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Lower body adynamia as a factor to reduce the risk of hypobaric decompression sickness.

BACKGROUND: We define lower body adynamia (LBA) as restricted lower body movement, particularly walking, during both the denitrogenation phase at site pressure and during the exercise phase while at altitude. HYPOTHESIS: Our null hypothesis is that subjects who are adynamic in the lower body but do upper body exercise will be at similar risk of decompression sickness (DCS) and venous gas emboli (VGE) as subjects who randomly walk but do no planned exercise while at altitude. METHODS: We selected a data set that contained 1401 altitude exposures with the following conditions: a) walking was part of the exercise at altitude; or b) there was no planned exercise done at altitude but walking was not restricted; or c) LBA was inforced, but upper body exercise was done at altitude. We used logistic regression (LR) on all 1401 exposures, a log logistic survival analysis (SA) on a subset of data from "a" and "c" (n = 234), and estimated a model for how the incidence of VGE changes through time. RESULTS: The estimated probabilities of DCS and VGE with 95% confidence intervals (Cls) from the LR with a simulation of a 3-h oxygen prebreathe, a 4-h exposure to 4.3 psia in a male, and exercise and LBA conditions as described above are: (see text). CONCLUSION: LBA that includes upper body exercise appears to be as protective against DCS and VGE as random walking by subjects who did no prescribed exercise while at altitude, and is more protective than exercise that included walking. Our conclusions are based on an assumption that we have adequately controlled, through our data selection process and the use of multivariable models, important variables in tests that were not done at the Johnson Space Center.

Cardiac Volume↗

Type II decompression sickness in naval hypobaric chambers: A case of mistaken identity?

INTRODUCTION: Historically, U.S. Navy clinicians have used the U.S. Navy Dive Manual for guidance in the diagnosis and treatment of injuries incurred during hyper- or hypobaric operations. Based on this manual, paresthesias are considered to be central nervous system manifestations and thus are classified as Type II (severe) decompression sickness (DCS). Yet given the highly successful response to treatment of peripheral nervous system manifestations of DCS in the literature, both the diving and aviation communities have questioned its classification as "severe" DCS. This record review was undertaken to examine U.S. Naval severe cases of altitude DCS with the goal of identifying dissimilarities between hypobaric facilities in classification and incidence. METHODS: Hypobaric exposures and cases were reviewed from quarterly training reports maintained at the Naval Operational Medicine Institute, Pensacola, FL, between January 1993 and April 2004. Cases were analyzed for age, gender, flight profile, symptom complex, type of DCS, and treatment provided. RESULTS: There were 50,355 hypobaric exposures resulting in 97 cases of altitude DCS. Of the 97 cases of diagnosed DCS, 58 were classified as Type II, while 39 were Type I. Of the 58 cases of Type II DCS, 29 were diagnosed as Type II by the sole finding of non-dermatomal paresthesias. DISCUSSION: Type II DCS, a designation traditionally reserved for severe DCS, is frequently diagnosed by the sole finding of non-dermatomal paresthesias in Naval hypobaric training. A review and revision of the U.S. Naval Aviation classification system for altitude DCS should be undertaken with emphasis on severity not symptomatology.

Adult↗

Evaluation of oxygen and pressure in treatment of decompression sickness in guinea pigs.

These experiments examined whether increasing the partial pressure of oxygen (PO2), hydrostatic pressure, or both were responsible for the improvement in effectiveness of recompression treatment previously observed in guinea pigs with increasing depths of air. Unanesthetized male guinea pigs (600-700 g) were subjected to 8.6 atm abs (871 kPa) air dives for 60 min and then decompressed at 1.82 atm (184 kPa)/min to the surface. Subsequently, animals usually displayed hypotension, cardiac arrhythmia, and tachypnea, indicative of a fatal bout (> 95% death rate) of decompression sickness (DCS). Animals that developed DCS were treated by recompressing to depths ranging from 2.5 to 11.6 atm abs (253-1175 kPa), with 14, 28, 42, or 100% O2/balance N2. This design produced PO2's at treatment depth ranging from 0.4 to 3.6 atm abs (41-365 kPa). Upon recompression, recovery of blood pressure, heart rate, and breathing rate generally occurred. The area under the breathing rate vs. time curve was used to examine the effectiveness of treatment over a period of 60 min. A dramatic improvement in recovery over time was observed with increasing recompression depth for all gas mixtures. Analysis indicated that the positive response to depth was related to increasing hydrostatic pressure, increasing PO2 had no statistically significant beneficial effect.

