RESPONSE TO NUTHALL ARTICLE
Dear Sirs:
We read the recent contribution to your esteemed journal by Nuthall,
et al (1) with extreme disappointment. Unfortunately, this article
distorts the true complication rate of low-pressure hyperbaric oxygen
therapy (LPHBOT) in the treatment of pediatric neurological conditions.
Noticeably missing from the paper is an estimate of the frequency with
which these complications occur. Without such perspective this article
misleads the medical community and fuels the unfounded fear that LPHBOT is
dangerous for children with cerebral palsy, when in fact it is both safe
and an extremely useful adjunctive therapy.
The first case mentioned in the article, vomiting with aspiration, is
a complication that can occur in an adult or pediatric patient with
gastroesophageal reflux in many medical settings, hyperbaric or
normobaric. Unfortunately, the article does not give enough information
for a critical appraisal of the patient’s care. Air swallowing at
anytime, but especially during an HBO treatment, can lead to gastric
distention which can worsen on ascent. It is easily avoided by simple
venting in patients with feeding tubes. The “tight-fitting” oxygen hood
implies neck constriction, but the hood used in multiplace chambers
throughout the United States and Canada in fact utilizes a comfortably
fitting latex neck dam. A competent attendant can easily remove the hood
if needed and suction should be available in the chamber. Aspiration is a
rare complication of HBOT, but does occur in the ill adult population. To
put the matter in perspective in the pediatric population, since the first
HBOT for a CP child in North America in 1992 (2) authors PGH and RAN have
logged over 35,000 treatments on brain injured children without a single
case of primary aspiration or air embolism. Approximately 7,000 of these
treatments were performed on an IRB-approved protocol. The point is that
this case report represents a very rare event indeed, and most likely a
completely avoidable one in a setting of adequate care. We believe the
slight risk is acceptable given the positive responses in the vast
majority of children treated.
The second case is an unfortunate example of an acutely ill child who
should have been denied treatment by proper pre-treatment evaluation the
day of the accident. The authors attribute the child’s cerebral infarct
to an oxygen embolism caused by primary arterial bubbles during
decompression or venous oxygen bubbles breaching the pulmonary filter or a
patent foramen ovale (PFO). In our opinion this diagnosis is exceedingly
unlikely, the mechanisms suggested by the authors nearly impossible to
account for their diagnosis, and their argument not supported by the
references cited. Primary arterial bubbles of any gas are only seen in
explosive decompressions (3). No such scenario is described in the
article. Primary venous bubbles occur in almost all decompressions, but
oxygen decompression sickness, and presumably bubbles, have only been
documented in animals at 3.53 atmospheres absolute (ATA) of oxygen (4)
which is over two times the oxygen exposure of this patient.
Furthermore, venous bubbles of any gas will form in proportion to the gas
load of the dive. This patient’s dive, 1.5 ATA, is a very shallow
exposure which would produce minimal or no bubbles. Venous bubbles that
do form during decompression have been measured to be mostly 19 to 180
microns with some larger bubbles upto 700 microns (5). While it is
possible for the bubbles to breach insulted lungs (parainfluenza induced
respiratory failure) or proceed through a PFO to cause an infarct they
would have to selectively coalesce and be retained in the much larger MCA.
This is highly unlikely, given the argument above and the fact that oxygen
bubbles should be readily metabolized, and hence transient.
Lastly, the two references cited to justify two of the proposed
mechanisms don’t apply to this case; both are articles on iatrogenic air
embolism (6, 7) and/or pulmonary barotrauma (6). In addition, the Muth
article (6) contradicts the authors’ mechanisms by stating, “Cerebral
arterial gas embolization typically involves the migration of gas to small
arteries (average diameter, 30 to 60 microns).” The MCA is much larger in
a 10 month old child. Muth further states that all patients with clinical
symptoms of arterial gas embolism should receive recompression treatment
with hyperbaric oxygen. To attribute this child’s cerebral infarct to an
oxygen embolism by any mechanism is nearly impossible. More likely, this
infarct was the result of a vasospastic event, fat embolism from infected
marrow, or some other etiology related to the child’s concurrent
infection.
Patient safety is paramount and we believe that physician attended
HBOT is mandatory. The Nuthall article begs the greater question of why
patients are driven to non-physician attended facilities to obtain medical
treatment. The British Columbia College of Physicians and Surgeons (8)
and an ex-president of the Undersea and Hyperbaric Medical Society (UHMS)
purportedly speaking for the UHMS (9) have now forbidden and threatened
doctors, respectively, should they treat non-UHMS approved pediatric
neurological disease with HBOT. This is a dangerous and intolerable
precedent. Off-label use of any FDA approved device or drug by a
qualified ethical physician constitutes the legal practice of medicine.
