Physiological responses to cold exposure in men: a disabled submarine study.

A disabled submarine (DISSUB) lacking power and/or environmental control will become cold, and the ambient air may become hypercapnic and hypoxic. This study examined if the combination of hypoxia, hypercapnia, and cold exposure would adversely affect thermoregulatory responses to acute cold exposure in survivors awaiting rescue. Seven male submariners (33 +/- 6 yrs) completed a series of cold-air tests (CAT) that consisted of 20-min at T(air) = 22 degrees C, followed by a linear decline (1 degrees C x min(-1)) in T(air) to 12 degrees C, which was then held constant for an additional 150-min. CAT were performed under normoxic, normocapnic conditions (D0), acute hypoxia (D1, 16.75% O2), after 4 days of chronic hypoxia, hypercapnia and cold (D5, 16.75% O2, 2.5% CO2, 4 degrees C), and hypoxia-only again (D8, 16.75% O2). The deltaTsk during CAT was larger (P < 0.05) on D0 (-5.2 degrees C), vs. D1 (-4.8 degrees C), D5 (-4.5 degrees C), and D8 (-4.4 degrees C). The change (relative to 0-min) in metabolic heat production (deltaM) at 20-min of CAT was lower (P < 0.05) on D1, D5, and D8, vs. D0, with no differences between D1, D5 and D8. DeltaM was not different among trials at any time point after 20-min. The mean body temperature threshold for the onset of shivering was lower on D1 (35.08 degrees C), D5 (34.85 degrees C), and D8 (34.69 degrees C), compared to D0 (36.01 degrees C). Changes in heat storage did not differ among trials and rectal temperature was not different in D0 vs. D1, D5, and D8. Thus, mild hypoxia (16.75% F1O2) impairs vasoconstrictor and initial shivering responses, but the addition of elevated F1CO2 and cold had no further effect. These thermoregulatory effector changes do not increase the risk for hypothermia in DISSUB survivors who are adequately clothed.

Subjective symptoms and postural control during a disabled submarine simulation.

To simulate conditions aboard a disabled submarine, 7 submariners were confined for 5 d to a normobaric environment of 16.75% O2, 2.5% CO2, 4 degrees C, and 85% relative humidity (RH). After 2 control days and 1 d of hypoxia, the remaining environmental conditions were imposed for the next 5 d, followed by 1 additional day of just hypoxia. Daily morning symptoms were assessed using the Environmental Symptoms Questionnaire (ESQ). Postural stability was determined on 4 occasions using a computerized balance system: control period, after 2.7 and 4.7 d of steady-state test conditions, and after 5.7 d (with return to normal ambient temp, RH, and CO2). Three balance tests were performed: eyes open, eyes closed, and a dynamic test. Postural stability deteriorated after 2.7 d (87% eyes open, P < 0.001 and 26% eyes closed, P = 0.01). ESQ symptom subsets for acute mountain sickness, exertion, fatigue, alertness, and ear/nose/throat were not significantly different. Cold symptom subsets were increased after 3-7 d (P < 0.001); distress and muscle discomfort subsets after 7 d (P = 0.02). Continued exposure to the combination of cold and hypoxia elicited subjective symptom changes and disturbances in postural stability that are statistically significant. These observations may be of practical importance when tasks aboard a disabled submarine involve balance and mobility.

Spirometric indices and the risk of pulmonary barotrauma in submarine escape training.

Between 1975 and 1997, a total of 115,090 ascents, from depths of between 9 and 28 m, have been made by trainees at the submarine escape training tank HMS Dolphin. During this 22-yr period, 53 incidents have occurred in which, after an ascent, the trainee required hospital or recompression therapy or both. Scrutiny of the incident records revealed unequivocal evidence of pulmonary barotrauma in six incidents with an additional four in which, despite a negligible gas burden, a confident diagnosis of acute neurologic decompression illness with short latency could be made. No causative mechanism other than arterial gas embolism following pulmonary barotrauma can be implicated in these four cases despite the absence of clinical or radiographic evidence of lung injury. In all 10 cases the forced vital capacity (FVC) of the trainees was less than the predicted value for their age and height, revealing a statistically significant (P< 0.01) association between values of FVC below predicted and pulmonary barotrauma. The median FEV1 for the 10 cases was also significantly (P < 0.05) less than the predicted value after allowing for age and height. No such association was found for the FEV1:FVC ratio. FVC would thus seem to be the measure of lung function most closely associated with increased risk of pulmonary barotrauma. Possible reasons for this finding are discussed. It is concluded that although the association between low FVC and pulmonary barotrauma is statistically significant, it is insufficiently specific for low FVC to serve as an exclusion criterion for submarine escape training.

A voxel-by-voxel multivariate analysis of cerebral perfusion defects in divers with 'bends'.

