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Weber's syndrome and sixth nerve palsy secondary to decompression illness: a case report.

We describe the first case of Weber's Syndrome to present as a manifestation of decompression illness in a recreational scuba diver. Weber's Syndrome is characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis. The patient was a 55 year-old male with a past medical history of a pulmonary cyst, in whom symptoms developed after a multilevel drift dive to a depth of 89 feet for 53 minutes, exceeding no-decompression limits. Symptom onset was within 30 minutes of surfacing and included the Weber's Syndrome, a sixth nerve palsy, dizziness, nausea, sensory loss, and ataxia. The patient received four U.S. Navy Treatment Tables with complete resolution of all neurological signs and symptoms. The mechanism of injury remains unclear, but may involve aspects of both air gas embolism and decompression sickness. Individuals with pre-existing pulmonary cysts may be at increased risk for dive-related complications.

Abducens Nerve Diseases↗

[Simulated diving tests in guinea pigs].

Simulated diving tests with helium oxygen mixture were carried out in guinea pigs. The water depth was 100M (1.1Mpa). Hearing ability of guinea pigs changes and inner ear lesions occurred after decompression. The tests proved that hearing changes were especially evident in 0.5-1.0 kHz in slow decompression group and were induced by barotrauma. In the fast decompression group, the hearing impairment in 0.5-1.0 kHz range was more prominent than that in the 2-8kHz. The hearing thresholds of the 3 guinea pigs having vestibular symptoms (nystagmus, rotatory movement of the body) were elevated in the 0.5-8.0 kHz range. The vestibular symptoms and the elevation of hearing threshold of these 3 guinea pigs were induced by inner ear decompression sickness. The middle ears showed bleeding, effusion and cell infiltration. Ultrastructural changes were derangement and lodging of stereocilia of hair cells and changes of organelle.

Animals↗

The biological effects of high pressures: underlying principles.

Physico-chemical principles set constraints on the response of biological systems to high-pressure gases and to pressure per se. They also indicate the mechanisms that may be involved. Classical thermodynamics, intermolecular forces and the theory of solutions and many other areas of physical chemistry have contributed to our understanding of the problems faced by divers breathing gases at high pressure, in particular the high pressure neurological syndrome, inert gas narcosis and decompression sickness. The value and the limitations of physico-chemical arguments when applied to the problems of underwater physiology are analysed.

Atmospheric Pressure↗

Recreational scuba injuries.

Decompression illness, which includes decompression sickness and arterial gas embolism, can be a complex and difficult diagnostic dilemma. The signs and symptoms are not well known and mimic other illnesses which often results in delay when seeking medical evaluation. Additionally, most physicians are not exposed to diving medicine and may not recognize a decompression illness injury. The Divers Alert Network (DAN) offers information to the diving public and telephone consultation for physicians who require assistance in the evaluation of scuba divers and management of dive accident cases. Divers Alert Network also publishes the national annual report on scuba diving morbidity and mortality. Services provided without charge are sponsored by the DAN membership. This article introduces the physician to decompression illness and the basic care and treatment of the injured scuba diver.

Decompression Sickness↗

Separation of basic parameters of decompression using fingerling salmon.

The experimental limitations inherent in use of air-breathing vertebrates for studies of decompression are chiefly due to the difficulty in estimating supersaturation levels associated with both symptoms of decompression sickness and bubble formation. The difficulty is because gas elimination begins upon reduction of pressure and therefore complicates any estimates of the supersaturations that promoted the bubbles or symptoms, or both, in the first place. Use of physostomatous fish such as salmonid fingerlings easily available from hatcheries allows decompression of both fish and surrounding water, thereby minimizing gas tension gradients from the fish to the water and the water to the fish. Depending upon the experimental conditions imposed, the important physical properties such as diffusivity and solubility of different diving gases, H2, Ne, He, and N2, can be separated or combined parametrically. Results of these studies indicate that initial bubble formation in vivo is relatively independent of solubility, whereas the bubble growth phase is more dependent on gas concentration.

Animals↗

Blood-brain and blood-lung barrier alteration by dysbaric exposure.

