Biomedical subjects

T S Neuman

Publications and source records attributed to T S Neuman.

24 records · Page 2Linked to original sources

PubMed1976

Hematologic changes in man during decompression: relations to overt decompression sickness and bubble scores.

In order to determine whether asymtomatic gas phase separation causes hematologic abnormalities, studies were carried out following two dive series, one to 210 feet of sea water (FSW) for 50 min and the other to 132 FSW for 30 min. Studies included white and red cell count, red cell indices, platelet count, ESR, fibrinogen, fibrin split products, prothrombin time, partial thromboplastin time, coagulation factors II, V, VII, VIII, and X, clot retraction, platelet aggregation and adhesion, euglobulin lysis time, and platelet factor III. Changes were seen in platelet and white cell count, prothrombin time and partial thrombo-plastin time. White cell count was the only variable which correlated with total bubble score. The results are presented and implications of the findings discussed.

Adult↗

PubMed1976

Gas phase separation during decompression in man: ultrasound monitoring.

During two dive series, one to 132 fsw and one to 210 fsw, Doppler ultrasonic bubble detectors were used to monitor venous gas bubbles in divers during decompression and for 30 min thereafter. Various decompression schedules were used. Bubble scores were evaluated by independent listerners to tape recordings in a blind manner. A significant increase in bubble scores throughout the stages of decompression and postdecompression was demonstrated as well as a statistically significant relationship between bubble score and decompression sickness. A reduction in mean bubble score was found in divers who made an additional deep decompression stop that was unrelated to the extension of the decompression time. The implications of these findings are discussed.

Adult↗

PubMedDate not supplied

The roentgenographic findings associated with air embolism in sport scuba divers.

Records on all patients with arterial gas embolism (AGE) presenting to UCSD from 1982-1989 and for whom chest radiographs were available were reviewed. Of the 31 patients, 13 roentgenograms (42%) showed evidence of pulmonary barotrauma demonstrated by pneumomediastinum (N = 8), subcutaneous emphysema (N = 3), pneumocardium (N = 2), pneumoperitoneum (N = 1), or pneumothorax (N = 1). Pneumopericardium was not seen. Sixteen (52%) of the 31 patients had pulmonary infiltrates. Radiographic evidence of barotrauma was on occasion subtle, and in four cases was overlooked. Evidence of barotrauma (i.e., extra-alveolar air) was often identified along the left cardiac border, aortic arch, descending aorta, and hilar vessels. Subtle findings of ectopic air can confirm the clinical diagnosis of AGE; however, radiographic evidence of concomitant near drowning occurs more frequently.

Adolescent↗

PubMedDate not supplied

Arterial gas embolism and hemoconcentration.

The charts of all patients with diving-related accidents presenting between 1983 and 1991 were reviewed. Individuals who sustained a neurologic deficit attributable to occlusion of part of the cerebral circulation within 10 minutes of surfacing from a dive and who had a depth time profile less than 80% of the U.S. Navy "no-stop" limits were considered to have had an arterial gas embolism. Their records were reviewed to determine the hematocrit upon first presentation and the final hematocrit prior to discharge or death. Twenty-three patients had hematocrit determinations on more than one occasion. There was a significant decrease from initial to final hematocrit for these patients. No source of significant blood loss was identified in any patient. A significant correlation was found between the magnitude of the fall in hematocrit and the eventual neurologic outcome. We conclude that gas embolism diagnosed using the above criteria produces hemoconcentration, and the degree of hemoconcentration correlates with the severity of the gas embolism. These observations suggest that the pathophysiology of gas embolism is more complex than previously thought and must include diffuse endothelial injury resulting in leak of fluid from the intravascular space.

Adolescent↗

PubMedDate not supplied

Abnormal serum biochemistries in association with arterial gas embolism.

Although diving-associated arterial gas emboli have been thought to embolize the cerebral circulation preferentially, more recent evidence suggests that gas bubbles disseminate widely and may cause dysfunction in multiple organ systems. We performed a retrospective survey of the records of patients presenting with diving-associated gas embolism over a 10-yr period to determine the maximal levels of serum transaminases and lactate dehydrogenase after a diving accident. Twenty-nine subjects with arterial gas embolism were identified whose dive profiles suggested that decompression sickness was unlikely. Maximal transaminase levels (aspartate amino transaminase = 442 +/- 187 IU/L; alanine amino transaminase = 315 +/- 205 IU/L) and lactate dehydrogenase level (800 +/- 227 IU/L) were significantly greater in the gas embolism patients than those levels measured in a group of normal individuals undergoing training dives of similar depth and duration. These preliminary studies suggest that arterial gas embolism frequently produces significant abnormalities in serum enzyme activity in sport divers whose dives would not be expected to produce decompression sickness. Arterialized gas bubbles may circulate widely, causing injury outside of the cerebral circulation.

Adolescent↗

PubMedDate not supplied

Fatal pulmonary barotrauma due to obstruction of the central circulation with air.

Cardiac arrest in cases of barotraumatic arterial gas embolism (AGE) is usually ascribed to reflex dysrhythmias secondary to brainstem embolization or secondary to coronary artery embolization. Several case reports suggest that obstruction of the central circulation (i.e., the heart, pulmonary arteries, aorta, and arteries to the head and neck) may play a role in the pathogenesis of sudden death in victims of pulmonary barotrauma. We report three consecutive cases of fatal AGE in patients in whom chest roentgenograms demonstrated confluent air lucencies filling the central vascular bed, the heart, and great vessels. In none of the victims was there evidence by history or at autopsy that the intravascular gas was iatrogenically introduced. Total occlusion of the central vascular bed with air is a mechanism of death in some victims of AGE, and resuscitation efforts for such patients should take this possibility into consideration.

Adult↗