Recurrence of Neurological Deficits in an F/A-18D Pilot Following Loss of Cabin Pressure at Altitude.

INTRODUCTION: Supersonic, high altitude aviation places its pilots and aircrew in complex environments, which may lead to injury that is not easily diagnosed or simply treated. Decompression illness (either venous or arterial) and environmental conditions (e.g., abnormal gases and pressure) are the most likely adverse effects aircrew often face. Though symptomatic aircrew personnel may occasionally require hyperbaric oxygen treatment, it is rare to require more than one treatment before returning to baseline function. CASE REPORT: This challenging aviation case details the clinical course and discusses the salient physiological factors of an F/A-18D pilot who presented with neurological symptoms following loss of cabin pressure at altitude. DISCUSSION: Most crucial to this discussion was the requirement for multiple hyperbaric oxygen treatments over several days due to recurrence of symptoms. The likelihood of recurrence during and after future flights cannot be estimated with accuracy. This case illustrates a degree of recurrences for neurological symptoms in aviation (hypobaric exposure to hyperbaric baseline environment) that has not previously been described. Robinson T, Evangelista JS III, Latham E, Mukherjee ST, Pilmanis A. Recurrence of neurological deficits in an F/A-18D pilot following loss of cabin pressure at altitude. Aerosp Med Hum Perform. 2016; 87(8):740-744.

Hyperbaric oxygen treatment reduced the lung injury of type II decompression sickness.

OBJECTIVE: To detect the ultrastructural changes in rabbits with type II decompression sickness (DCS), and study the therapeutic effects of hyperbaric oxygen (HBO). METHODS: Twenty-seven male New Zealand rabbits were randomly divided equally into the DCS group, HBO treatment group and control group. Experimental models of each group were prepared. Lung apex tissues were harvested to prepare paraffin- and EPON812-embedded tissues. RESULTS: In the DCS group, macroscopic and histological examination revealed severe and rapid damage to lung tissue. Ultrastructural examination revealed exudation of red blood cells in the alveolar space. Type I alveolar epithelial cells exhibited retracted cell processes and swollen mitochondria, and type II cells showed highly swollen mitochondria and decrease in cytoplasmic lamellar bodies. Dilatation and congestion of capillary vessels were accompanied by swelling of endothelial cells and incomplete basement membrane. In the HBO treatment group, the findings were somewhat similar to those in the DCS group, but the extent of damage was lesser. Only a small amount of tiny bubbles could be seen in the blood vessels. Type I alveolar epithelia cells and endothelial cells of the capillaries illustrated slight shortening of cells, swollen cytoplasm and decreased cell processes. Type II alveolar epithelial cells showed slight swelling of the mitochondria, decreased vacuolar degeneration of lamellar bodies, and increase in the number of free ribosomes. CONCLUSIONS: Our microscopic and ultrastructural findings confirm that the lung is an important organ affected by DCS. We also confirmed that HBO can alleviate DCS-induced pulmonary damage.

A systematic review of factitious decompression sickness.

We present a case of factitious decompression sickness (DCS) involving a patient emergently treated at a hyperbaric medicine facility in New Zealand. Patients with factitious disorder feign illnesses such as DCS in order to receive care and attention despite the lack of an underlying illness. Other studies have suggested that 0.6% to as many as 9.3% of hospital admissions are factitious in nature. Therefore we believe that factitious DCS is occurring more often than hyperbaric clinicians suspect. DCS can be life-threatening, and hyperbaric medicine clinicians will almost always "err on the side of caution" when patients are referred with symptoms of DCS. Because DCS can be diagnosed based on subjective symptoms and self-reported history, there are opportunities for factitious patients to receive hyperbaric therapy. The costs associated with factitious DCS include transport, staff resources and preventing patients with treatable conditions from accessing the hyperbaric chamber. We performed a systematic review of the literature and found eight additional reported cases of confirmed or suspected factitious DCS. We report our findings and recommendations for hyperbaric medicine specialists regarding the recognition and management of factitious DCS.

Huperzine A ameliorates cognitive deficits and oxidative stress in the hippocampus of rats exposed to acute hypobaric hypoxia.

Acute exposure to high altitudes can cause neurological dysfunction due to decreased oxygen availability to the brain. In this study, the protective effects of Huperzine A on cognitive deficits along with oxidative and apoptotic damage, due to acute hypobaric hypoxia, were investigated in male Sprague-Dawley rats. Rats were exposed to simulated hypobaric hypoxia at 6,000 m in a specially fabricated animal decompression chamber while receiving daily Huperzine A orally at the dose of 0.05 or 0.1 mg/kg body weight. After exposure to hypobaric hypoxia for 5 days, rats were trained in a Morris Water Maze for 5 consecutive days. Subsequent trials revealed Huperzine A supplementation at a dose of 0.1 mg/kg body weight restored spatial memory significantly, as evident from decreased escape latency and path length to reach the hidden platform, and the increase in number of times of crossing the former platform location and time spent in the former platform quadrant. In addition, after exposure to hypobaric hypoxia, animals were sacrificed and biomarkers of oxidative damage, such as reactive oxygen species, lipid peroxidation, lactate dehydrogenase activity, reduced glutathione, oxidized glutathione and superoxide dismutase were studied in the hippocampus. Expression levels of pro-apoptotic proteins (Bax, caspase-3) and anti-apoptotic protein (Bcl-2) of hippocampal tissues were evaluated by Western blotting. There was a significant increase in oxidative stress along with increased expression of apoptotic proteins in hypoxia exposed rats, which was significantly improved by oral Huperzine A at 0.1 mg/kg body weight. These results suggest that supplementation with Huperzine A improves cognitive deficits, reduces oxidative stress and inhibits the apoptotic cascade induced by acute hypobaric hypoxia.