It is to the medical profession’s embarrassment that families are forced
to seek care from facilities which may be ill-equipped or staffed by
personnel who lack medical training.
The call for a randomized controlled trial, while desired, strikes a
loud and clear double standard. There exists far more evidence to support
cerebral palsy as a UHMS HBOT “accepted indication”(10) than existed for
cerebral abscess, the last indication added to the list in 1996. In
addition, reviews of the accepted indications list by author PGH in 1998
for a presentation at the Advanced Topics Course in Hyperbaric
Medicine(11), by evaluators for the Calgary Regional Health Authority in
1999 (12), and Blue Cross/Blue Shield in 2000 (13) found that as many as 6
-7 of the accepted thirteen diagnoses are not supported by either
controlled clinical trials and/or adequate research. The statement by the
Nuthall article that neither they nor the UHMS can recommend HBOT for CP
in the absence of randomized (Nuthall) controlled (UHMS and Nuthall)
clinical trials is inconsistent.
In conclusion, we must correct the Nuthall article’s frightening
implication and inform the medical community that low-pressure HBOT for
pediatric brain injury is a very low risk medical treatment, supported by
our combined experience of greater than 35,000 patient treatments.
Thank you,
Paul G. Harch, M.D.
Hyperbaric Medicine Fellowship Director
Clinical Assistant Professor
Department of Medicine
Section of Emergency and Hyperbaric Medicine
LSU School of Medicine
New Orleans, Louisiana
Jamie Deckoff-Jones, M.D.
New England Hyperbaric Center
Great Barrington, Massachusetts
Richard A. Neubauer. M.D.
Ocean Hyperbaric Center
Lauderdale-by-the-Sea, Florida
References:
1. Nuthall G, et al. Electronic article: Hyperbaric Oxygen Therapy
for Cerebral Palsy; Two Complications of Treatment. Pediatrics,
12/2000:106(6);e80-85.
2. Harch PG, et al. HMPAO SPECT Brain Imaging and Low Pressure HBOT
in the Diagnosis and Treatment of Chronic Traumatic, Ischemic, Hypoxic,
and Anoxic Encephalopathies. Undersea Hyper Med, 6/1994;21(Suppl):30.
3. Hills BA. Decompression Sickness, Volume 1: The Biophysical
Basis of Prevention and Treatment. John Wiley and Sons, New York, 1977.
P.65
4. Vann RD, Thalmann ED. Chapter 14, Decompression Physiology and
Practice, p.396. The Physiology and Medicine of Diving, 4th Edition.
Editors Bennett and Elliott. W. B. Saunders Co, Ltd., London, 1993.
5. Hills BA, Butler BD. Size Distribution of Intravascular Air
Emboli Produced by Decompression. Undersea Biomed Res, 9/1981;8(3):163-
170.
6. Muth CM, Shank ES. Gas Embolism. New England Journal of
Medicine, 2/17/2000;342(7):476-482.
7. Murphy BP, et al. Cerebral Air Embolism Resulting from Invasive
Medical Procedures. Ann Surg, 1985;201:242-245.
8. Locklear KR. College of Physicians and Surgeons of British
Columbia Announce Standards for Non-Hospital Medical Hyperbaric Oxygen
Facilities. Hyper Med Today, 2000;1(2):20-21.
9. Kindwall EW. Research in Hyperbaric Medicine. Hyper Med Today,
2000;1(1):10-12.
10. Harch PG. McGill University Pilot Study of HBOT in the Treatment
of Spastic Diplegia Cerebral Palsy. Hyper Med Today, August-September,
2000;1(3):44-45, and 49.
11. Harch PG. Hyperbaric Oxygen Therapy in Acute Neurological
Indications. 7th Annual Advanced Topics Course in Hyperbaric Medicine,
Richland Memorial Hospital, Columbia, South Carolina. April, 1998.
Available in text and on videotape from the Department of Hyperbaric
Medicine, Richland Memorial Hospital.
12. Mitton C, Hailey D. Health Technology Assessment and Policy
Decisions on Hyperbaric Oxygen Treatment. Inter J Tech Assess in Health
Care, 1999;15(4):661-70.
13. Hyperbaric Oxygen Therapy for Wound Healing, Part I. TEC
Assessment Program, August, 1999;14(15):1-34. Available from Blue Cross
Blue Shield Association.
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