HYPERBARIC OXYGEN THERAPY IN NEONATES


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E. Cuauhtimoc Sanchez R., M.D. Medical Director

Servicio do Medicina Hiperbarica, Hospital Angeles del Pedregal, Camino a Santa Teresa No. 1055, Col. Heroes de Padierna, Mexico, D.F. 10700 Telephone 652-2011, 652-3011 ext. 2185, fax:568-8083, Email: danmex@scubalatin.com.mx

Introduction

The use of Hyperbaric Oxygen Therapy (HBOT) is extensive in adults and is becoming more common in the pediatric patient. Nevertheless, there is great reluctance to treat neonates in hyperbaric chambers. The use of HBOT in pediatric patients was relative common in the former USSR and by 1981 there were reports of over 1868 cases treated. However, there are very few reports of neonates being treated with HBOT and most of them date from the 60's. We have started treating neonates in our monoplace chambers (Sechrist Series 3200) for the following conditions: acute severe intestinal ischemia, necrotizing enterocolitis, and acute ischemic/anoxic encephalopathy.

Severe Intestinal Ischemia and Necrotizing Enterocolitis

There are reports on the use of HBOT in relation to intestinal pathologies, such as, radiation necrosis, intestinal pneumatosis, intestinal ischemia, intestinal ischemia/reperfusion injury, intestinal obstruction, Crohn's disease, systemic inflammatory response, bacteria translocation, intestinal sepsis, and necrotizirig enterocolitis. All of these reports support the use of HBOT.

Hyperbaric oxygen therapy is not only useful for the intestinal pathology, but also for the systemic effects of which include disseminated intravascular coagulation (DIC), the systemic inflammatory response (SIR) and shock. Normally, neonates who are treated in the first 6 hours, respond in the first one or two treatments. It is rare for these patients to need more than 2 treatment, and it is only in those cases where there are surgical complications that further treatments may be required.

The effects of HBOT in neonates are visible within the first minutes post-treatment. In infants with severe intestinal ischemia and necrotizing enterocolitis there is a significant reduction of abdominal circumference, gut edema and pneumatosis. They also have stabilization of the systemic responses (DIC, SIR and shock). Oral feeding is usually restored in the first 24-h post-HBOT.

Ischemic/Anoxic Encephalopathy

Again, the reported experience of neonates with this condition dates from the 60's and is mainly from the former USSR. The rationale for the use of HBOT for this condition is to prevent the development of the primary ischemic/anoxic lesion and secondary ischemic/reperfusion injury. We recommend treating these patients in the first 6 hours post-delivery.

Our patients were studied with EEG and transfontanellar ultrasound to determine a baseline. All of the patients were re-studied 4-6 hours after HBOT and there was no evidence of cerebral edema after the first treatment. A neonatologist and neurologist have been performing the follow-up and all patients have had adequate psychomotor development according to their age. There were no side effects in this group of patients, one with history of being premature with a hyaline membrane was treated preventively with inhaled surfactant and did not developed pulmonary oxygen toxicity. All the neonates were studied pre and post-treatment by fundascopic examination to rule out retinopathy of the premature. We have studied them every month, and so far there has been no evidence of it in our patients.

Oxygen Toxicity

The lack of information about oxygen toxicity in neonates has hindered the development of HBOT in these patients. According to the established milestones for ocular development, the distal third of the vasculature will develop up to the 34 th week of pregnancy. The retinopathy of the premature is generally due to breathing sustained high percentage of oxygen (above 45%) for long periods in incubators. Presently, the retinopathy of the premature is considered to be like an ischemia/reperfusion injury. HBOT has been used to manage, and to prevent ischemia/reperfusion injury. Also, short exposures to low pressures (2.0 atmosphere absolute or 202kPa for 45 minutes once or twice a day will be unlikely to cause this lesion and may even prevent it. Toxicity to the CNS is very unlikely to occur at 2.0 atm abs or less, as it usually occurs in compromised patients treated at much higher pressures (3.0 atm abs).

