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Dysbaric osteonecrosis appears to be independent of decompression sickness. The 2 conditions, however, may share etiologic and pathogenetic factors. The incidence of osteonecrosis is influenced by the number of hyperbaric exposures, extent of pressure, decompression profile and possibly by the rate of compression and degree of obesity. Though etiology and pathogenesis are unclear, osteonecrosis is probably due to ischemia, with gas bubbles causing direct or indirect circulatory impairment. In vitro experiments, as well as human and animal studies, suggest multiple pathogenetic mechanisms: intraosseous vessel compression by extravascular bubbles; vessel obstruction by bubbles, fibrin thrombi, platelet aggregates, clumped erythrocytes or coalesced lipids; and narrowing of arterial lumina by bubble-induced myointimal thickening. Obstructing materials, whether autochthonous or embolic, may result from blood-bubble interface reactions. Rheologic changes and blood flow redistribution could play contributing roles. It seems likely that multiple pathogenetic factors act in concert or sequentially. Proposed nonischemic changes, such as hyperoxic injury gas-induced osmosis, or autoimmunity, lack sufficient supporting evidence. The peculiar vulnerability of bone may be related to gas supersaturation of the fatty marrow; sensitivity to extravascular gas pressure because of tissue rigidity; poor vascularization; and the presence of uranium 238 which promotes nucleation and subsequent gas bubble formation.
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PMID:Dysbaric osteonecrosis. Etiological and pathogenetic concepts. 63 12

The histopathology of dysbaric osteonecrosis and the influence of the number of exposures, compression rate, and obesity on the incidence and latency of the lesion were studied in 438 mice (2505 bones were examined). The animals were subjected to 75 psig air pressure for 2-6 hours (single or multiple exposures). Compression was rapid or stage. Decompression was safe. Osteonecrosis developed in the epiphysis of the tibia and/or femur in 34.1% of obese and in 5.8% of thin animals after a latent period of 2 to at least 12 months. It was concluded that: 1. dysbaric osteonecrosis appears to be independent of decompression sickness; 2. in obese mice the incidence is higher and the latent period shorter; 3. multiple exposures result in higher incidence and earlier lesions than single exposure; 4. the incidence is lower with stage than with rapid compression; 5. the pathogenesis of osteonecrosis may involve several factors (circulatory impairment by extravascular or intravascular bubbles, emboli, thrombi, vasoactive substances, gas-induced osmosis, autoimmunity) acting in concert or in sequence.
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PMID:Dysbaric osteonecrosis in mice. 95 27

In the largest compressed air tunnelling project using the Blackpool Decompression Tables in Hong Kong, 912 men had radiological examination of major joints and 12 definite and 30 suspected cases of dysbaric osteonecrosis were detected by the compressed air physician. Distribution of the lesions was symmetrical and 43.1 per cent were juxta-articular. All the cases were asymptomatic. The infrequent occurrence of osteonecrosis in Hong Kong in general and in this project in particular suggests that the Blackpool Tables were relatively effective in preventing the disease. Definite and suspected cases were pooled together for the study of risk factors for osteonecrosis. Logistic regression analysis showed that the number of bends ever experienced, number of hours worked in the present contract, age and obesity were important independent risk factors. Because of the impossibility of a suitably long follow-up for all workers, the prevalence of osteonecrosis may be under-reported in Hong Kong.
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PMID:Dysbaric osteonecrosis in a compressed air tunnelling project in Hong Kong. 157 28

Among aviators, decompression sickness is a condition that occurs almost exclusively at altitudes above 6,098 m (20,000 ft). Several reports have been published describing the development of decompression sickness after altitude exposures of 3,049 to 4,878 m (10,000-16,000 ft). In most of these cases, the affected individual had a previous history of pain in the involved area due to prior trauma or surgery, or had other risk factors for decompression sickness, such as obesity. Few of these reports have confirmed the presence of decompression sickness by a test of pressure. A case is reported here of multiple joint pains developing after a rapid decompression at 2,439 m (8,000 ft), which improved during descent and rapidly resolved with recompression therapy. There was no prior history of joint pain, trauma, or diving. A brief discussion of decompression sickness is included.
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PMID:A case of decompression sickness at 2,437 meters (8,000 feet). 225 76

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.
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PMID:Analysis of some individual risk factors for decompression sickness in Hong Kong. 277 60