Past analysis of dysbaric-induced cerebral perfusion defects, demonstrated by 99Tcm-hexamethylpropylene amine oxime (99Tcm-HMPAO) single photon emission tomography in divers using quantitative and/or univariate techniques, has resulted i considerable controversy regarding the significance of these lesions compared to those seen in control subjects, correlations with clinical findings and the role of 99Tcm-HMPAO as a prognostic indicator in decompression sickness. We tried to address these problems by using a multivariate approach to a voxel-by-voxel analysis, involving the use of principal components, to determine ranges of normality in 50 reference controls. In subsequent images, abnormality was defined as 10 spatially connected voxels at an appropriate significance level of three standard deviations. The images of 50 divers with clinically diagnosed 'bends' were compared with those of a further 40 normal population controls with no previous history of loss of consciousness, head injury or dysbarism. The results showed that 19 of 50 divers with 'bends' and 3 of 40 population controls had significant perfusion defects, representing a significant difference between divers with dysbarism and population controls at the level P < 0.002. It is concluded that dysbarism causes significant cerebral cortical perfusion defects in affected divers both in 'silent' and symptomatic (clinically correlated) areas.

Outcome of neurological decompression illness: development of a manifestation-based model.

A significant proportion neurological decompression illness cases remain symptomatic after the first recompression treatment. Currently, the factors that predict an incomplete resolution are poorly defined. In this study, 214 cases of neurological decompression illness were reviewed and classified according to the presenting manifestations and outcome after a standard therapeutic regimen. The neurological manifestations were classified by type (loss of sensory or motor function, or loss of consciousness) and then by either the number of sites involved or the location of each manifestation. Cases with both sensory and motor manifestations were less likely to have complete resolution than those with sensory or motor manifestations alone. Cases with manifestations involving the legs were less likely resolve completely than those with manifestations in the arms, especially if both sensory and motor manifestations were reported. Based on these data, a linear logistic model was developed to predict the probability of incomplete resolution after the first recompression treatment depending on the type and location of the manifestations.

The distribution of limb pain in decompression sickness.

BACKGROUND: For many years there has been a widely held but largely unsubstantiated belief that pain in the upper limb in decompression sickness (DCS) is associated with bounce diving, whereas compressed air workers, saturation divers and high altitude aviators are more susceptible to involvement of the lower limbs. HYPOTHESIS: The hypothesis of counter current exchange of inert gas, modulated by changes in tissue temperature, has been evaluated as a possible mechanism to explain the reported distribution of limb pain in DCS. METHODS: An extensive review of over 19,000 cases of limb pain decompression illness has been undertaken from case reports stored in the diving accident database at the Institute of Naval Medicine, in the published literature, and from unpublished clinical and experimental reports. RESULTS: There was a predominance of upper limb involvement in bounce divers and, in contrast to traditional teaching, in aviators. By contrast, the lower limbs were more commonly involved in compressed air workers and saturation divers. CONCLUSION: Each of the occupational exposures has been discussed individually with reference to counter-current exchange and other factors as potential influences on the distribution of disease. We conclude that counter-current exchange of inert gas may be implicated in the distribution of limb pain in DCS.

Electroencephalographic study of divers with histories of neurological decompression illness.

OBJECTIVE: To determine whether divers with histories of neurological decompression illness are electroencephalographically distinguishable from non-divers. METHODS: The electroencephalograms (EEGs) from 68 divers with histories of neurological decompression illness and 45 non-diver controls were examined independently by two clinical neurophysiologists. RESULTS: The diver and non-diver groups were electroencephalographically indistinguishable. CONCLUSION: There is no electroencephalographic evidence for the existence of cerebral dysfunction in divers with histories of decompression illness.

Mate preference and avoidance in female rats following treatment with scopolamine.

The effects of the muscarinic antagonist, scopolamine, on the behavior of female rats in a mate preference test were determined. Ovariectomized rats were primed with sufficient doses of estradiol benzoate (0.25 micrograms for 3 days) and progesterone (500 micrograms) to activate full sexual receptivity. Beginning 15 min after intraperitoneal injection of saline (0.4 ml/kg) or scopolamine hydrochloride (1 mg/kg), females were tested in an arena divided into three compartments. Females treated with scopolamine clearly avoided a compartment occupied by a gonadally intact stimulus male, instead preferring a compartment occupied by a castrated male or an empty neutral compartment. Direct contact with an intact male was a critical feature of this avoidance because females treated with scopolamine did not avoid intact males that were confined within a chamber that prevented physical contact between the male and female. Results indicate that female rats treated with scopolamine avoid direct physical contact with sexually active males, possibly due to an alteration in sexual motivation and/or the aversive nature of this interaction.

Neurophysiological assessment of divers with medical histories of neurological decompression illness.

