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PubMedDate not supplied

Preoxygenation time versus decompression sickness incidence.

Preoxygenation, breathing 100% oxygen prior to decompression, has been used for well over half of this century to reduce decompression sickness (DCS) incidence. Duration of preoxygenation has been reported to be inversely related to subsequent DCS incidence. A direct comparison of DCS incidence at 30,000 ft versus preoxygenation time is needed to allow better-informed decisions regarding the cost vs. benefit of increasing preoxygenation time to prevent DCS. To obtain such a comparison, we accomplished a retrospective study of exposures to 30,000 ft (226 mm Hg; 4.37 psia) while performing mild exercise. The 86 male exposures were preceded by preoxygenation times of one to four hours. Venous gas emboli (VGE) and DCS symptom development were monitored and recorded. Although more protection was demonstrated with increasing preoxygenation time, the cost-to-benefit ratio also increases with each additional increment of preoxygenation time. The diminishing return of increasing preoxygenation to reduce DCS would eventually impact mission planning and crew duty limitations. Alteration in the physiology of denitrogenation, such as inclusion of exercise during preoxygenation, may provide better and more cost-effective DCS protection than simply increasing preoxygenation time.

Aerospace Medicine↗

PubMedDate not supplied

[Probability of altitude decompression sickness during a suited exit from a space ship having a near-Earth atmosphere].

A large number (550) pressure chamber experiments in which 200 suited subjects simulated an egress from the spacecraft (decompression from 760 to 20--10 mm Hg) showed a relationship between decompression sickness frequency and severity, space suit absolute pressure (160--310 mm Hg), time of the exposure (1--10 hours) and desaturation (15--60 min), and exercise load (150--400 Cal/hr). Without desaturation there were no decompression sickness symptoms at a suit pressure of 270--310 mm Hg. An egress into space in a suit at a pressure of 160--230 mm Hg after 15--60 min desaturation induced bends of different severity. Less frequent cases of decompression sickness in our experiments as compared with the literature data (obtained on unsuited subjects) can be attributed to the peculiar kinematics of movements and excessive pressure in the suit.

Adult↗

PubMed1995

Role of ischemia in rats with spinal cord injury induced by decompression sickness.

The microsphere technique was used to determine whether blood flow to the central nervous system and various organs is impaired in rats with spinal cord injury induced by decompression sickness. For this purpose cannulas were placed in the left ventricle of the rats for the injection of microspheres and in the tail artery as the reference site for withdrawal of blood for the calculation of cardiac output (CO) and blood flow (BF) and for measurement of blood pressure (BP) and heart rate (HR). The rats were then subjected to a simulated dive that by electrophysiologic criteria rapidly (within 60 min after diving) induces severe neurologic deficits in the cord. Microspheres were used to determine CO and BF before and at 10, 60, and 180 min after diving. CO, BP, and HR were not affected by diving. BF to various regions of the brain, heart, bone, and fat was also not affected by diving. BF decreased in the lung (40%) and skeletal muscle (50%) and increased in spinal cord (20%) at 10 min after diving. At 60 and 180 min after diving the only alterations seen were increases in hepatic arterial and portal BF. Analysis of the distribution of cardiac output showed that diving induced changes that essentially paralleled the BF changes described above. We conclude that perfusion in the central nervous system is maintained in rats with spinal cord injury induced by decompression sickness. These results indicate that ischemia does not play a role in the pathophysiology of neuronal injury in this model of decompression sickness.

Animals↗

PubMed1999

Three cases of spinal decompression sickness treated by U.S. Navy Treatment Table 7.

For patients of type 2 decompression sickness, recompression therapy using U.S. Navy Treatment Table 6 (TT6) and its extensions is the most common means of treatment. However, some cases are resistant to the recompression therapy, and the outcome of TT6 is not always satisfactory. Although a new table, the U.S. Navy Treatment Table 7 (TT7) was described in 1985 in the U.S. Navy Diving Manual, to date few cases who were treated using TT7 have been reported. Here, we report three cases of spinal decompression sickness who received treatment according to TT7. Two were sports scuba divers, and the other a commercial diver. TT7 was applied later than 4 d after onset in all three cases; two patients were remarkably improved during the recompression therapy, while the other improved to a certain extent after additional repetitive TT6. Mild impairment of lung function, probably due to pulmonary oxygen toxicity, was observed on lung function testing in one case. In all cases, after additional TT6 and/or rehabilitation, patients were able to return to active daily living.

