet air " . This can mean nitrous oxide. Thus the long

reply.

The two abstracts below are offered, with permission, from the files of the CK2

group

files. Thanks to, " A " and Sym!!

Please note that under the more extreme article Dr Erbe is quoted as saying, " I

don't

think these results should cause panic among the general public, "

The important lessons are that B-12 and methionine can be dangerously depleted

by

Nitrous Oxide and it looks like a good idea to be aware of the patient's levels.

Many

parents are finding methylcobalamin injections and other supplementation to

support

methionine metabolism are important therapies in their ASD child precisely

because

there seems to be some metabolic (even genetic) fragility or dependance which

needs

to be taken into account.. For families who already know their MTHFR status this

should

be a wake-up call.

The long post below is not written by me. I am not the anesthesia nurse. I got

permission to

send this. I would read it carefully, copy it, and talk it over with my child's

healthcare provider.

HTH - someone's child get painless - and safe - help.

...

> I have been reading a lot of post about anesthesia problems. I am a

> nurse anesthetist. Hopefully I can explain a few things to everyone.

>

> Our children are deficient in B12. When we start the B12 shots, most

> of us see great improvement in our children. Do a Google search on

> B12 and nitrous oxide. Inhaling nitrous can deplete B12. It seems to

> start to cause problems after 30 minutes of exposure and with multiple

> exposures.

>

> Where I practice, this is how we take care of children. Usually for a

> pre-op we give them Versad in some grape juice. (Versad is a

> valium-type drug that relaxes you and makes you forget.) Then the

> children are brought to the operating room and a mask is placed on

> their face. High flow of nitrous, O2 and Sevoflourane ( Halothane is

> not used anymore) are used to get the child asleep and then an IV is

> started. Nitrous is usually given for the whole case. When an adult

> is given a general anesthetic, they have an IV. Diprivan( a

> pentothal-type drug) is used for induction of anesthesia, and Versad

> and a narcotic are usually given. Anesthesia is maintained with either

> of the gases Sevoflourane or Suprane. If the case is short we can use

> just Diprivan given IV as the anesthetic. There are many ways to do an

> anesthetic but this is just the basics.

>

> My advice if your child has to have an anesthetic is to ask to speak to

> the anesthesia personnel before you go to the hospital. Stress to them

> that your child has a B12 deficiency and to limit the use of nitrous.

> Tell them there are reports of serious regressions after anesthetics.

> If they cannot start an IV on your child, they can give nitrous for

> just a few minutes and then turn it off, or not use it at all and just

> give oxygen with the gas. In my practice I have stopped giving

> nitrous to my adults because of the link to nausea.

>

> About the MTHFR gene...well, we all cannot go out and get genetic

> testing, but we can assume we have a defect in folate metabolism. Last

> year I started having numbness in my hands and face. The MRI was

> negative and no one could tell me what was wrong. From my own research

> I thought it was from being exposed to the nitrous for over 20 years.

> I found that I got numbness when I would be in a room doing children

> all day. Since then I avoid doing children. My doctor also put me on

> folic acid for a high homocystine level. I am now also on B12.

> Unfortunately mainstream medicine does not link autism and B12. They

> still think it is a deficiency of Ritallin or Resperidal.

> I hope this helps.

Arch Dis Child 2001;85:510 ( December )

Letters to the editor

Nitrous oxide and vitamin B12

EDITOR,

----------

The paper by Kanagasundaram et al1 on the use of nitrous oxide to

alleviate pain and anxiety during painful procedures fails to mention

the effect of this gas on cobalamin metabolism. Nitrous oxide

inactivates cobalamin (1), the active derivative of vitamin B12 and

essential cofactor for the transfer of the methyl group from

methyltetrahydrofolate to homocysteine to form methionine. For subjects

with good body stores of cobalamin this effect is unimportant, but

no-one using this agent should remain unaware of the potentially

devastating complications in the nervous system of using nitrous oxide

in subjects who are of borderline or deficient vitamin B12 status.

Onset of subacute combined degeneration affecting the brain and spinal

cord is a well documented event when individuals with low body stores

of cobalamin are exposed to nitrous oxide.(2)

There is a long list of situations which put children at special risk

of cobalamin deficiency

----------

for example, diets low in animal products, synthetic feeding of any

description, small bowel malfunction, any prolonged illness with

disturbance of feeding behaviour, especially if combined with increased

metabolic demands

----------

for example, systemic malignancy or chemotherapy. Children with chronic

conditions often need painful procedures, and depleted cobalamin stores

may not be apparent unless measurements of serum B12 are made

routinely. What is more, repeated use of nitrous oxide depletes the

body stores of cobalamin even in well people.

