Low Pressure HBOT for Paediatric Brain Injury, A Minimal Risk Medical Treatment

Low Pressure Hyperbaric Oxygen Therapy for Pediatric Brain Injury, a Minimal Risk Medical Treatment Response to Nuthall Article

Dear Sirs:

We read the recent contribution to your esteemed journal by Nuthall¹, et al 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 gastro esophageal 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 and 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 IRS-approved protocol. The point is that this case report represents a very rare 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 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 up to 700 microns ⁵. While it is possible for the bubbles to breach insulted lungs (Para influenza 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 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 professions 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, 1212000:106(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, 4^th Edition. Editors Bennett and Elliott. W. B.Saunders Co, Ltd., London, 1993.
5. Hills BA, Butler BD. Size Distribution of Intravascular Air Emboli Prcxl.lced by Decompression. Undersea Biomed Res, 9/1981;8(3):163-170.
6. Muth CM, Shank ES. Gas Embolism. New England Journal of Medicine, 2/1712000;342(7):476-482.
7. Murphy BP, et al. Cerebral Air Embolism Resulting from Invasive Medical Procedures. Am 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 Hyperbanc 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.