Determination of therapeutic blood levels of methamphetamine and pentobarbital by GC.
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Biomedical subjects
Publications and source records attributed to G W Moore.
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A case-control study was performed to identify risk factors for developing and dying from necrotizing enterocolitis (NEC). Eighty-six infants observed at The Johns Hopkins Hospital who had clinical and/or pathological evidence of this disease during the past 10 years were studied. Birth weight matched autopsied control infants without NEC were also studied for comparison with the autopsied infants who died with NEC. Patients with NEC had a mean birth weight of 1,620 +/- 198 g, and those who died from NEC had even lower birth weights (1,418 +/- 109 g). The development of NEC was correlated with significantly higher frequencies of oral feeding (p less than 0.005) and septicemia (p less than 0.001). Death with NEC was correlated with earlier onset and more extensive disease (both p less than 0.05), hypotension (p less than 0.001), septicemia (p less than 0.001), persistent respiratory distress (p less than 0.05), a patent ductus arteriosus (p less than 0.05), and lower 5-min Apgar scores (p less than 0.05). These findings suggest that NEC is caused by overwhelming hypotensive/ischemic injury to the intestines in association with enterosepticemia. Intestinal immaturity and oral feedings appear to be important predisposing factors in this condition.
The distribution of flow divider offset, branch angle, and angular asymmetry in a collection of 70 human aortic bifurcations are reported. A computer algorithm was used to determine these parameters objectively. The mean values with standard deviations and ranges are: 1) magnitude of flow divider offset = 1.4 +/- 1.4 mm (range = 0.04 to 8.1 mm); 2) branch angle = 35.0 degrees +/- 11.1 degrees (range = 10.4 degrees to 61.3 degrees); and 3) angular asymmetry = 15.3 degrees +/- 12.9 degrees (range 0.2 degrees to 56.1 degrees). Since these parameters have been shown to have a significant influence on hemodynamic shear, their variability suggests a corresponding variability in the fluid dynamic stresses to which the bifurcations were exposed in life.
Diagnoses made at autopsy are usually yes-no (binary) decisions inferred from clinicopathologic data. A major conceptual problem in determining cause of death is that variables used in classifying some patients may be missing in other patients. A model with too few logical implications will be mathematically incomplete for small data sets; but a model with too many implications may be inconsistent with large data sets. We examined the 155 patients autopsied after coronary artery bypass surgery from The Johns Hopkins Hospital autopsy data base of 43,200 cases. Diagnoses entered on a word processor and transmitted to a minicomputer were solved by the Quine-McCluskey algorithm. Our analysis disclosed that 41% of patients suffered a fatal complication of cardiac surgery; 43% had established surgical complications or unrelated causes of death; and in 17% of cases the cause of death was unexplained. Computerized symbolic logic analysis of medical information is useful in testing the completeness of a proposed set of causes of death.
A previous study of hyaline membrane disease of the newborn demonstrated that the hyaline membrane was derived from necrotic epithelial cells, and it was suggested that a no flow-reflow episode affecting the pulmonary circulation might account for the cell necrosis. An unexpected statistical finding in that study was a highly significant negative correlation between hyaline membrane disease and chorioamnionitis. Because it seemed to us that fetal infection could be expected to produce the circulatory pathophysiology suggested to produce hyaline membrane disease, we reexamined the issue by reviewing a group of autopsied infants. Data were collected on clinicopathologic variables from 42 stillborn and 54 liveborn infants less than or equal to 12 h of age with lung and placenta slides available for review. Correlations and multivariate regression analysis showed that the inflammatory responses in membranes, cord, and lung are interrelated but that hyaline membrane disease develops independently. However, lattice theory analysis, which represents the pathogenesis of a progressive disease process as edges along a mathematical lattice or hyperdimensional cube, showed that this separation was not absolute. Despite the negative correlation of hyaline membrane disease and fetal pneumonia, there were 10 (10%) patients with both conditions and a total of 19 (20%) with hyaline membrane disease and inflammation of membranes, cord, and/or lung. We suggest that the coexistence of hyaline membrane disease and fetal pneumonia in some patients implies a possible pathogenetic relationship between the two entities. Given the nature of the two processes, it seems likely that the direction of causality is that fetal pneumonia would give rise to the hyaline membrane disease of the newborn.
The basis for persistence of the left superior vena cava (LSVC), usually associated with cardiac malformations, is poorly understood. We examined 351 staged, serially sectioned human embryos in the Carnegie Embryological Collection and 1208 specimens with congenital cardiovascular malformations in the Pathology Collection of the Johns Hopkins Hospital. A standardized questionnaire was answered for each embryo and autopsy case and a computer program was employed to tabulate concurrent anatomic features. In the normal embryos a symmetric venous system appeared with the heart tube at Carnegie stage 9; the sinoatrial junction translocated to the right and the relationship of the coronary sinus to the LSVC was established by stage 12. The LSVC was patent through stage 20 and subsequently underwent luminal obliteration by compression between the left atrium and the hilum of the left lung. Among the 1208 hearts with a congenital abnormality, 104 (9%) had a persistent LSVC with a coronary sinus connection. Statistically, significantly more frequent associations were found between persistent LSVC and atrioventricular canal defects, cor triatriatum, and mitral atresia and a significantly less frequent association was observed between persistent LSVC and atrial septal defect or patent foramen ovale as a primary defect. The normally late embryonic obliteration of the LSVC suggests that its persistence would be secondary to reduce cardiac compression or to blood flow redistribution at an early stage, and the malformations associated with persistent LSVC support that view. Identification of a persistent left superior vena cava with coronary sinus connection should suggest an associated malformation, especially atrioventricular canal, cor triatriatum, or mitral atresia.
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