Pathophysiology of bends and decompression sickness. An overview with emphasis on treatment.

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.

Recent observations on the neurobehavioral toxicity of carbon disulfide.

Visual thresholds, fluorescein angiography, color fundus photography and tests of motor function were used to examine the effects of carbon disulfide (CS2) on macaque monkeys. After reliable baseline measures were obtained, two monkeys were exposed to 256 ppm CS2, 6 hours a day, 5 days each week for 7 weeks. A third monkey was tested similarly but received a sham exposure over the same period. Visual acuity of the exposed monkeys dropped more than 5 fold during exposure and showed a partial subsequent recovery only in one monkey. Flicker resolution, on the other hand, was only slightly and transiently impaired. Tests of motor function also showed only brief and partial disruption. No evidence was seen in either exposed monkey of the retinal vascular changes that are currently the major diagnostic signs in human carbon disulfide poisoning.

Extraocular muscle surgery in the presence of complete paralysis of the fifth, sixth and seventh cranial nerves.

A nine-year-old boy developed paralytic left esotropia secondary to an intracranial lesion. He also exhibited total loss of function of the left fifth and seventh cranial nerves. Extraocular muscle surgery in this situation was felt to be dangerous to the operated eye. The degree of risk however could not be determined from published reports. Surgery was performed and was complicated by severe corneal ulceration. Use of a therapeutic contact lens presumedly helped in finally achieving a satisfactory result.