Forced expiratory spirograms following decompression sickness.
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During construction of the Coxwell sewer tunnel and subway in Toronto, a number of patients with decompression sickness failed to respond completely to repressurization alone. After the addition of hypothermia, significant improvement occurred. These observations stimulated an experimental study in which 36 rabbits were exposed to 60 or 70 p.s.i. for 1 h. After sudden decompression over 70 s, they were either observed, cooled in air at 0 degrees C, or cooled in water at 3 degrees C. Immersion in water significantly reduced the mortality rate, while cooling in air did not. These experimental results supported the clinical observations that hypothermia was an effective therapeutic adjunct in the treatment of decompression sickness.
Twelve professional divers had visual complaints after decompression sickness. Severe accommodative and convergence insufficiency, heretofore unrecognized, was detected and studied. Two rhesus monkeys were subjected to similar hyperbaric conditions and then examined before death for study of their eyes and brains. The animals seemed to have accommodative and convergence insufficiency.
BACKGROUND: In a porcine model of neurological decompression sickness (DCS), perivascular leukocyte activation was a consistent finding in biopsies of associated cutaneous DCS. This prompted examination of other organs for similar changes; multifocal leukocyte activation was found in the lungs (pneumonitis) and liver (hepatitis). HYPOTHESIS: DCS in pigs induces leukocyte aggregation and activation in the liver and lungs. METHODS: Male Yorkshire swine, trained to run on a modified treadmill, were compressed to 200 ft of seawater (fsw) in a dry, air-filled compression chamber. Decompression varied according to the profile under study. RESULTS: In 106 pigs, evidence for association of leukocyte aggregation and activation with the clinical diagnosis of neurologic DCS was sought. The incidence of pneumonitis (20/68, 29% with DCS; 4/38, 10% without DCS) and hepatitis (23/68, 33% with DCS; 4/38, 10% without DCS) were strongly correlated with the incidence of neurologic DCS via Pearson Chi-squared analysis (p = 0.026 pneumonitis and p = 0.008 hepatitis). Additionally, Kruskal-Wallis rank analysis for numbers of organs involved and incidence of neurologic DCS showed a strong correlation between the increasing occurrence of neurologic DCS and the involvement of both the liver and lungs (p = 0.004). CONCLUSIONS: The results imply that, at least in pigs, DCS induces leukocyte aggregation and activation in the liver and lungs. These organs are not normally considered targets of DCS. Leukocyte aggregation in these organs may be related to their roles as highly perfused organs. Leukocyte aggregation may be a marker for DCS, providing further evidence for wider, systemic effects of DCS.
A case of decompression sickness is described in an uniformed diver who developed lymphatic manifestations after recompression treatment. No definite contributing factors to this rare disorder were established. A brief review of cutaneous lesions in decompression sickness is also presented.
The intensity of a pain-only decompression sickness (DCS) symptom with respect to time at altitude increases, peaks, and then declines in some cases. A similar pattern is also seen in a graph of the probability density function [f(t)] for DCS. The f(t) is the proportion of DCS per unit time with respect to time at altitude. The integration of f(t) with respect to time provides the cumulative probability of DCS [P(DCS)]. We suspect that the perceived intensity of pain with a given stimulus intensity is related to the P(DCS); it may be related to the intensity of the stimulus to a power (alpha). Our stimuli are defined as pressure ratio [PR = (phi P1N2/ P2)-11] or pressure difference [delta P = phi P1N2-P2], where phi P1N2 is the N2 partial pressure calculated in the 360 min half-time (t1/2) compartment or t1/2 is estimated with other parameters and P2 is ambient pressure after the ascent. Both stimuli represent a potential released volume of gas. We tested the null hypothesis that alpha > 1 was no better than alpha = 1 in PR alpha and delta P alpha in a log logistic survival analysis of 1085 exposures in hypobaric chambers. The log likelihood number increased from -1198 for alpha = 0 for the null model to -724 for PR alpha when alpha = 3.52 with a 42 min t1/2 and -714 for delta P alpha when alpha = 8.44 with a 91 min t1/2. We conclude that the improvement in our expressions for decompression dose with alpha > 1 is not by random chance and that alpha may link the physics of gas evolution to the biology of pain perception. Because of our empirical approach, we do not exclude other possible interpretations.