A 51-year-old civilian pilot flying a high performance aircraft for the USAF presented for medical attention approximately 1.5 hours after developing substernal chest pain and dyspnea while flying unpressurized at FL 280 (8,534 meters) for 30 minutes. In spite of recompression about 3 hours later, the pilot expired while ascending from 6 atmospheres, 2.5 hours into the dive. This represents the first reported fatality due to altitude-induced decompression sickness since 1959. Pathologically, this case is similar to cases presented in the past. In addition, this case serves to reemphasize many of the "risk factors" for decompression sickness, especially age and obesity. Furthermore, the evidence presented points to maintaining only the highest standards of physical health in those who fly high performance aircraft.
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PMID:Fatal pulmonary decompression sickness: a case report. 324 Feb 20

The relationship between the health status and physical characteristics of 185 U.S. Navy divers and their risk for experiencing decompression sickness was examined utilizing historical cohort design. Data on multiphasic medical examinations performed on these men between 1972-1978 were obtained. Cases of decompression sickness before and after examination were identified. Divers who did experience decompression sickness either before or after examination had significantly higher measures of skinfold thickness and weight when compared to those who remained free of decompression sickness. Those divers in the highest quartile of each of three significant skinfold thicknesses measured had risks for decompression sickness that were generally 9 to 10 times as great as those calculated for the combined lower 3 quartiles and 5 to 6 times as great as the average crude risk calculated for all Navy divers over the past 5 yr. These findings suggest that obesity may be a contributory factor to the occurrence of decompression sickness.
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PMID:Health risk factors for the development of decompression sickness among U.S. Navy divers. 653 16

Obesity is one of the factors which increase the risk of decompression sickness. It has been suggested that any diver whose weight is more than 20% in excess of that derived from currently accepted tables should therefore be stopped from diving until he has lost enough weight. Published tables of average and standard weights for men, however, are unsuitable for application to men recruited for commercial diving, as the populations on which the tables were based differ in important respects from divers. Furthermore, the tables may assume that men are weighed and measured clothed and in shoes, whereas in most medical examinations the measurements are made on men without shoes and partially clad . Analysis of weight measurements of 1520 divers whose records are in the Decompression Sickness Central Registry in Newcastle upon Tyne suggests that divers as a group are substantially heavier than other populations on whom height-weight tables have been based. A table derived from American data of 1935-53 is often used as a guide. If this table is used the percentage of divers rejected as overweight may be as high as 13.6%. More recent and more appropriate data on heights and weights are required for use as reference standards for divers, or perhaps another measurement indicating obesity should be used.
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PMID:Optimum weights for commercial divers. 672 56

The case of a decompression sickness in woman, diving to 26 meter depth is reported. The patient was helped by instructor's computer (error!) and she presented risk factors for embolic disease (obesity, smoke, estroprogestinic therapy). She presented with many symptoms of decompression sickness during immersion and during re-ascent (headache, vertigoes and paresthesias). She was not treated on the place of incident, but only 36 hours later at our center of hyperbaric medicine. Her Magnetic Resonance imaging showed hyperintensity lesions of white matter.
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PMID:[NMR in the diagnosis and treatment of neurologic lesions in decompression sickness]. 1047 48

We have previously established that ATP binds to mammalian metallothionein-2 (MT). The interaction between ATP and MT and the associated conformational change of the protein affect the sulfhydryl reactivity and zinc transfer potential of MT [Jiang, L.-J., Maret, W., and Vallee, B. L. (1998) The ATP-metallothionein complex. Proc. Natl. Acad. Sci. U.S.A. 95, 9146-9149]. NMR spectroscopic investigations have now provided further evidence for the interaction. (35)Cl NMR spectroscopy has further identified chloride as an additional biological MT ligand, which can interfere with the interaction of ATP with MT. (1)H NMR/TOCSY spectra demonstrate that ATP binding affects the N- and C-terminal amino acids of the MT molecule. Scanning tunneling microscopy recorded images of single MT molecules in buffered solutions. Moreover, this technique demonstrates that the otherwise nearly linear MT molecule bends by about 20 degrees at its central hinge region between the domains in the presence of ATP. These results may bear on the development of mild obesity in MT null mice and the role of MT in the regulation of energy balance. The interaction suggests a mechanism for the cellular translocation, retention, and reactivity of the ATP*MT complex in the mitochondrial intermembrane space. Both MT and ATP are localized there, and MT and thionein alternately bind and release zinc, thereby affecting mitochondrial respiration.
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PMID:The ATP/metallothionein interaction: NMR and STM. 1181 64


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