Pulmonary oxygen toxicity in general, is not seen in HBOT protocols. It is sometimes seen in the treatment of divers when long periods are spent at high pressure -typically 2.8 atm abs on military therapeutic tables. Probably this type of oxygen toxicity is related to the action oof reactive species of oxygen (free radicals) on the lipid part of surfactant (DPPC). Nevertheless, in our experience we have only found pulmonary oxygen toxicity in neonates with history of hyaline membrane and/or bronchopulmonary dysplasia after 1 or 2 treatments. In non-compromised neonates it takes more than 2 treatments to see evidence of toxicity. Fortunately, it responds well to inhaled steroids and/or surfactants.

Special Considerations in the Management of Neonates

There are several factors which should be considered in the management of neonates under hyperbaric conditions, especially in a monoplace chamber.

1. Our studies have involved patients older than 34 weeks of pregnancy and above 1.2 kg.

2. The patient should always be accompanied by a neonatologist and/or hyperbaric physician, as an inside attendant.

3. There is no ventilator suitable for these patients and they should be bagged when necessary by the inside attendant.

4. To avoid hypothermia, all the clothes (100% cotton) used to cover the neonates should be warmed in a vapor autoclave and kept at 38C before covering the patient (never heat them in a microwave oven because of the risk of ignition).

5. A transcutaneous oxygen monitor (TCOM) can be used in the second left intercostal space, or around that area, as an indirect measure for adequate ventilation and oxygenation. A reading should be taken at normal atmospheric pressure when the patient has a haemoglobin saturation of 95% and this can be used as a baseline. If during HBOT the patient has a value below the baseline, there is a problem with the ventilation of the patient.

6. Our treatment protocol for neonates is 2.0 atm abs for 45 minutes (20 min oxygen, 5 min air, and 20 min oxygen) qid or bid.

7. In neonates the CNS oxygen toxicity is rare, but pulmonary oxygen toxicity is not. Special care should be taken for patients with history of hyaline membrane and/or bronchopulmonary dysplasia. It can be handled with preventive inhaled steroid and/or surfactant. Those patients that develop pulmonary oxygen toxicity should receive inhaled steroids and/or surfactant before the next treatment.

8. Evaluation of the eye in neonates is important. It should include fundascopic examination and/or visual evoked potentials. Always get a baseline and we have continued follow up every month until 18 months of age. Neonates require special handling in a hyperbaric chamber, particularly in a monoplace unit.

It is mandatory to have an inside assistant and to do other measures (mentioned above) to provide an adequate inside environment for the neonate. They are also specially prone to oxygen toxicity, particularly of the lungs. Nevertheless, they respond very quickly and may require only one treatment to resolve the local ischemic/hypoxic condition and the systemic response (DIC, SIR, or shock) to this event. We observe that these patients treated early (<6 h of the event) have dramatic reversal of their condition and HBOT is a safe and cost-effective adjunctive treatment There is a need to undertake large randomized, controlled studies to establish the efficacy of HBOT in ischemic/hypoxic conditions.

ACKNOWLEDGEMENTS

Our work in neonates was done with the invaluable collaboration, effort and support of the following individuals:

  • Gabriela Montes, MD -Neonatologist, Hospital Angeles del Pedregal, Mexico, D.F.
  • Lisardo Garcia, M.D. Fellow in Hyperbaric Medicine, Palmetto Richland Memorial Hospital, Columbia, SC.
  • Gerardo Qroz, MD. Neonatologist, Hospital Angeles del Peciregal, Mexico, DF.
  • Robert Borer, MD. Associate Director, Hyperbaric Medicine Department, Long Beach Memorial Hospital, Los Angeles, CA
  • Dick Clarke, CHT - Program Director, Hyperbaric Medicine
  • All of the Hyperbaric Medicine Service Staff and Residents of Neonatology of the Hospital Angeles del Pedregal, Mexico, D.F.

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