Animals↗

Prevention of decompression sickness in current and future fighter aircraft.

United States Air Force oxygen regulators set to "NORMAL OXYGEN" deliver up to 60% nitrogen to the pilot at cockpit altitudes of 15,000 to 20,000 ft (4573-6096 m). Research chamber exposure to these altitudes while breathing 50% nitrogen has resulted in high grades of venous gas emboli. Expansion of existing gas emboli following an unplanned decompression to ambient aircraft altitude (e.g., loss of canopy) could result in rapid development of decompression sickness (DCS) symptoms. To reduce this potential problem, regulators in current fighters should be set to "100% OXYGEN" until descent from cruise to increase denitrogenation. The United States' Advanced Tactical Fighter and the European Fighter Aircraft may be designed to cruise above 50,000 ft (15,240 m), where cockpit altitudes exceed 20,000 ft with a 5-psi differential (psid) cockpit pressurization schedule. Increasing cockpit differential pressure to 7 psid while breathing 100% oxygen would greatly reduce the chance of significant emboli formation and the potential for DCS, but would slightly elevate the risks associated with pulmonary overpressure during rapid decompression.

Air Pressure↗

Arterial gas embolism as a pathophysiologic mechanism for spinal cord decompression sickness.

A continuous infusion of air (1.0 ml.min-1) was delivered via a fine aortic cannula into the arterial circulation of 7 anesthetized dogs until no spinal cord function could be elicited by somatosensory evoked potentials. The animals were then rapidly perfusion-fixed and the spinal cords removed for histological examination. The appearance of the embolized cords differed substantially from eight spinal cords injured by fulminant decompression sickness (DCS). The embolized cords appeared essentially normal whereas the DCS cords featured extravascular, nonstaining, space-occupying lesions (SOLs) scattered throughout the cord, mainly in the white matter. Two spinal cords injured by DCS with a delayed onset (30 min from surfacing) appeared similar to the embolized cords. These findings are compatible with the hypothesis that two mechanisms are involved in the onset of spinal cord DCS. Fulminant disease is associated with SOLs, which are probably caused by the in situ evolution of a gas phase. Disease with a delayed onset is more likely to be caused by an ischemic mechanism, which in the acute phase is histologically indistinguishable from gas embolism.

Animals↗

Comparative data from 2250 male and female sports divers: diving patterns and decompression sickness.

BACKGROUND: The aim of the study was to compare the diving habits and histories of men and women in recreational scuba diving. METHODS: More than 10,000 questionnaires were circulated to recreational divers in the United Kingdom. Retrospective, broad-based information was requested concerning general health, smoking, alcohol, recreational drug use, diving habits and histories, and physician-confirmed and self-diagnosed episodes of decompression sickness (DCS). Data relating only to women were also gathered. Questionnaires were anonymous. RESULTS: Over four years, 2250 divers responded, 47% of whom were women. Of the 458,827 dives reported, 310% were by women. Differences in diving habits were observed between men and women, which included number of dives per annum, maximum depths dived, and dives with extra stops. When the level of experience was taken into account in this study group, the estimated rate of DCS in men was 2.60 times greater than for women. CONCLUSIONS: In this study, comparison between men and women in recreational diving differed from the initial evaluation when underlying factors were taken into account. Future studies should attempt to control for underlying factors in the data gathering and data analysis.

Adolescent↗

Decompression sickness during simulated extravehicular activity: ambulation vs. non-ambulation.

BACKGROUND: Extravehicular activity (EVA) is required from the International Space Station on a regular basis. Because of the weightless environment during EVA, physical activity is performed using mostly upper-body movements since the lower body is anchored for stability. The adynamic model (restricted lower-body activity; non-ambulation) was designed to simulate this environment during earthbound studies of decompression sickness (DCS) risk. DCS symptoms during ambulatory (walking) and non-ambulatory high altitude exposure activity were compared. The objective was to determine if symptom incidences during ambulatory and non-ambulatory exposures are comparable and provide analogous estimates of risk under otherwise identical conditions. METHODS: A retrospective analysis was accomplished on DCS symptoms from 2010 ambulatory and 330 non-ambulatory exposures. RESULTS: There was no significant difference between the overall incidence of DCS or joint-pain DCS in the ambulatory (49% and 40%) vs. the non-ambulatory exposures (53% and 36%; p > 0.1). DCS involving joint pain only in the lower body was higher during ambulatory exposures (28%) than non-ambulatory exposures (18%; p < 0.01). Non-ambulatory exposures terminated more frequently with non-joint-pain DCS (17%) or upper-body-only joint pain (18%) as compared with ambulatory exposures, 9% and 11% (p < 0.01), respectively. DISCUSSION: These findings show that lower-body, weight-bearing activity shifts the incidence of joint-pain DCS from the upper body to the lower body without altering the total incidence of DCS or joint-pain DCS. CONCLUSIONS: Use of data from previous and future subject exposures involving ambulatory activity while decompressed appears to be a valid analogue of non-ambulatory activity in determining DCS risk during simulated EVA studies.

