In people with traumatic brain injury, while the addition of HBOT may reduce the risk of death and improve the final GCS, there is little evidence that the survivors have a good outcome. The improvement of 2.68 points in GCS is difficult to interpret. This scale runs from three (deeply comatose and unresponsive) to 15 (fully conscious), and the clinical importance of an improvement of approximately three points will vary dramatically with the starting value (for example an improvement from 12 to 15 would represent an important clinical benefit, but an improvement from three to six would leave the patient with severe and highly dependent impairment). The routine application of HBOT to these patients cannot be justified from this review. Given the modest number of patients, methodological shortcomings of included trials and poor reporting, the results should be interpreted cautiously. An appropriately powered trial of high methodological rigour is required to define which patients, if any, can be expected to benefit most from HBOT.
In people with traumatic brain injury, the addition of HBOT significantly reduced the risk of death but not of favourable clinical outcome. The routine application of HBOT to these patients cannot be justified from this review. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT.
Exhaled nitric oxide (eNO) detects airway inflammation. Hyperbaric oxygen therapy (HBOT)
is used for tissue hypoxia, but can cause lung damage. We measured eNO following
inhalation of oxygen at different tensions and pressures. Methods. Part 1, eNO was
measured before and after HBOT. Part 2, normal subjects breathed 40% oxygen. Results.
Baseline eNO levels in patients prior to HBOT exposure were significantly higher than in
normal subjects (P < .05). After HBOT, eNO significantly decreased in patients (15.4 ± 2.0 versus 4.4 ± 0.5 ppb, P < .001), but not in normal subjects, after either 100% O2 at increased pressure
or 40% oxygen, 1 ATA. In an in vitro study, nitrate/nitrite release decreased after 90 minutes
HBOT in airway epithelial (A549) cells. Conclusion. HBO exposure causes a fall in eNO.
Inducible nitric oxide synthase (iNOS) may cause elevated eNO in patients secondary to
inflammation, and inhibition of iNOS may be the mechanism of the reduction of eNO seen
with HBOT.
Arterial gas embolism may occur as a complication of diving or certain medical procedures. Although relatively rare, the consequences may be disastrous. Recent articles in the critical care literature suggest the non-hyperbaric medical community may not be aware of the role for hyperbaric oxygen therapy in non-diving related gas embolism. This review is part of an Australian appraisal of experience in the management of arterial gas embolism over the last 10 years. We identified all patients referred to Prince of Wales Hospital Department of Diving and Hyperbaric Medicine with a diagnosis of arterial gas embolism from 1996 to 2006. Twenty-six patient records met our selection criteria, eight iatrogenic and 18 diving related. All patients were treated initially with a 280 kPa compression schedule. At discharge six patients were left with residual symptoms. Four were left with minor symptoms that did not significantly impact quality of life. Two remained severely affected with major neurological injury. Both had non-diving-related arterial gas embolism. There was a good outcome in the majority of patients who presented with arterial gas embolism and were treated with compression.
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