WDA visits Washington.
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Biomedical subjects
Publications and source records attributed to W Gill.
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Nineteen patients who had profound hypotensive shock were studied to correlate the light and electron microscopic appearances of the liver with the clinical and biochemical evidence of hepatic dysfunction. Despite the multiple etiologic factors that can result in jaundice in these patients, a fluctuating pattern occurs which enables the correlation of a bilirubin peak with the predominating etiologic factor. Immediately after shock, there was enzymatic and light and electron microscopic evidence of hepatocellular damage, resulting in a jaundice peak on the eighth to tenth day after the shock episode. This was followed by repair and regeneration of the liver as well as an increase in cholestatic enzyme levels. Later, bilirubin peaks occurred when hepatocellular function was further decreased or overloaded against this background of dysfunction related to the episode of shock. Recovery of hepatic function could continue or be delayed by intercurrent disease, particularly systemic infection. Support of hepatic function, similar to that available for pulmonary and renal failure may, in the future, be used to effect the prognosis of these patients.
Urinary cyclic adenosine monophosphate levels were measured in 150 patients with accidental injury of varying causes. Thirty-eight healthy adults of both sexes serving as controls excreted 2.21 to 6.85 micromoles of cyclic adenosine monomphosphate per gram of creatinine, mean 4.34 +/- 1.25. In 120 patients with trauma on admission, the excretion was increased by 15.7 per cent, p less than 0.05, and the changes showed a time related pattern. In patients admitted within the first 30, 60 and 120 minutes after trauma, the mean excretion was changed by 19, 10 and minus 2.8 per cent, respectively, and in those admitted between two and 24 hours by 30 per cent. Twelve patients with differing types of trauma showed a mean 24 hour excretion reaching its peak on the first day, 44 per cent, and declining to its nadir of 2.25 micromoles per gram of creatinine on the third day, minus 47 per cent, p less than 0.01. A second rise reached its peak on the fifth day, p less than 0.05. Thereafter, the excretion fluctuated widely with peaks significantly above and below the control range, and we were unable to correlate these changes with any specific factors. In post-traumatic acute renal failure, the nucleotide excretion fell within several hours and usually reached low values, that is, below 0.25 micromoles per 1,000 milliliters per 24 hours within one to three days. In general, the excretory pattern for cyclic adenosine monophosphate followed that of creatinine clearance, but in the diuretic phase of the recovering kidney, the cyclic adenosine monophosphate levels remained more depressed than those of creatinine. The high sensitivity of urinary cyclic adenosine monophosphate to abnormalities in renal function suggests its potential as a clinical indicator.
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A review of the literature on zinc and wound healing shows the many gaps of knowledge which still exist. This study of the histologic appearance of wound healing in rats fed various diets demonstrates the serum zinc levels achieved by such diets. No significant improvement was observed in the rate of healing for any one group, but a number of histologic differences were observed.
The relation between serum osmolality and blood-alcohol was studied prospectively in 565 acute trauma patients. The two measurements were closely correlated. It is therefore possible to estimate the blood-alcohol from serum osmolality to assist in the clinical management of acutely injured patients.
A technique for abdominal lavage is described and was used to evaluate the abdomen of 671 multiple trauma victims. In 44 per cent (299 cases) there was a bloodstained return and these were regarded as positive. Patients with a positive result underwent exploratory laparotomy which revealed that 89 per cent had significant intra-abdominal trauma requiring a surgical procedure, 8 per cent had trauma which did not require any active surgical correction and 3 per cent had no abdnormal findings. Of all the lavages performed, there were 0-11 per cent false positive and 0-03 per cent false negative results. The value of the test in the context of multiple trauma is emphasized.
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This is a follow-up study of male and female offspring of mothers who were part of a double-blind placebo controlled investigation during the years 1951-1952, originally aimed at determining the usefulness of DES administration in maintaining pregnancy. So far, 84 DES-exposed females, 43 female controls, 42 DES-exposed males and 37 male controls have been examined. Circumferential ridges of the vagina and cervix were seen in 39% of the DES-exposed females but in none of the controls. Colposcopy revealed vaginal epitheleal changes in 78% of the DES-exposed females 2% of the female controls. Cytology proved to be reliable as a screening test for vaginal epithelial changes in the DES-exposed female. Urine cytology was negative for tumor cells in all patients. The main abnormal finding in the DES-exposed males was that cysts in the epididymis were detected in 10%. No cases of cancer were observed in either the male or female offspring.
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Perumbilical portal vein catheters and arterial and central venous catheters were inserted in 16 patients recovering from trauma or other shock-producing events, and in 5 patients who later developed shock. This permitted serial measurement of blood gases, pH, and the levels of ammonia, lactate and certain other metabolites in all three circulatory systems simultaneously. Nine of the trauma patients were never in shock, had no liver disease or injury and consequently formed a baseline group for comparison with the shock patients. In the shock patients there was a significant degree of hypoxemia in the portal venous blood and an increase in the arterialportal oxygen saturation difference. Their portal venous blood showed a lower pH and a higher pCO(2) than did the portal blood of the patients who had never been in shock. In 3 of the 4 shock patients who died, the total blood lactate showed a greater increase in portal venous than in the arterial or central venous blood. In shock there was also an increase in portal venous blood ammonia which was later accompanied by increments in arterial and central venous blood ammonia. This suggests impairment of hepatic urea synthesis, allowing escape of ammonia through the liver. These phenomena, when added to the finding previously reported of an elevated portal venous pressure in some shock patients, lend support to the hypothesis that in certain cases of shock there is increased impedance to flow of portal blood through the liver with resultant stasis in the portal-splanchnic bed and ischemichypoxic hepatocellular injury.