Given the scale of use which would result from routine use of nitrous

oxide in children undergoing painful procedures, there should be real

concern about the potential for an accident in a child with occult

cobalamin deficiency. The message must be: never forget vitamin B12

when thinking of using nitrous oxide.

ISABEL SMITH

Clinical Audit Department, Great Ormond Street Hospital, Great Ormond

Street, London WC1N 3JH, smithi@g...

References

1.

Kanagasundaram SA, Lane LJ, Cavaletto BP, et al. Efficacy and safety

of nitrous oxide in alleviating pain and anxiety during painful

procedures. Arch Dis Child 2001;84:492-495[Abstract/Free Full Text].

2.

Lee P, I, Piesowicz A, et al. Spastic parapareisis after

anaesthesia. Lancet 1999;353:554[Medline].

© 2001 by Archives of Disease in Childhood

=============================================

check methionine before giving nitrous oxide anesthesia to our kids

Nitrous Oxide Anesthesia Implicated in Death of Child With MTHFR

Deficiency

By J. Brown, MD

NEW YORK (Reuters Health) Jul 02 - Nitrous oxide anesthesia

administered to a child born with an undiagnosed deficiency in a

key metabolic enzyme appears to have caused the child's death,

according to a report published in the July 3rd issue of The New

England Journal of Medicine.

The deficient enzyme, 5,10-methlyenetetrahydrofolate reductase

(MTHFR), is involved in the metabolism of folate and in the

production of methionine, which is needed for a variety of

important biochemical reactions, senior author Dr. Kirk Hogan,

from the University of Wisconsin in Madison, and colleagues

note.

In the current case, because of the enzyme deficiency, the child

probably had baseline methionine levels that, although low, were

survivable. Unfortunately, in this situation treatment with

nitrous oxide, an agent known to block methionine synthesis,

may have resulted in fatally low levels.

The case involved a male infant who appeared normal until 3 months of

age when he presented with a mass in the left leg. Excisional biopsy of

the lesion was performed under anesthesia that included nitrous oxide.

The procedure lasted 45 minutes and the pathology results indicated

fibrosarcoma.

The child was taken back to the OR four days later for complete

resection of the mass. Once again, nitrous oxide-containing anesthesia

was administered, but this time the procedure lasted 270 minutes. Still,

the patient was discharged on postoperative day 7 in seemingly good

health.

Seventeen days after discharge, the infant was admitted to the

hospital with seizures and apnea episodes. The patient was found to

be severely hypotonic and CT scan revealed generalized brain atrophy

with enlarged prepontine and medullary cisterns. In addition, plasma

methionine levels were low, while homocysteine levels were elevated-

-both findings consistent with a MTHFR deficiency.

Forty-six days after surgery, the infant died after respiratory arrest.

Postmortem examination showed extensive damage to the

central nervous system.

Although it was not known at the time of surgery, two of the child's

relatives had elevated homocysteine levels. However, none had ever

been treated with nitrous oxide.

The case was initially reported in 1987, but at that time the

technology was not available to test for MTHFR activity or for

mutations in the corresponding gene, Dr. W. Erbe, co-author

of a related editorial, told Reuters Health.

When Dr. Hogan's team went back and tested fibroblast samples from the

patient and his family, they found a novel MTHFR mutation associated

with severely decreased enzyme activity.

" I don't think these results should cause panic among the general

public, " Dr. Erbe, from the University at Buffalo, noted. " There were

clues in this particular case that suggested a problem before the

nitrous oxide was given, " he added.

Moreover, the MTHFR mutation in the current case appears to be

rather rare,

Dr. Erbe said. " There is a MTHFR mutation that is present in up to

50% of the population, but there is no evidence that nitrous oxide

is unsafe for carriers of this mutation. "

However, in children with developmental delay or altered homocysteine

metabolism, methionine levels should be determined before using

nitrous oxide-containing anesthesia, he noted.

Carcinogenesis. 2003 Jun;24(6):1097-103. Epub 2003 Apr 24.

Folate status, metabolic genotype, and biomarkers of genotoxicity in

healthy subjects.