Decompression Sickness↗

Importance of surface tension in therapeutic compression in decompression sickness.

The aim of this investigation was to study the effect of environmental pressure and surface tension on the size of gas bubbles in tissues and on their inner pressure. Due to the action of surface tension, the pressure inside the bubbles is always greater than the surrounding pressure. This phenomenon is the more marked, the smaller are the bubbles. Therapeutic compression leads to diminution of the volume of gas bubbles and thus to a rise of that portion of their inner pressure which is due to surface tension. In small bubbles the surface tension may cause their dissolution and disappearance. It is therefore correct to implement therapeutic compression in decompression sickness as soon as possible before the fusion of a significant number of small bubbles into larger ones occurs.

Atmospheric Pressure↗

Decompression sickness and recreational scuba divers.

OBJECTIVES: The aim of this study is to clear the status of recreational scuba divers in Japan for promoting safety in recreational diving. METHODS: A five year (from 1996 to 2001) questionnaire survey was performed of Japanese divers at the Osezaki area in Japan. The subjects of this survey included diving instructors as well as recreational divers. Based on the obtained data, the study investigated the theory predicted incidence of decompression sickness (DCS) among Japanese recreational divers. RESULTS: The average (SD) of the maximum depth for diving was 37.4 (13.1) metres, which was deeper than the recommended depth of recreational diving. The incident rate of nitrogen narcosis (12%) was the most frequent, followed by barotraumas of the ear (11%) and barotraumas of the paranasal sinus (5.6%). The rate of DCS was 1.9 % (60 divers) during investigated period, and that DCS occurred once per 19 011 dives in calculation. CONCLUSIONS: This investigation showed that the status of leisure diving in Japan is still serious, because DCS would be expected to occur once a weekend in Japan. It is speculated that many divers may develop DCS while moving through high altitudes after diving, particularly at the Osezaki diving spot in Japan. Based on the results of this study, it is emphasised that every Japanese leisure diver should take an increasing interest in the safety of diving activity.

Adult↗

Blood and blood vessel wall changes induced by decompression sickness in dogs.

Healthy female dogs of mixed breed were anesthetized with pentobarbital sodium and given 51Cr-labeled autologous red blood cells and 125I-labeled anticanine vessel wall fiber (collagen and elastin) antibody. The anesthetized dogs were exposed to the equivalent of a 220-ft dive on air for 40-45 min (descent rate 75 ft/min, ascent rate 60 ft/min). The animal's condition was adjusted by additional shorter and/or shallower dives. Four dogs had mild decompression sickness (DCS), and seven had severe DCS judged by electrocardiogram. Three of the seven died before completion of the experiment. Permeability of the endothelial sheet of jugular veins and carotid arteries to the tracer (125I-gamma-globulin) was significantly increased in animals with severe but not mild DCS. There was slight hemoconcentration (increased capillary and venular permeability). Scanning electron microscopy showed that the endothelium was grossly intact with no evidence of mechanical damage, but giant cells (derived from monocytes) frequently adhered to the endothelium. Leukocytes and platelets adhered occasionally. Fibrin monomer was found in the plasma. Thus DCS is accompanied by endothelial cell alteration and limited blood cell adhesion to vessel walls in addition to activation od the clotting mechanism.

Animals↗

Screening test for decompression sickness.

The fibrin-fibrinogen degradation products (FDP) tests were studied in 18 patients having a history of illness associated with diving. FDP tests were performed prior to hyperbaric oxygen therapy (OHP). Eight patients were serious neurologic signs had positive FDP tests and required repetitive therapy. Six patients had negative FDP tests with local musculoskeletal complaints and all were asymptomatic following the first OHP treatment. Three patients were found to be suffering from other diseases. These three patients had normal levels of FDP. One patient treated at another facility 3 months earlier and having paraplegia had a positive FDP test. Serious decompression sickness with neurologic complaints appear to have some degree of disseminated intravascular coagulation (DIC) as reflected by the FDP tests. The FDP test appears to be a useful screening test that may be able to delineate therapy.

