Does hyperbaric oxygen cause narcosis or hyperexcitability? A quantitative EEG analysis.

Divers breathe higher partial pressures of oxygen at depth than at the surface. The literature and diving community are divided on whether or not oxygen is narcotic. Conversely, hyperbaric oxygen may induce dose-dependent cerebral hyperexcitability. This study evaluated whether hyperbaric oxygen causes similar narcotic effects to nitrogen, and investigated oxygen's hyperexcitability effect. Twelve human participants breathed "normobaric" air and 100% oxygen, and "hyperbaric" 100% oxygen at 142 and 284 kPa, while psychometric performance, electroencephalography (EEG), and task load perception were measured. EEG was analyzed with functional connectivity and temporal complexity algorithms. The spatial functional connectivity, estimated using mutual information, was summarized with the global efficiency network measure. Temporal complexity was calculated with a "default-mode-network (DMN) complexity" algorithm. Hyperbaric oxygen-breathing caused no change in EEG global efficiency or in the psychometric test. However, oxygen caused a significant reduction of DMN complexity and a reduction in task load perception. Hyperbaric oxygen did not cause the same changes in EEG global efficiency seen with hyperbaric air, which likely related to a narcotic effect of nitrogen. Hyperbaric oxygen seemed to disturb the time evolution of EEG patterns that could be taken as evidence of early oxygen-induced cortical hyperexcitability. These findings suggest that hyperbaric oxygen is not narcotic and will help inform divers' decisions on suitable gas mixtures.

Hyperbaric oxygen for decompression sickness.

Decompression sickness (DCS, "bends") is caused by formation of bubbles in tissues and/or blood when the sum of dissolved gas pressures exceeds ambient pressure (supersaturation). This may occur when ambient pressure is reduced during any of the following: ascent from a dive; depressurization of a hyperbaric chamber; rapid ascent to altitude in an unpressurized aircraft or hypobaric chamber; loss of cabin pressure in an aircraft; and during space walks.

Persistent extravascular bubbles on radiologic imaging after recompression treatment for decompression sickness: A case report.

Decompression sickness (DCS) is a condition arising when dissolved inert gas in tissue forms extravascular and/or intravascular bubbles during or after depressurisation. Patients are primarily treated with 100% oxygen and recompression, which is often assumed to lead to resolution of bubbles. After this, repeated hyperbaric exposures can be provided in case of persistent symptoms, with oxygen delivery to ischaemic tissues, anti-inflammatory properties and reduction of oedema considered the main mechanisms of action. In this case report we present the history and imaging of a diver diagnosed with DCS that was treated with two US Navy Treatment Table 6 recompressions, but who still had multiple extravascular bubbles apparent on CT-imaging after these hyperbaric treatments. Based on these findings we hypothesise that, contrary to general belief, it is possible that large extravascular bubbles can persist after definitive treatment for DCS.

Emerging indications for hyperbaric oxygen.

PURPOSE OF REVIEW: To identify and discuss emerging trends in the therapeutic use of hyperbaric oxygen. RECENT FINDINGS: There has been a maturing of the clinical evidence to support the treatment of sudden hearing loss, a wide range of problematic chronic wound states and the prevention and treatment of end-organ damage associated with diabetes mellitus. On the other hand, the controversy continues concerning the use of hyperbaric oxygen therapy (HBOT) to treat sequelae of mild traumatic brain injury. HBOT remains poorly understood by many medical practitioners despite more than 50 years of clinical practice. Pharmacological actions arise from increased pressures of oxygen in the blood and tissues. Most therapeutic mechanisms identified are not the simple result of the reoxygenation of hypoxic tissue, but specific effects on immunological and metabolic pathways by this highly reactive element. HBOT remains controversial despite biological plausibility and a solid clinical evidence base in several disease states. SUMMARY: Multiple proposals for new indications for HBOT continue to emerge. Although many of these will likely prove of limited clinical importance, some show significant promise. Responsible practitioners remain acutely aware of the need for high-quality clinical evidence before introducing emerging indications into routine practice.

In-water recompression.

Divers suspected of suffering decompression illness (DCI) in locations remote from a recompression chamber are sometimes treated with in-water recompression (IWR). There are no data that establish the benefits of IWR compared to conventional first aid with surface oxygen and transport to the nearest chamber. However, the theoretical benefit of IWR is that it can be initiated with a very short delay to recompression after onset of manifestations of DCI. Retrospective analyses of the effect on outcome of increasing delay generally do not capture this very short delay achievable with IWR. However, in military training and experimental diving, delay to recompression is typically less than two hours and more than 90% of cases have complete resolution of manifestations during the first treatment, often within minutes of recompression. A major risk of IWR is that of an oxygen convulsion resulting in drowning. As a result, typical IWR oxygen-breathing protocols use shallower maximum depths (9 metres' sea water (msw), 191 kPa) and are shorter (1-3 hours) than standard recompression protocols for the initial treatment of DCI (e.g., US Navy Treatment Tables 5 and 6). There has been no experimentation with initial treatment of DCI at pressures less than 285 kPa since the original development of these treatment tables, when no differences in outcomes were seen between maximum pressures of 203 kPa (10 msw) and 285 kPa (18 msw) or deeper. These data and case series suggest that recompression treatment comprising pressures and durations similar to IWR protocols can be effective. The risk of IWR is not justified for treatment of mild symptoms likely to resolve spontaneously or for divers so functionally compromised that they would not be safe in the water. However, IWR conducted by properly trained and equipped divers may be justified for manifestations that are life or limb threatening where timely recompression is unavailable.