Failure of certain circulating substances to penetrate specific organs led to the concept of blood-organ barriers. Such barriers can be altered by various physical or chemical means. This report concerns modification of the blood-brain barrier (BBB) and blood-lung barrier (BLB) by dysbaric exposure. Trypan blue was intravenously administered to 19 experimental rabbits (subjected to compression-decompression) and to 11 controls (kept at ambient pressure). Gross and microscopic examination and measurements of dye extracted from tissues revealed greater dye penetration into lung and brain of the experimental animals. Dye concentration in brain was 12.10 microgram/g tissue in experimental and 2.93 microgram in control animals; in lungs it was 935 microgram and 434 microgram, respectively (0.01 greater than P 0.001). Increased permeability of BBB and BLB was associated with intravascular bubbles. The mechanism of BBB and BLB alteration may involve chemical agents activated by gas-blood interface or vascular injury produced by bubbles. These observations could have pathogenetic implications in decompression sickness and may suggest new methods for facilitating penetration of therapeutic agents into the brain.

Animals↗

[Neuroradiological studies in diving accidents].

In case of a type II decompression sickness (with cerebrospinal injury), the decision on how to structure a prompt hyperbaric treatment rests on an anamnesis and the clinical investigation. In looking for an associated contingent barotrauma, one has to be satisfied with an X-ray of thorax and abdomen. The myelopathy which results from a decompression mishap with medullary involvement forms a very peculiar clinical entity defined by a fascicular injury at several levels. For several years now, clinical radiologists resort to a new medical imaging technique: Nuclear Magnetic Resonance (NMR-)Imaging. For the first time, this technique allows the imaging of intramedullary lesions due to a decompression accident. Other neuroradiological investigations (such as myelography, spinal tomodensitometry, medullary angiography, isotopic tests) are without merit for evaluating decompression accidents with medullary involvement. NMR-Imaging has the potential too, of revealing ischemic cerebral injuries, even if the clinical brain impairment is often silent and therefore overlooked. The role of NMR-Imaging for evaluating cerebrospinal aspect of decompression accidents is not yet finalized. However, NMR-Imaging will give without any doubt a boost to the pathophysiological knowledge of decompression mishaps.

Adult↗

Deep diving mammals: Dive behavior and circulatory adjustments contribute to bends avoidance.

A mathematical model was created that predicted blood and tissue N(2) tension (P(N2)) during breath-hold diving. Measured muscle P(N2) from the bottlenose dolphin after diving repeatedly to 100 m (Tursiops truncatus [Ridgway and Howard, 1979, Science, 4423, 1182-1183]) was compared with predictions from the model. Lung collapse was modelled as a 100% pulmonary shunt which yielded tissue P(N2) similar to those reported for the dolphin. On the other hand, predicted muscle P(N2) for an animal with a dive response, reducing cardiac output by 66% from surface values (20.5 to 6.8l x min(-1)), also agreed well with observed values in the absence of lung collapse. In fact, modelling indicated that both cardiovascular adjustments and dive behaviour are important in reducing N2 uptake during diving and enhancing safe transfer of tissue and blood N2 back to the lung immediately before coming to the surface. In particular, diving bradycardia during the descent and bottom phase together with a reduced ascent rate and increase in heart rate reduced mixed venous P(N2) upon return to the surface by as much as 45%. This has important implications as small reductions in inert gas load (approximately 5%) can substantially reduce decompression sickness (DCS) risk by as much as 50% (Fahlman et al., 2001, J. Appl. Physiol. 91, 2720-2729).

Acclimatization↗

Diving injuries.

This is a collective review about the pathophysiology, diagnosis, and management of SCUBA and diving injuries by the emergency physician. These injuries can be classified into those resulting from the toxic effects of the inhaled gas, from the pressure changes in the water and gas mixture while diving, and from decompression sickness. With the increasing popularity of SCUBA diving, it is hoped that this discussion will enable a recognition of these injuries and therefore minimize the morbidity and mortality from them.

Athletic Injuries↗

Decompression outcome following saturation dives with multiple inert gases in rats.