Adolescent↗

[Medical aspects of diving in otorhinolaryngology. I. Barotrauma and decompression sickness].

Recreational scuba diving has become immensely popular in recent years and is no longer restricted to individualists or adventurers. During a dive, the human body with its gas-filled cavities is exposed to an increased ambient pressure. In the present review article, aspects of diving and hyperbaric medicine related to the otolaryngology field are presented. The basics of physics, physiology and pathophysiology that are essential to understand the effects of an increased and varying ambient pressure are reviewed. Barotrauma of the outer, middle and inner ear, the paranasal sinuses, face, teeth and larynx are explained and classified in those during the compression and decompression phase. This is followed by a discussion of inner ear decompression sickness. The present article will provide a background and foundation for both, an adequate treatment of these diseases and a critical and responsible health education of the diver.

Athletic Injuries↗

Oxy-helium treatment for refractory neurological decompression sickness: a case report.

A 49-yr-old male presented with paraparesis and urinary incontinence that appeared 10 min after surfacing from a dive. Treatment was started on an extended USN table 6, but the symptoms persisted. Twenty-four hours later, he was treated with oxy-helium table CX-30, resulting in marked improvement in gait and in sensory and motor function. Urodynamic examination indicated an upper motor neuron lesion; bilateral decreased amplitude of the somatosensory evoked potential was found on stimulation of the tibial nerves; no response below the upper limbs was elicited on central motor conduction time (CMCT) testing; MRI showed lesions in the lower dorsal cord. The patient's condition was further improved by an additional 10 hyperbaric oxygenation sessions, with complete restoration of urinary control and virtually complete sensory and motor recovery. Follow-up urodynamic studies were normal. CMCT recordings showed a bilateral lower limb small-amplitude response. The present case reinforces the limited clinical data regarding the value of oxy-helium in the treatment of neurological decompression sickness, even when primary treatment with oxygen tables is unsuccessful.

Ataxia↗

Somatosensory evoked potentials and neuraxial blood flow in central nervous system decompression sickness.

Seven adult, conditioned dogs were anesthetized with pentobarbital sodium and prepared for measurement of upper lumbar, mid-thoracic and lower cervical spinal evoked potentials (SEPs), cortical evoked potential (CEP), and aortic, right ventricular, and cerebrospinal fluid pressures. Following preparation, one animal was monitored by means of repeated evoked potentials for 2 h, at which time a [14C]iodoantipyrine autoradiographic blood flow study was performed. The 6 other animals were exposed to simulated dives in a compression chamber while anesthesia was maintained through a chamber penetration. These animals developed decompression sickness (DCS) of varying severity upon returning to the surface, and the corresponding decrements in neuronal function of the cord and the brain were measured by means of serial SEP and CEP recording. Following this evoked potential recording, [14C]iodoantipyrine autoradiographic blood flow studies were performed. The results indicated that clear reductions in SEP and CEP amplitude were associated with very low blood flows, which were in the 'neuron-disabling' range. Spinal and cortical somatosensory evoked potentials provide a valuable index with which to monitor and manage a model of spinal cord DCS.

Animals↗

Relation of breathing oxygen-argon gas mixtures to altitude decompression sickness.

A 95% oxygen-5% argon breathing mixture produced by a molecular sieve generator was shown to be similar to a 95% O2-5% N2 mixture for breathing during 1-h exposures at 7,620 m (25,000 ft) or 10,972 m (35,000 ft), as determined by the detection of proportionate numbers of intravascular bubbles in the pulmonary artery of dogs. Comparable results were obtained with 95% O2-5% He or 100% O2. The partial pressures of a 5% mixture at 7,620 and 10,972 m were 14.1 and 8.6 torr, respectively, and were apparently low enough so that the nonmetabolizable gases did not result in differences in the incidence of intravascular bubble formation or decompression sickness. Argon at the 10% level showed a nonsignificant trend to produce more bubbles. Individual susceptibility or resistance to form bubbles was observed with the different gases. Denitrogenation with either 5 or 10% mixtures of the inert gases was quite effective, as shown by a reduction in the number of intravascular bubbles detected.

Aerospace Medicine↗