OBJECTIVE: To examine the possibility that subclinical damage may persist after clinical recovery from neurological decompression illness. METHODS: The neuraxes of 71 divers with medical histories of neurological decompression illness and 37 non-diver controls were examined by recording the somatosensory evoked potentials produced on stimulation of the posterior tibial and median nerves. RESULTS: Although the tests gave some objective support for the presence of "soft" residual neurological symptoms and signs, no evidence was given for the presence of subclinical damage. CONCLUSIONS: The contention that neurological damage persists after full clinical recovery from the neurological decompression illness was not supported.

Effects of a muscarinic antagonist on various components of female sexual behavior in the rat.

The effects of the muscarinic antagonist scopolamine on lordosis, solicitation, pacing, approach, attractivity, and activity were evaluated in ovariectomized rats brought into sexual receptivity with estrogen and progesterone. Systemic (1 mg/rat) or intraventricular (10 micrograms bilaterally) administration of scopolamine significantly reduced the incidence of lordosis and solicitation behaviors and disrupted typical pacing of sexual contacts with a stimulus male. In addition, females avoided contact with a stimulus male, but not a stimulus female, following intraventricular infusion of scopolamine. The levels of general activity and frequencies of sexual contacts were similar in females treated intraventricularly with scopolamine and vehicle solutions. Consequently, scopolamine disrupted various components of sexual behavior, including lordosis, solicitation, pacing, and approach, without altering female attractivity or general activity.

Case control study of cerebral perfusion deficits in divers using 99Tcm hexamethylpropylene amine oxime.

In a preliminary report, Adkisson et al. (Lancet 1989; 2:119-121) used 99Tcm-hexamethylpropylene amine oxime (HMPAO) single photon emission computed tomography (SPECT) to provide evidence for cerebral perfusion deficits in 28 cases of dysbarism. The report caused concern because these deficits were found even in cases in which the clinical manifestations were limited to the spinal cord. To address this issue further, a case-control study of cerebral perfusion using 99Tcm-HMPAO SPECT is reported. Four groups of 10 subjects were studied: a) divers scanned on average 11 days after treatment of neurologic decompression illness, b) divers scanned 3-5 yr after treatment for neurologic decompression illness, c) diver controls, and d) population controls. All groups were matched for age, and the divers were further matched for general diving experience. The scans were randomized and reported blind to history. Despite a trend toward larger numbers of deficits in individuals with decompression illness, the 4 groups were statistically indistinguishable. Furthermore, no correlation was found between the location of the perfusion deficits and the clinical presentation. These results indicate that 99Tcm-HMPAO SPECT scanning requires further evaluation before clinical significance can be ascribed to perfusion deficits found in divers.

An introduction to decompression illness.

Decompression illness was formerly an occupational hazard confined to professional divers and compressed-air workers. With the increasing popularity of recreational diving it has come to involve a wider cross-section of the population. Furthermore, the proportion of cases presenting with the more serious manifestations of the disease appears to be rising.

Maxillary sinus barotrauma with fifth cranial nerve involvement.

A case of neurapraxia of the infraorbital nerve occurring as a result of maxillary sinus barotrauma in a diver is presented. Existing reports of a similar nature are reviewed and the pathogenesis of cranial nerve involvement in barotrauma is discussed. Guidelines for treatment are suggested.

Ten years of diving-related illness in the Royal Navy.

The period from 1 January 1980 to 31 December 1989 produced a total of 244 training and operational diving accident reports involving Royal Navy and Royal Marines personnel. Because the incidence figures fluctuated widely year by year, a clear trend over the decade failed to emerge. However, the incidence of Type II decompression sickness, as a percentage of total decompression sickness, was greater in the second half of the decade than in the first, a trend similar to, although more moderate than, recent experience of dysbaric illness amongst sport divers. Student divers were disproportionately highly represented in the statistics, particularly with regard to pulmonary barotrauma and near-drowning.

Bubble-induced dysfunction in acute spinal cord decompression sickness.

Five anesthetized dogs undertook a chamber dive, on air, to 300 feet of seawater for 15 min. After the dive, spinal cord decompression sickness was detected by recording a reduced amplitude of the somatosensory evoked potential compared with predive base-line values. After the diagnosis of decompression sickness and rapid perfusion fixation of the animal, the spinal cord was removed and examined histologically. Numerous space-occupying lesions (SOL) that disrupted the tissue architecture were found in each cord, mainly in the white matter. The size and distribution of the SOL were determined using computerized morphometry. Although SOL occupied less than 0.5% of the white matter volume, we tested a number of algorithms to assess whether the SOL may have been directly involved in the loss of spinal cord function that followed the dive. We determined that the loss of somatosensory evoked potential amplitude may be attributed to the SOL if 30-100% of the spinal cord fibers that they displaced were rendered nonconducting. A number of possible mechanisms by which SOL may interfere with spinal nerve conduction are discussed.