Adult↗

PubMed1980

Permeability changes in cerebral, iridic, and retinal vessels during experimental decompression sickness in the rat.

An investigation has been made of the effect of acute decompression sickness upon the permeability of the cerebral, iridic, and retinal vessels of the rat, with sodium-fluorescein as intravenous tracer. No permeability changes were observable during the first 15 min subsequent to decompression, following exposure to 5.1 bar for 50 min. Focal leaky areas were found in the brain parenchyma after exposures to 5.1 bar for 120 min. Although sodium-fluorescein partially permeated the pial vessels in controls, the treatment in a hyperbaric chamber seems to increase the diffusion of the tracer from the pia into the cerebral cortex. Nevertheless, both the iridic and retinal vessels remained "tight." The factors which increase the permeability of microvasculature in brain and possible reasons for the negative results obtained with the iris and retina in decompression sickness are discussed.

Air Pressure↗

PubMed2002

Recurrent inner ear decompression sickness associated with a patent foramen ovale.

Isolated inner ear injuries occurring during shallow scuba dives are an uncommon manifestation of decompression sickness in recreational divers. We describe a patient who presented with the typical symptoms of inner ear involvement after 2 independent dives within the decompression limits. The diver reported symptoms of unilateral (right-sided) hearing loss, tinnitus, and vertigo after dives to 35 and 50 m. After treatment with hyperbaric oxygen, his symptoms completely resolved. To confirm the hypothesis of inner ear decompression sickness (IEDCS), we examined the patient for a right-to-left shunt by cranial Doppler ultrasound and found a patent foramen ovale. The existence of a patent foramen ovale is suspected to be a risk factor for developing neurological symptoms of decompression sickness. There was no evidence of any other risk factors, so we suggest that the relevant right-to-left shunt in our patient may have been the predisposing factor that caused the inner ear symptoms during his scuba dive.

Adult↗

PubMed1981

Acute decompression sickness--report of an autopsy case with widespread fat embolism.

A case of acute decompression sickness presenting severe clinical features was reported. At the time of autopsy, intra- and extravascular air bubbles were found in various organs. Pulmonary fat embolism was also prominent in association with severe circulatory disturbances of the lungs. The spinal cord showed edematous and congestive swelling which was intimately related to the coagulation of blood within the epidural veins that contained innumerable fat droplets. Intravascular fat seemed to be created in and released from the injured adipose tissue, especially that of the bone marrow during decompression and to have acted as an accelerator of intravascular coagulation. The pathophysiological significance of the fat embolism for the development and the progression of decompression sickness is discussed.

Adult↗

PubMed2003

Case history of serious altitude decompression sickness following rapid rate of ascent.

Neurologic and respiratory decompression sickness (DCS) symptoms occurring in the same individual represent complications rarely observed in altitude research. A case is presented of multi-symptom serious DCS resulting from exposure to 12,192 m (40,000 ft). Following 90 min of preoxygenation, the patient was decompressed in a hypobaric chamber from ground level to 12,192 m in 30 s. After 69 min at altitude he developed substernal chest pressure and the flight was immediately terminated. During the chamber descent the patient appeared disoriented. By 5486 m (18,000 ft) his chest pressure had resolved. The post-flight medical exam revealed multiple neurological abnormalities. He underwent a Table VI hyperbaric oxygen treatment with complete resolution of all abnormal neurological findings.

Aerospace Medicine↗

PubMed2001

The effect of exposure to 35,000 ft on incidence of altitude decompression sickness.

