Biomedical subjects
Publications and source records attributed to R Aronow.
We report the ingestion of ammonium dichromate by a child that resulted in multiple-organ-system failure and death. Exchange transfusion and hemodialysis were ineffective in removing significant amounts of chromium or causing sustained clinical improvement. We suggest that immediate, large doses of the reducing agent ascorbic acid would allow effective reduction of hexavalent chromium with less cellular toxicity.
The cause of microcytosis and anemia in lead poisoning was investigated using red blood cell distribution width as a screening parameter in 21 consecutive patients with lead poisoning and seven nonrandomly selected patients with iron deficiency and lead poisoning. Of the 21 consecutive patients, 11 had microcytosis as defined by a mean corpuscular volume of less than 72 fL, nine had thalassemia trait (alpha or beta), one had both alpha thalassemia trait and iron deficiency, and one had iron deficiency. The red blood cell distribution width was less than 17.0 in those with thalassemia trait and greater than 17.0 in the iron-deficient subjects. Results of our study suggest that microcytosis in children with lead poisoning is due to coexistent iron deficiency or thalassemia trait. The red blood cell distribution width may be of value in the rapid assessment of the cause of microcytosis in children with lead poisoning.
Suicide attempts during pregnancy usually present as intentional drug overdoses after interpersonal conflicts. During a recent four-year period, 119 (0.07%) of all 179,893 telephone inquiries at a metropolitan poison control center involved drug overdoses by 111 pregnant women. This was usually the first such attempt and telephone notification occurred primarily within the first hour. The ingested substance was known in 109 (98%) cases and consisted mostly of an excess of a single drug. The 50 different types of over-the-counter and prescription medications consisted primarily of analgesics (most notably acetaminophen), vitamins or iron, sedatives, antibiotics, and antihistamines or decongestants. No maternal deaths were reported. Signs or symptoms were nonexistent or mild in 61 (55%) women, and major or life-threatening in 50 (45%) women. Compliance with recommendations given by telephone and referral to the primary physician or emergency room was good, especially when major symptoms or life-threatening illnesses were apparent. Close emotional support and a search for depression during pregnancy and the postpartum period are recommended.
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In a patient severely poisoned with theophylline, saturation kinetics were demonstrated at serum concentrations > 35 micrograms/ml with subsequent conversion to first order kinetics (t 1/2 = 5.4 h). Peritoneal dialysis was used to enhance the drug's removal. The mean theophylline clearance was greater for dialysate (5.11 ml/min) than for urine (1.98 ml/min) or gastric fluid (0.32 ml/min). Urinary elimination occurred as a constant first order process (t 1/2 = 4.3 h). Peritoneal dialysis is a valuable early adjunct in the management of severe theophylline intoxication.
The use of peritoneal dialysis as an adjunct to management of theophylline intoxication is presented. Due to the nature of the case, detailed pharmacokinetic explanation was not possible. The data indicate that appreciable quantities of theophylline can be removed using peritoneal dialysis.
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Emergency physicians should be prepared to treat overdosage from phencyclidine, a common street drug abused throughout North America. A dearth of laboratory resources to establish the diagnosis makes it essential that diagnoses include awareness of symptomatology. A specific therapeutic approach utilizing ion-trapping by continuous gastric suctioning and acidification of urine and/or blood can be used successfully to treat these patients.
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In spite of continued lead intake, the oral chelate d-penicillamine was effective in reducing blood lead levels of lead-poisoned weanling rats on three different low-residue diets: a standard rat diet, a low calcium diet, and the trace metal salt modified EPA diet. A significant lessening of weight gain was evident in those on the low calcium diet.
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It has been known for many years that the eating of leaded paint is the prime cause of lead poisoning and elevated blood leads of children living in deteriorated housing. Recently, there has been speculation that children may eat dirt and dust contaminated with lead exhausted from cars and that this amount of ingested lead is sufficient to contribute significantly to the childhood lead problem. This study used a naturally occurring radioactive tracer (lead-210) to determine the relative amounts of dust and other lead-containing materials (e.g., paint) eaten by young children. This tracer is present in very low concentrations in paint and in significantly higher concentrations in fallout dust. Stable lead and lead-210 were analyzed in fecal material from 8 children suspected of having elevated body burdens of lead and 10 children living in good housing where lead poisoning is not a problem. The normal children averaged 4 micrograms lead per gram dry feces, with a range of 2 to 7. Of the eight children suspected of having elevated lead body burdens, two had fecal lead values within the normal range. However, the remaining six were 4 to 400 times higher. Despite these differences in fecal lead between the two groups, the groups were essentially identical in the lead-210 content of their feces. The "elevated" children averaged 0.040 picocurie lead-210 per gram dry feces, while the normal group averaged 0.044. The results provide sound evidence that these children suspected of elevated lead body burden were not ingesting dust or air-suspended particulate.
It has been known for many years that the eating of leaded paint is the prime cause of lead poisoning and elevated blood leads of children living in deteriorated housing. Recently, there has been speculation that children may eat dirt and dust contaminated with lead exhausted from cars and that this amount of ingested lead is sufficient to contribute significantly to the childhood lead problem. This paper reports on a twopart study conducted to evaluate the validity of the dirt-and-dust hypotheses. The first part of the study was made to determine the source of lead in dirt to which children are normally exposed. Dirt samples were taken in old urban areas around 18 painted frame houses and 18 houses of brick construction. Samples also were taken around seven old frame farmhouses remote from traffic. Based on the fact that lead concentrations in the dirt were similar in city and rural yards at corresponding distances from the houses, it is clear that nearly all of the lead in dirt around these houses is due to paint from the houses. Lead antiknock additives are therefore not a significant contributor to the lead content of dirt around houses where children usually play. The second part of the study used a naturally occurring radioactive tracer (210)Pb to determine the relative amounts of dust and other lead-containing materials (e.g., paint) eaten by young children. This tracer is present in very low concentrations in paint and in significantly higher concentrations in fallout dust. Stable lead and (210)Pb were analyzed in fecal material from eight children suspected of having elevated body burdens of lead and ten children living in good housing where lead poisoning is not a problem. The normal children averaged 4 mug Pb/g dry feces, with a range of 2 to 7. Of the eight children suspected of having elevated lead body burdens, two had fecal lead values within the normal range. However, the remaining six were 4 to 400 times as high. Despite these differences in fecal lead between the two groups, the groups were essentially identified in the (210)Pb content of their feces. The "elevated" children averaged 0.040 pCi of (210)Pb dry feces, while the normal group averaged 0.044 pCi/g. The results provide sound evidence that these children suspected of elevated lead body burden were not ingesting dust or air-suspended particulate.