This investigation examined the question of whether gas mixtures containing multiple inert gases provide a decompression advantage over mixtures containing a single inert gas. Unanesthetized male albino rats, Rattus norvegicus, were subjected to 2-h simulated dives at depths ranging from 145 to 220 fsw. At pressure, the rats breathed various He-N2-Ar-O2 mixtures (79.1% inert gas-20.9% O2); they were then decompressed rapidly (within 10 s) to surface pressures. The probability of decompression sickness (DCS), measured either as severe bends symptoms or death, was related to the experimental variables in a Hill equation model incorporating parameters that account for differences in the potencies of the three gases and the weight of the animal. The relative potencies of the three gases, which affect the total dose of decompression stress, were determined as significantly different in the following ascending order of potency: He less than N2 less than Ar; some of these differences were small in magnitude. With mixtures, the degree of decompression stress diminished as either N2 or Ar was replaced by He. No obvious advantage or disadvantage of mixtures over the least potent pure inert gas (He) was evident, although limits to the expectation of possible advantage or disadvantage of mixtures were defined. Also, model analysis did not support the hypothesis that the outcome of decompression with multiple inert gases in rats under these experimental conditions can be explained totally by the volume of gas accumulated in the body during a dive.

Animals↗

Explosive decompression of subjects up to a 20,000-m altitude using a two-pressure flying suit.

The RSAF two-pressure flying suit system to protect the pilot at high altitude has been tested from different medical safety aspects. To secure adequate alveolar oxygen pressure, the suit admits up to 70 mm Hg (9.3 kPa) positive pressure breathing by counter-pressure against the thorax and by a 3.2 times higher pressure in the anti-G suit. After 1 h of oxygen breathing, subjects were exposed to explosive decompression from an altitude of 9,000 m to 17,500 or 20,000 m in 0.5 s in a hypobaric chamber. No symptoms of decompression sickness or of alveolar rupture with gas embolism to the central nervous system were seen. Pulmonary X-rays after the test did not reveal any signs of lung rupture with extrapulmonary gas leakage. With the precordial Doppler ultrasound technique, intracardial gas bubbles (silent bubbles) could be detected only in one subject after explosive decompression to a 20,000-m altitude in the 10 experiments.

Adult↗

Evaluation of standard decompression schedule by agarose gel method.

The Standard Decompression Schedule was evaluated by the method of bubble formation in agarose gel, the result of which can be summarized as follows: 1) The number of bubbles formed in agarose gel corresponded well with the exposed pressure. 2) The technique of this method was simple and the number of bubbles was accurately counted. 3) Eventually, this method was useful for examining the decompression schedules. 4) It is not always safe to follow the Standard Decompression Schedule in some pressure conditions. 5) As to the period of time that a person is able to tolerate a high pressure condition, the prescription of the Standard Decompression Schedule is not necessarily correct. 6) The number of bubbles was small by the proper decompression schedule, for example, in the cases of exposure above the 60-meter depth of water. 7) This method can be applied for the prevention of decompression sickness when the agarose gel samples are attached to the workers during the compressed air work. 8) The number of bubbles was inconsistent with the coefficient of body pressure (1. N2 in the body), therefore it is not necessarily safe to rely only on the coefficient of body pressure. 9) To prevent osteonecrosis, the Standard Decompression Schedule is not proper, a deeper first stop and slower ascent being recommended.

Decompression↗

Breathing volumes and gas exchange during simulated rapid free ascent from 100 msw.

The crew of a disabled submarine can be rescued by means of free ascent through the water to the surface. Pulmonary gas exchange was studied during simulated rapid free ascent in subjects standing immersed to the neck in a pressure chamber. The pressure was rapidly increased to 1.1 MPa [100 meters seawater (msw)] followed by decompression at 0.03 MPa/s (3 msw/s). Effective inspired tidal volume, as estimated by an Ar dilution method, fell gradually to zero during decompression from 20 to 0 msw. Directly determined expired tidal volumes were increased up to two to three times at the time of return to surface pressure compared with pre- and postdecompression volumes. End-tidal PCO2 was increased on compression and fell to a nadir of 3.4 kPa (25 Torr) at the time of return to surface pressure. Thus, intrapulmonary gas expansion caused simultaneous inspiratory hypoventilation and expiratory hyperventilation. If O2-enriched gas is to be used to reduce the risk of decompression sickness, it should be administered early during decompression to alter the intrapulmonary gas composition. The time course of arterial PCO2 changes as reflected by end-tidal values during short-lasting compression/decompression would act to promote inert gas supersaturation in the brain.

Adult↗

Cochleo-vestibular disturbances in diving.