INTRODUCTION: Exposure to 35,000 ft without preoxygenation (breathing 100% oxygen prior to decompression) can result in severe decompression sickness (DCS). Exercise while decompressed increases the incidence and severity of symptoms. Clarification of the level of activity vs. time to symptom onset is needed to refine recommendations for current operations requiring 35,000-ft exposures. Currently, the U.S. Air Force limits these operations to 30 min following 75 min of preoxygenation. The objective of this study was to determine the effect of exercise intensity on DCS incidence and severity at 35,000 ft. METHODS: Following 75 or 90 min of ground-level preoxygenation, 54 male and 38 female subjects were exposed to 35,000 ft for 3 h while performing strenuous exercise, mild exercise, or seated rest. The subjects were monitored for venous gas emboli (VGE) with an echo-imaging system and observed for signs and symptoms of DCS. RESULTS: Exposures involving strenuous and mild exercise resulted in higher incidence (p < 0.05) and earlier onset of symptoms (p < 0.05) of DCS than exposure at rest. Mild and strenuous exercise during exposure did not differ in incidence or rate of onset. Incidence at 30 min of exposure was 8% at rest and 23% while exercising. CONCLUSION: The results showed that current guidelines for 35,000-ft exposures keep DCS risk below 10% at rest. Exercise, even at mild levels, greatly increases the incidence and rate of onset of DCS.

Aerospace Medicine↗

PubMed1991

[Neurological decompression sickness].

We have examined 34 divers, mean age 30 years, after treatment for neurological decompression sickness. The initial symptoms often indicated mild sensory or motor involvement. After recompression treatment five of 19 divers with primary affection of the brain had slight hemiparesis or dysphasia. Nine of 14 divers with primary affection of the spinal cord showed signs of spinal cord dysfunction following treatment. Only 16 divers were recompressed within six hours after start of the neurological symptoms. It is concluded that neurological decompression sickness is a serious disorder with a high rate of residual findings. The condition should be treated with prompt recompression, administration of oxygen, and intravenous fluid.

Adult↗

PubMed2001

Radionuclide lung imaging in respiratory decompression sickness: potential role in the diagnosis and evaluation of hyperbaric therapy.

Of the more than 3.5 million trained divers in the United States, many will experience various illnesses specific to divers. Most of these illnesses are related to the changes in absolute pressure that divers experience while diving. During and after ascent, a diver is at risk for decompression sickness and pulmonary barotrauma. A very rare casualty is pulmonary decompression sickness from immersion. This is a literature review and case report of a young woman with acute respiratory decompression sickness who had defects on perfusion lung imaging after a diving accident and after hyperbaric oxygen therapy. However, the perfusion defects reverted to normal in less than 24 hours. Possible explanations for the changes in the appearances of the scans are offered and discussed. This case report shows the potential utility of lung scanning in the diagnostic examination of these patients and the evaluation of the adequacy of treatment with hyperbaric oxygen therapy. A greater use of ventilation-perfusion lung scans in the treatment of such patients may establish its role more definitely.

Adult↗

PubMed1975

Management of severe decompression sickness with treatment ancillary to recompression: case report.

Recompression remains the primary form of treatment in decompression sickness, but severe cases require ancillary treatment. The case of a compressed air worker with decompression sickness is presented who, in addition to recompression, required 5.5 of I.V. fluids in the first 8 h, heparin, digitalis, steroids, and respiratory support, to prevent death. The report includes a description of the precipitation causes, the course during recompression, the drugs and dosages used, and comments on respirator treatment.

Adult↗

PubMedDate not supplied

[Prevention of altitude decompression sickness during short flights in a depressurized cabin at high altitudes].

Forty altitude chamber experiments were carried out in which 18 test subjects participated. The purpose of the experiments was to prevent decompression sickness in a pilot using an altitude compensatory suit and oxygen mask. It was demonstrated that oxygen breathing on the ground and at an altitude of 8 km for 20 and 50-60 min eliminated severe symptoms and lowered the frequency of occurrence of mild symptoms of decompression sickness during the subsequent 10-20 and 60-120 min exposures to altitudes of 40,000 and 11,000 m respectively. An increase in the absolute pressure to 240-290 mm Hg in the altitude garment prevented decompression sickness of altitudes of 11,000-15,000 m and eliminated it if it occurred at lower barometric pressure.

Adult↗

PubMed1978

The kangaroo rat as a model for type I decompression sickness.