Total and Differential Phylloquinone (Vitamin K1) Intakes of Preterm Infants from All Sources during the Neonatal Period.

All newborns require phylloquinone after birth to prevent vitamin K deficiency bleeding. Babies born prematurely may be at particular risk of deficiency without adequate supplementation during infancy. The main sources of phylloquinone in preterm babies during the neonatal period are the prophylactic dose of phylloquinone given at birth, and that derived from parenteral and/or enteral feeding. This observational study formed part of a prospective, multicentre, randomised, controlled trial that examined the vitamin K status of preterm infants after random allocation to one of three phylloquinone prophylactic regimens at birth (0.5 or 0.2 mg intramuscularly or 0.2 mg intravenously). In this nutritional sub-study we quantified the proportional and total phylloquinone intakes of preterm infants within the neonatal period from all sources. Almost all infants had average daily phylloquinone intakes that were in excess of the currently recommended amounts. In infants who did not receive parenteral nutrition, the bolus dose of phylloquinone given at birth was the major source of phylloquinone intake, whereas in infants who received parenteral nutrition, the intake from the parenteral preparation exceeded that from the bolus dose by a ratio of approximately 3:1. Our study supports the concern of others that preterm infants who receive current parenteral nutrition formulations may be receiving excessive vitamin K.

Unestablished indications for hyperbaric oxygen therapy.

Unestablished indications are conditions in which systematic clinical use of hyperbaric oxygen treatment (HBOT) is not supported by adequate proof of benefit. HBOT is vulnerable to use in many such conditions for various reasons, perhaps the most important being that a placebo or participation effect may create an impression of efficacy. The systematic use of HBOT in unestablished indications raises ethical concerns about provision of misleading information, giving false hope, and taking payment for therapy of doubtful benefit. Any practice perceived as unethical or unscientific has the potential to draw the wider field into disrepute. Of substantial contemporary relevance is the use of HBOT in treatment of various forms of chronic brain injury; in particular, cerebral palsy in children and the sequelae of mild traumatic brain injury in adults. There are now multiple, randomised, blinded, sham-controlled trials of HBOT in both indications. None of these studies showed benefit of HBOT when compared to sham control, though the sham and HBOT groups often both improved, indicating that a placebo or participation effect influenced outcomes. These results almost certainly explain those of open-label trials (lacking sham controls) in which HBOT frequently seems beneficial. Advocates for HBOT in chronic brain injury claim that the sham treatments (usually 1.3 ATA pressure exposure whilst air breathing) in the blinded trials are actually active treatments; however, the same dose of oxygen can be achieved at 1 ATA breathing 27% oxygen. To counter this argument, advocates also claim that the extra 0.3 ATA of pressure is somehow independently beneficial, but this notion has limited biological plausibility and there is little supporting evidence. Chronic brain injuries remain unestablished indications at this time and, in our opinion, should not be systematically treated with HBOT.

The use of deep tables in the treatment of decompression illness: the Hyperbaric Technicians and Nurses Association 2011 Workshop.

In August 2011, a one-day workshop was convened by the South Pacific Underwater Medicine Society and the Hyperbaric Technicians and Nurses Association to examine the use of deep recompression treatment tables for the treatment of decompression illness in Australia and New Zealand. The aim of the workshop was to develop a series of consensus statements to guide practice around the region. The workshop chose to focus the discussion on the use of 405 kPa (30 msw) maximum depth tables using helium-oxygen breathing periods, and covered indications, staffing and technical requirements. This report outlines the evidence basis for these discussions and summarises the series of consensus statements generated. These statements should assist hyperbaric facilities to develop and maintain appropriate policies and procedures for the use of such tables. We anticipate this work will lead to the formulation of a standard schedule for deep recompression to be developed at a future workshop.

Recompression and adjunctive therapy for decompression illness.

