Mahon RT, Dainer HM, Gibellato MG, Soutiere SE. Short oxygen prebreathe periods reduce or prevent severe decompression sickness in a 70-kg swine saturation model. J Appl Physiol 106: 1459-1463, 2009. First published January 29, 2009 doi:10.1152/japplphysiol.91058.2008 survivors are expected to achieve saturation with inert gas. However, rescue procedures may not accommodate staged decompression, raising the potential for severe decompression sickness (DCS). Alternatives to standard recompression therapy are needed. It has been demonstrated in humans that isobaric oxygen "prebreathing" (OPB) can accelerate decompression in a DISSUB scenario. In-70 kg swine saturated at 2.82 atm absolute (ATA), 1 h of OPB eliminated death and reduced severe DCS. We hypothesized that even shorter periods (Ͻ1 h) of OPB before no-stop decompression from saturation at 2.82 ATA could reduce the incidence of DCS in a large animal model. Catheterized Yorkshire swine (68.8 Ϯ 1.7 kg) in individual Plexiglas boxes within a large animal hyperbaric chamber were compressed to 2.82 ATA for 22 h. Following saturation and while still at depth, breathing gas was switched to Ͼ95% O 2 for 45 min (OPB45), 15 min (OPB15), or 5 min (OPB05) of OPB, or no OPB (control). The chamber was then decompressed without stops (0.91 ATA/min). Observers then entered the chamber and recorded signs of DCS for 2 h. All OPB periods significantly reduced the risk of developing type II DCS. OPB45 eliminated severe DCS. Controls had a 2.5 times greater risk of developing type II DCS than OPB05 (P ϭ 0.016). OPB45 and OPB15 significantly reduced type I DCS compared with controls. These results support the potential of OPB as an alternative to staged decompression and that OPB could be expected to improve outcome in a DISSUB rescue scenario. disabled submarine; nonrecompressive therapy; preoxygenation; prebreathe EXPOSURE to hyperbaric air causes the human body to absorb inert gas. Levels of absorption are based on depth and duration as well tissue perfusion and gas solubility. After remaining at depth for an extended period of time the tissue beds become saturated with inert gas. When a diver's tissues become saturated with inert gas, further exposure at depth no longer increases the inert gas load (4,7,18). Decompression from saturation is generally a lengthy undertaking, with decompression from just 60 feet of sea water (fsw) requiring 14 -16 h of staged decompression (22,29).In certain situations this lengthy decompression may not be feasible. One such scenario is a disabled submarine (DISSUB). It is possible that the internal pressure of a DISSUB would increase based on partial flooding and the use of emergency air-breathing systems (25). Under such circumstances, it is likely that submariners waiting for the deployment of submarine rescue assets will achieve inert gas saturation. Lengthy decompression onboard a rescue vehicle, with their limited passenger capacity, imperils remaining survivors who are likely facing air contamination, fire, and other hazards. Lengthy d...
Disabled submarine (DISSUB) survivors will achieve inert gas tissue saturation within 24 h. Direct ascent to the surface when saturated carries a high risk of decompression sickness (DCS) and death, yet may be necessary during rescue or escape. O(2) has demonstrated benefits in decreasing morbidity and mortality resulting from DCS by enhancing inert gas elimination. Perfluorocarbons (PFCs) also mitigate the effects of DCS by decreasing bubble formation and increasing O(2) delivery. Our hypothesis is that combining O(2) prebreathing (OPB) and PFC administration will reduce the incidence of DCS and death following saturation in an established 20-kg swine model. Yorkshire swine (20 +/- 6.5 kg) were compressed to 5 atmospheres (ATA) in a dry chamber for 22 h before randomization into one of four groups: 1) air and saline, 2) OPB and saline, 3) OPB with PFC given at depth, 4) OPB with PFC given after surfacing. OPB animals received >90% O(2) for 9 min at depth. All animals were returned to the surface (1 ATA) without decompression stops. The incidence of severe DCS < 2 h after surfacing was 96%, 63%, 82%, and 29% for groups 1, 2, 3, and 4, respectively. The incidence of death was 88%, 41%, 54%, and 5% for groups 1, 2, 3, and 4, respectively. OPB combined with PFC administration after surfacing provided the greatest reduction in DCS morbidity and mortality in a saturation swine model. O(2)-related seizure activity before reaching surface did not negatively affect outcome, but further safety studies are warranted.
Nontraumatic spontaneous intracranial hemorrhage occurs most commonly into the subarachnoid space and brain parenchyma, in contrast to subdural and epidural hematomas that are usually traumatic. The differential diagnosis of nontraumatic subarachnoid hemorrhage includes intracranial aneurysm rupture and vascular malformations, both of which may be investigated noninvasively with computed tomography and magnetic resonance imaging. An isolated intraparenchymal hematoma may be caused by hypertensive vasculopathy, amyloid angiopathy, vascular malformations, or by primary or secondary neoplasms. Knowledge of the appearance of intracerebral vascular malformations will help clinicians request appropriate further imaging and direct treatment.
Profile 1 performed best, shortening decompression with no death or severe DCS, yet it may still exceed emergency operational utility in an actual submarine rescue.
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