This study involved 720 exposures of 70 kangaroo rats trapped in West Texas and showed that decompression-induced tail biting in this animal provides a good animal model for marginal limb bends in man. That this phenomenon can be reversed by recompression and pathological examination of the tail both indicated that a similar mechanism is probably involved in kangaroo rats and humans. Quantitatively, the most susceptible 20% of kangaroo rats can reproduce the no-stop decompression limits for man for exposure times ranging from 5 min to 8 h, for both air and helium-oxygen. Even the average minimum no-tail-biting depth of 46.2 fsw (2.40 ATA) for this species is much closer to the minimum bends depth of man than to the equivalent depth for other animals of its size, and is as good as the goats'. Its size and habits make the kangaroo rat much more convenient than other animals to use as a model for marginal decompression sickness, and particularly attractive economically for testing long helium-oxygen schedules and other means of decompression sickness prevention.

Animals↗

PubMed2005

Headache and altitude decompression sickness: joint pain or neurological pain?

INTRODUCTION: Exposure to reduced ambient pressure may result in decompression sickness (DCS). Headache is among the DCS symptoms encountered and is usually regarded as neurological DCS, which is traditionally classified as serious DCS. Since cranial sutures may be considered joints, it is possible that some headaches are actually joint pain and when associated with decompression sickness need not be neurological DCS. METHODS: Records were individually recovered from the Davis Hyperbaric Laboratory at Brooks City-Base, TX. Information was extracted using a detailed survey instrument. Possible joint pain headache cases were identified using three criteria: headache localized at a suture, normal neurologic exam, and resolution within 30 min of hyperbaric oxygen treatment. RESULTS: A total of 729 records documenting treatment for DCS were scrutinized. Of these, 70 cases of altitude DCS with headache were examined. Analysis, using the three criteria, showed 23% (16 cases) of altitude headache DCS symptoms could potentially be re-classified as joint pain. CONCLUSION: Generally, headache DCS is considered neurological DCS. However, since cranial sutures are joints, both histologically and functionally, and since DCS most commonly affects joints, headache DCS may, at times, be joint pain DCS. Indeed, retrospective data analysis suggests that this possibility exists. Such a reclassification from neurological to joint pain DCS would lessen the aeromedical impact of a DCS headache.

Adult↗

PubMed1978

Acute decompression sickness: 50 cases.

In a review of the most recent 50 consecutive cases of acute decompression sickness in US Navy divers undergoing training at the Naval School, Diving and Salvage, in no instance was recompression following the initial treatment necessary, nor was there any permanent morbidity post-treatment. Factors common to this series are 1) strict physical screening and conditioning; 2) physician and diver awareness of the signs and symptoms of decompression sickness; 3) short surface interval between symptom onset and recompression; 4) aggressive diagnostic and therapeutic use of hyperbaric oxygenation, and 5) judicious use of adjunctive measures such as intravenous fluid and dexamethasone (Decadron). In the ideal management, the physician sees the patient shortly after symptom appears. As soon as central nervous system involvement appears, 100% oxygen by mask is administered and the patient is recompressed supine to 60 feet of sea water.

Decompression Sickness↗

PubMed1988

The role of computed tomography in the assessment of neurologic sequelae of decompression sickness.

Computed tomographic (CT) scans were performed on 47 patients who had received recompression treatment for decompression sickness. A retrospective review of the case notes disclosed that 24 of the 47 patients had symptoms that suggested cerebral involvement. None of the reported CT abnormalities could be correlated with the clinical manifestations at presentation. It was concluded that the CT scan is not a cost-effective investigative tool for the posttreatment evaluation of decompression sickness.

Brain↗

PubMed1994

Assessment of spinal cord trauma using evoked potentials in a rat model of decompression sickness.

A rapid quantitative technique for assessing spinal cord trauma in a rat model of decompression sickness is described. Evoked potentials are measured from the lower limbs of rats before and after dives with compressed air in a hyperbaric chamber. Under chloral hydrate anesthesia, the sciatic nerve is stimulated at the sciatic notch with needle electrodes and platinum/iridium electrodes are used to record the action potentials from the plantar muscles. Analysis showed that the sensory reflex response was markedly depressed in the rats soon after diving and did not recover for up to 5 days. The motor response was similarly affected although to a lesser degree. The latency of the reflex response also became prolonged after 3 days. The significant and complex pattern of neurological dysfunction shown by this electrophysiologic technique validates the use of the rat model for the study of spinal cord decompression sickness. This technique should aid studies aimed at testing new therapies for this disease.

Action Potentials↗