Abstract
by improving tissue perfusion and causing activated platelets to return to their normal morphology (Gilroy et al., 1969). Haemoconcentration, which may be accompanied by cerebral oedema, is a feature of severe decompression sickness, and plasma expansion alone has been used successfully in two cases (Brunner et ah, 1964). In the present case the initial packed cell volume was 48%, suggesting haemoconcentration and cerebral oedema, and thus mannitol was given. The use of heparin in fat embolism has been described (Cobb et al., 1968), its actions on lipoprotein lipase and plate lets probably being the most important. Heparin has also been used successfully as adjuvent therapy to recompression in five cases (Barth?l?my, 1963). Also rapidly decompressed dogs when treated with heparin (2 mg/kg) have shown 100% survival, while the controls died (Pauley and Cockett, 1970). In the present case 100% oxygen was given to counteract the patient's arterial hypoxaernia, which may have been caused by microemboli in the pulmonary circulation, and to increase the capillary-alveolar diffusion gradient for nitrogen elimin ation. At present, recompression is the only generally accepted treatment for type II decompression sickness. The rationale for medical treatment of such cases, however, is supported by the successful management of this patient.
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