Insidious development of high-tone sensorineural hearing loss may be associated with diving, but the evidence is not certain and further research is needed. 'Internal ear barotrauma' can cause an acute or relatively acute onset of hearing loss and/or vertigo, and it may be that 'alternobaric vertigo' provides a link between the insidious and acute forms of labyrinthine injury in diving. With deep diving, decompression sickness and other syndromes can also affect the cochleo-vestibular system. These aetiologies and effects will be discussed, together with evidence from an audiometric survey of naval divers and of 5 experimental deep divers.

Cochlea↗

[Decompression injuries].

A decompression accident occurs during uncontrolled dive ascent with diving equipment. Through the rapid decrease in the surrounding pressure, gas bubbles form in the blood and tissues. Depending upon the mechanism of onset, the decompression illness (DCI) is classified as decompression sickness (DCS) or arterial gas embolism (AGE). The therapy consists of administering, as quickly as possible, 100% oxygen as well as a volume substitution. The treatment is continued in a recompression chamber.

Decompression Sickness↗

Decompression incidence in air- and liquid-breathing hamsters.

The effects of hyperbaric compression on heart rate, rectal temperature, respiratory rate, bubble formation, and survival were studied in three groups of anesthetized golden hamsters (Mesocricetus auratus). Group I (15 animals) breathed air while exposed to 7 ATA of pressure for 1 h in a hyperbaric chamber; Group II (13 animals), at the same pressure level (7 ATA) and for the same time period (1 h), breathed an oxygenated fluorocarbon liquid (temperature 27 degrees C) that was open to the chamber atmosphere; Group III (10 animals), at the same pressure and time period as the other groups, were sealed in a flexible plastic bag filled with oxygenated fluorocarbon as a breathing mixture. A fourth, Group IV (12 animals), breathed oxygenated fluorocarbon for 1 h at 1 ATA. Survival after rapid decompression in each group varied, 9 animals died in Group I, 12 animals in Group II, whereas none of the animals died in either Groups III or IV. Thirty minutes after decompression postmortem examinations of all the animals demonstrated the presence of large amounts of gas bubbles in the right ventricle and some gas bubbles in the left ventricle of all the hamsters in Groups I and II. No gas bubbles were found in the hearts of the Group III animals. Group III animals, breathing a liquid unsaturated by an inert gas, survived rapid explosive decompression without the signs and symptoms of decompression sickness. Immersion in the liquid fluorocarbon produced a profound decrease in heart rate, rectal temperature, and respiration in Groups II, III, and IV.

Air↗

Diving decompression fails to activate complement.

The present study evaluated complement activation during decompression after air dives in a hyperbaric chamber. Intravascular bubbles were quantified by Doppler ultrasound scoring. Eighteen subjects completed 92 dives, of which 74 produced bubbles. Complement activation was assessed by plasma C3a des Arg and red-cell-bound C3d before and after each dive. These parameters of in vivo complement activation failed to show significant activation. In vitro complement activation susceptibility tests on pre-dive sera were performed to explore their association with in vivo complement activation and intravascular bubbles. Such tests failed to identify a distinct complement-sensitive group and did not correlate with in vivo complement activation during the dives and/or intravascular bubble appearance. Two subjects developed decompression sickness but were not different from the rest of the group regarding in vitro complement sensitivity or complement activation during dives.

Adult↗

Compatible atmospheres for a space suit, space station, and shuttle based on physiological principles.

Fundamental physiological principles have been invoked to design compatible environments for a space suit, space station, and the space craft used to transport the astronauts from Earth. These principles include the long-term memory of tissues for a bubble-provoking decompression, the intermittent nature of blood flow in the tight connective tissues(s) responsible for the bends whose incidence in aviators has been shown to be related to bubble volume by the Weibull distribution. In the overall design an astronaut breathing a mixture of 30% O2 in N2 for 4-5 h in a space craft at 11.9 psia can transfer to a space station filled with the same mix at 8.7 psia and, after a further 4-5 h, go EVA at any time without any oxygen prebreathing at any stage. The probable incidence of decompression sickness has been estimated as less than 0.5% using the present suit operating at 4.3 psia but the risk could be reduced to zero if the suit pressure were increased to 6.5 psia.

Aerospace Medicine↗