BACKGROUND: Decompression illness (DCI) is due to bubble formation in the blood or tissues following the breathing of compressed gas. Clinically, DCI may range from a trivial illness to loss of consciousness, death or paralysis. Recompression is the universally accepted standard treatment of DCI. When recompression is delayed, a number of strategies have been suggested in order to improve the outcome. OBJECTIVES: To examine the effectiveness and safety of both recompression and adjunctive therapies in the treatment of DCI. SEARCH METHODS: In our previous update we searched until October 2009. In this version we searched CENTRAL (The Cochrane Library, October 2011); MEDLINE (1966 to October 2011); CINAHL (1982 to October 2011); EMBASE (1980 to October 2011); the Database of Randomised Controlled Trials in Hyperbaric Medicine (October 2011); and handsearched journals and texts. SELECTION CRITERIA: We included randomized controlled trials that compared the effect of any recompression schedule or adjunctive therapy with a standard recompression schedule. We did not apply language restrictions. DATA COLLECTION AND ANALYSIS: Three authors extracted the data independently. We assessed each trial for internal validity and resolved differences by discussion. Data were entered into RevMan 5.1. MAIN RESULTS: Two randomized controlled trials enrolling a total of 268 patients satisfied the inclusion criteria. The risk of bias for Drewry 1994 was unclear as this study was presented as an abstract, while Bennett 2003 was rated as at low risk. Pooling of data was not possible. In one study there was no evidence of improved effectiveness with the addition of a non-steroidal anti-inflammatory drug (tenoxicam) to routine recompression therapy (at six weeks: relative risk (RR) 1.04, 95% confidence interval (CI) 0.90 to 1.20, P = 0.58) but there was a reduction in the number of compressions required when tenoxicam was added from three to two (P = 0.01, 95% CI 0 to 1). In the other study, the odds of multiple recompressions were lower with a helium and oxygen (heliox) table compared to an oxygen treatment table (RR 0.56, 95% CI 0.31 to 1.00, P = 0.05). AUTHORS' CONCLUSIONS: Recompression therapy is standard for the treatment of DCI, but there is no randomized controlled trial evidence for its use. Both the addition of a non-steroidal anti-inflammatory drug (NSAID) and the use of heliox may reduce the number of recompressions required, but neither improve the odds of recovery. The application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation. Benefits may be largely economic and an economic analysis should be undertaken. There is a case for large randomized trials of high methodological rigour in order to define any benefit from the use of different breathing gases and pressure profiles during recompression therapy.

Pulmonary barotrauma and cerebral arterial gas embolism during hyperbaric oxygen therapy.

Hyperbaric oxygen therapy (HBOT) is used to treat a variety of disorders. It is a safe treatment modality, but rare catastrophic complications may occur. In this case report, we describe the occurrence of irreversible spastic quadriparesis in a patient who suffered a cerebral arterial gas embolism (CAGE) during decompression from HBOT. The patient had a history of respiratory disease and was subsequently found to have bullous changes in the left lung, which almost certainly predisposed to this rare event. We discuss appropriate pretreatment screening to prevent such events and highlight the paradox that HBOT, the cause of the CAGE, is also the treatment of choice.

Vitamin K prophylaxis for preterm infants: a randomized, controlled trial of 3 regimens.

OBJECTIVE: Preterm infants may be at particular risk from either inadequate or excessive vitamin K prophylaxis. Our goal was to assess vitamin K status and metabolism in preterm infants after 3 regimens of prophylaxis. METHODS: Infants <32 weeks' gestation were randomized to receive 0.5 mg (control) or 0.2 mg of vitamin K1 intramuscularly or 0.2 mg intravenously after delivery. Primary outcome measures were serum vitamin K1, its epoxide metabolite (vitamin K1 2,3-epoxide), and undercarboxylated prothrombin assessed at birth, 5 days, and after 2 weeks of full enteral feeds. Secondary outcome measures included prothrombin time and factor II concentrations. RESULTS: On day 5, serum vitamin K1 concentrations in the 3 groups ranged widely (2.9-388.0 ng/mL) but were consistently higher than the adult range (0.15-1.55 ng/mL). Presence of vitamin K1 2,3-epoxide on day 5 was strongly associated with higher vitamin K1 bolus doses. Vitamin K1 2,3-epoxide was detected in 7 of 29 and 4 of 29 infants from the groups that received 0.5 mg intramuscularly and 0.2 mg intravenously, respectively, but in none of 32 infants from group that received 0.2 mg intramuscularly. After 2 weeks of full enteral feeding, serum vitamin K1 was lower in the infants who received 0.2 mg intravenously compared with the infants in the control group. Three infants from the 0.2-mg groups had undetectable serum vitamin K1 as early as the third postnatal week but without any evidence of even mild functional deficiency, as shown by their normal undercarboxylated prothrombin concentrations. CONCLUSIONS: Vitamin K1 prophylaxis with 0.2 mg administered intramuscularly maintained adequate vitamin K status of preterm infants until a median age of 25 postnatal days and did not cause early vitamin K1 2,3-epoxide accumulation. In contrast, 0.2 mg administered intravenously and 0.5 mg administered intramuscularly led to vitamin K1 2,3-epoxide accumulation, possibly indicating overload of the immature liver. To protect against late vitamin K1 deficiency bleeding, breastfed preterm infants given a 0.2-mg dose of prophylaxis should receive additional supplementation when feeding has been established.