Individual risk factors for decompression sickness (DCS) were studied in 932 men who had worked for 12 shifts or more at maximum working pressure (MWP) of 1 bar or above in a compressed air tunneling project in Hong Kong. Two dependent variables were used: presence or absence of bends and number of bends experienced by a man. Three hundred and fifty-six men (38.2%) had one or more bends. Univariate analysis showed that many variables were associated with presence or absence of bends. Logistic regression showed that the best equation included five independent variables: MWP, number of exposures, past number of bends, job (being a miner), and Quetelet Index (or Body Mass Index). The number of bends was also associated with many variables. Stepwise multiple regression revealed five important independent variables: ethnicity, MWP, Quetelet Index, number of exposures, and past number of bends. Obesity and past number of bends were therefore important risk factors for DCS after taking into account MWP and number of exposures. The age effect observed in univariate analysis could be due to obesity. Miners and Japanese had higher risks of DCS, probably due to their strenuous labor.
A case of first degree atrio-ventricular block, probably representing cardiac involvement by decompression sickness, is presented. The conduction defect resolved spontaneously 36 h after the initiating decompression insult, and was not accompanied by any other cardiovascular changes. The contribution of a recompression treatment, which alleviated accompanying Type I decompression sickness (DCS) symptoms, to the resolution of cardiac DCS is not certain. Cardiac symptoms of DCS do not receive enough consideration. It is suggested that an electrocardiogram should, whenever possible, form part of the basic evaluation of suspected DCS and of the initial workup of candidates for diving. A flow diagram for management of cardiac DCS is proposed.
BACKGROUND: Sports diving is a popular recreational activity. Sports divers presenting with acute decompression sickness may exhibit residual neurologic and neuropsychological symptoms during follow-up, in spite of appropriate treatment. MATERIAL AND METHODS: A retrospective review of medical records was carried out for sports divers admitted to the department of neurology at Haukeland University Hospital during 1997. RESULTS: 11 out of 20 divers experienced residual neurological symptoms after treatment. Five responded poorly to treatment, with 50% or more residual clinical score. These patients tended to be older, had performed deeper dives, and more repetitive diving. Seven divers had increased slow wave activity in EEG on initial recording, in two the EEG changes persisted after treatment. INTERPRETATION: In this small series of sports divers with decompression sickness and arterial gas embolism, most neurologic symptoms responded to hyperbaric treatment. However, more than one half of the divers had residual neurological symptoms on discharge. Sensory loss and asymmetrical reflexes were the most common residual findings.
The incidence of altitude decompression sickness (ADS) was studied in 23 altitude scientists during repeated altitude exposure to 15,000-29,000 ft (4572-8839 m) in a decompression chamber. Prior to each altitude exposure, a 30-60-mm pre-breathing period with 100% oxygen took place. Ascent was made to an altitude at a rate of 2000 ft X min-1. The altitudes studied ranged from 15,000-29,000 ft (4572-8839 m). Symptoms reported appear consistent with previous reports. Incidence of ADS at 26,000-29,000 ft (7925-8839 m) was 29.7%, during 274 chamber flights and 1264.6 h of altitude time. Incidence appeared related to frequency of exposure, severity of altitude, and physical activity. Incidence was not related to age, duration of exposure, or body index (weight/height 2). This high incidence of ADS reported in this study is similar to that reported by NASA.
It can be expected that the differential diagnosis problem of decompression sickness will increase in the future due to the increasing number of divers. During the last 30 years, 232 divers were treated for decompression sickness (DCS) at the Naval Medical Institute (NMI) in Split, Croatia. In 66 cases (28%), physicians at various diving sites reached diagnosis with difficulty, and 86 divers (37%) came directly to the NMI without seeing a physician first. Physicians at remote diving locations frequently have only basic knowledge of diving medicine and are often inexperienced. The language barrier was a major obstacle in obtaining a medical history and examination of foreign divers. Consultations at the NMI proved a major contribution to correct diagnosis and treatment. We present six illustrative cases from NMI Archives that demonstrate how prejudices, panic, and inexperience could create problems in establishing DCS diagnosis.
