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Pathophysiology of Bends and Decompression SicknessAn Overview With Emphasis on Treatment
Abraham T. K. Cockett, MD;
Stephen M. Pauley, MD;
Donald N. Zehl, MD;
Andrew A. Pilmanis, PhD;
Willia S. Cockett
Arch Surg. 1979;114(3):296-301.
Abstract
• Current concepts in the pathophysiology of decompression sickness are reviewed. Mild, moderate, and severe forms of this syndrome resulting from gaseous and lipid emboli are described. Therapy is aimed at restoring or specifically treating each alteration. Plasma volume deficit is restored by colloidal re-expansion. Decompression sickness is partially treated when recompression alone is used. Blood lipid alterations are managed by use of antilipemic agents. Dextran is mentioned. Divers at depths of 61 m display changes in hematocrit, platelet, and blood lipid profiles. Cord paralysis may occur from bubbles in the vena cava. Retrograde migration blocks the venous circulation of the spinal cord. Ultrasonic devices can detect "silent" bubbles during decompression. Recompression, when available, is a lifesaving treatment for diving accidents involving saturation diving. Air embolism is discussed. Monitoring emboli by EEG and fundoscopy are reported.
(Arch Surg 114:296-301, 1979)
Author Affiliations
From the Departments of Urology (Drs Cockett, Pilmanis, and Pauley and Ms Cockett) and Ophthalmology (Dr Zehl), University of Rochester (NY) School of Medicine and Dentistry.
Footnotes
Accepted for publication Oct 24, 1978.
Reprint requests to Box 656, 601 Elmwood Ave, Rochester, NY 14642 (Dr Cockett).
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