Hyperbaric oxygen in patients with ischemic stroke following cardiac surgery: a retrospective observational trial.

BACKGROUND: Hyperbaric oxygenation (HBO2) involves breathing 100% oxygen under elevated ambient pressure in a hyperbaric chamber, thereby dissolving oxygen in the plasma. This results in an increase of arterial partial pressure of oxygen (pO2). Though well established in experimental studies, HBO2 treatment for ischemic stroke is still under discussion. METHODS: From 2002-2014 HBO2 (2.2 bar, 90 minutes one/day; average number per patient: 4.7) was applied in 49 consecutive patients (32 males, 17 females, mean age: 68.8 years, range 31.2 - 83.9) with acute neurological deficit following cardiac surgery (CABG 15; combined surgery 14; valve surgery 11; aneurysm repair 8; malformation 1). Patients' history including TIA or stroke and carotid artery pathology were documented. Both degree and type of neurological deficit was evaluated by a scoring system (0-4) before and after HBO2 treatment. RESULTS: Before HBO2 therapy, the average motor deficit score was 2.45 and the average speech disorder score was 0.55, as compared with an average motor deficit of 1.12 and an average speech disorder of 0.27 afterward (α=0.0001, α=0.009). The majority of patients had an overall improvement of 2 score-points after HBO2 therapy (n=23 patients). Probit analysis showed that for a 50% response/probability (LC50) of having an overall outcome of ≥2 scoring points, an estimate of 4.3 HBO2 therapy sessions is necessary. CONCLUSIONS: HBO22 therapy was associated with significant improvement in patients with acute neurological deficits due to ischemic stroke following cardiac surgery. Though this fact suggests gas embolism as the most likely cause of stroke in this collective, other underlying pathologies cannot be ruled out. Randomized studies are needed for further evaluation.

Hyperbaric oxygen therapy for intensive care patients: position statement by the European Committee for Hyperbaric Medicine.

Many of the accepted indications for hyperbaric oxygen treatment (HBOT) may occur in critically ill patients. HBOT itself may cause a number of physiological changes which may further compromise the patient's state. Guidelines on the management of critically ill patients in a hyperbaric facility have been founded on the conclusions of the 2007 European Committee for Hyperbaric Medicine (ECHM) meeting. With regard to patient management, HBOT should be included in the overall care of ICU patients only after a risk/benefit assessment related to the specifics of both the hyperbaric centre and the patient's clinical condition and should not delay or interrupt their overall management. Neither patient monitoring nor treatment should be altered or stopped due to HBOT, and any HBOT effects must be strictly evaluated and appropriately mitigated. With regard to the hyperbaric facility itself, the hyperbaric chamber should be specifically designed for ICU patients and should be fully equipped to allow continuation of patient monitoring and treatment. The hyperbaric chamber ideally should be located in, or around the immediate vicinity of the ICU, and be run by a sufficiently large and well-trained team of physicians, nurses, chamber operators and technicians. All devices to be introduced into the chamber should be evaluated, tested and acknowledged as safe for use in a hyperbaric environment and all procedures (standard and emergency) should be tested and written before being implemented.

Severe hydrogen sulphide poisoning treated with 4-dimethylaminophenol and hyperbaric oxygen.

UNLABELLED: INTRODUCTION Hydrogen sulphide (H2S) is a highly toxic gas which originates mainly during breakdown of organic matter under anaerobic conditions. After inhalation, H2S binds to mitochondrial respiratory enzymes preventing oxidative phosphorylation, thereby causing reversible inhibition of aerobic metabolism and cellular anoxia. The use of hyperbaric oxygen therapy (HBOT) for H2S poisoning remains controversial, but has a similar underlying rationale to that in carbon monoxide poisoning. METHODS: A retrospective review of patients with severe H2S intoxication who presented during 2006 and 2007 was carried out. Ten victims of severe occupational H2S poisoning were identified, of whom four died at the site of the accident. Two further patients required cardiopulmonary resuscitation at the site of the accident and the remaining four all received 100% oxygen followed by endotracheal intubation and artificial ventilation prior to hospital admission. In these six cases, 4-dimethylaminophenol was administered on admission as an antidote, followed immediately by HBOT using the schedule otherwise used in carbon monoxide intoxication. CLINICAL OUTCOME: The two patients who required cardiopulmonary resuscitation at the site of exposure died of cerebral ischaemia or pulmonary oedema on the first and seventh days after the accident respectively. The remaining four patients recovered without any neurological sequelae and were discharged for outpatient care after a median of nine days (range 8-12 days). No antidote-related adverse effects could be detected. Acid-base status and oxygenation improved and methaemoglobin fell with the first HBOT in all six cases. CONCLUSION: In severe H2S intoxication, supportive HBOT may play a useful role in improving oxygenation and acid-base status quickly and counteracting the decrement in oxygen carriage caused by methaemoglobinaemia due to antidote administration.