In the last decade there has been an increase in the incidence of decompression sickness in Ireland. The modern diver, equipped with specially developed diving equipment, is exposed to abnormal physiological conditions. This has resulted in a spectrum of medical conditions, which need to be recognised, diagnosed and treated. The department of Underwater Medicine at University College Hospital, Galway, is the only referral centre in the Republic of Ireland for patients suffering from decompression sickness. Early recognition and referral for treatment dramatically improves patient outcome. A one year's review of patients referred for treatment is presented.
Most published reports on the treatment of altitude-induced decompression sickness (DCS) deal exclusively with patients treated with hyperbaric oxygenation. Little information exists on the role of normobaric (ground level) oxygenation as a primary treatment modality for altitude-induced DCS. This study reports the U.S. Air Force experience in the treatment of Type 1 altitude chamber DCS with ground level oxygenation (GLO2) during the period 1 January 1989 to 31 December 1991. Data collected included age, sex, time of symptom development, type of initial treatment, and response to GLO2 administration. There were 221 cases of Type 1 DCS, of which 46 were treated with compression therapy without initial use of GLO2. Of the 175 cases treated with GLO2, 40 failed to resolve and were treated with compression therapy. The remaining 135 cases all resolved with GLO2, obviating the need for HBO therapy. Only 8 patients had a recurrence of symptoms after resolution with GLO2, all of which subsequently resolved with compression therapy. Factors associated with a favorable response to GLO2 are discussed.
This paper reports two cases involving divers who presented with painful hands and were treated for decompression sickness. Although treatment was successful, their symptoms and diving history suggest non-freezing cold injury, the so-called immersion hand, rather than decompression sickness. For long exposures or cases where the diver may have inadequate insulation, thermal protection of hands is recommended even in water as warm as 16 degrees C.
BACKGROUND: Current therapy for altitude decompression sickness (DCS) includes hyperbaric oxygen therapy and ground-level oxygen (GLO). The purpose of this paper is to describe the Air Force Research Laboratory experience in the extensive use of GLO for the treatment of altitude DCS in research subjects. METHODS: Data were collected from 2001 altitude chamber subject-exposures. These data, describing DCS symptoms, circulating intracardiac venous gas emboli, and treatment procedures used were collected for each subject exposure and stored in an altitude DCS database. RESULTS: In the database of 2001 subject exposures, 801 subjects (40.0%) were diagnosed with altitude DCS. Subjects reporting DCS symptoms were immediately recompressed to ground level. Of the 749 subjects who received 2 h GLO, 739 (98.7%) resolved completely and required no further treatment. CONCLUSIONS: Although not an operational study, these data provide indirect support for the current USAF guidelines for the treatment of altitude DCS with GLO.
U-2 pilots are at an increased risk of decompression sickness compared with other aviators in the U.S. Air Force. This is due to the extreme altitudes at which the missions take place. Presented here is a case of decompression sickness that occurred in a U-2 pilot who was wearing a full-pressure suit while flying at an altitude greater than 70,000 ft, with a pressurized cabin altitude of 29,200 ft. This case demonstrates the continued need for pilot education and awareness of DCS risk factors and symptoms.
A middle-aged professional diver with neurological decompression sickness, seen in Tikur Anbessa Hospital, Addis Abeba, in February 1989, is reported. Early recognition and prompt treatment, and, most of all, prevention are of paramount importance to avoid permanent neurological deficits.
A mixed-gas model for rats was developed to further explore the role of different gases in decompression and to provide a global model for possible future evaluation of its usefulness for human prediction. A Hill-equation dose-response model was fitted to over 5,000 rat dives by using the technique of maximum likelihood. These dives used various mixtures of He, N(2), Ar, and O(2) and had times at depth up to 2 h and varied decompression profiles. Results supported past findings, including 1) differences among the gases in decompression risk (He < N(2) < Ar) and exchange rate (He > Ar approximately N(2)), 2) significant decompression risk of O(2), and 3) increased risk of decompression sickness with heavier animals. New findings included asymmetrical gas exchange with gas washout often unexpectedly faster than uptake. Model success was demonstrated by the relatively small errors (and their random scatter) between model predictions and actual incidences. This mixed-gas model for prediction of decompression sickness in rats is the first such model for any animal species that covers such a broad range of gas mixtures and dive profiles.