Biomedical subjects
Publications and source records attributed to J F Wiley.
Astemizole, a nonsedating antihistamine, caused a prolonged corrected QT interval, ventricular dysrhythmias, and atrioventricular heart block after overdose in five children. Cardiotoxic effects lasted an average of 2 1/2 days. Children poisoned with astemizole need emergent medical evaluation, a 12-lead electrocardiogram with calculation of the corrected QT interval, and continuous cardiac monitoring for 24 hours.
To determine the risk of increased blood lead levels in children with aural, nasal, or gastrointestinal foreign bodies, the authors prospectively obtained venous blood lead and erythrocyte protoporphyrin levels from 40 study patients and two control groups without foreign bodies (65 patients presenting to a medical clinic and 40 patients presenting to an emergency department). A questionnaire was used to assess environmental and behavioral risk factors for lead poisoning in the three groups. Mean blood lead level was higher in children with foreign bodies (P less than .001), and they were more likely to have a venous blood lead value of more than 1.2 mumol/L (25 micrograms/dL, P less than .01) than patients in either control group. Seventy-eight percent of study patients had no prior lead screening by parent's report vs 64% of emergency department control subjects and 55% of medical clinic control subjects. Control patients in the emergency department had the same incidence of elevated blood lead values as patients enrolled from the medical clinic (6%). No differences in environmental risk factors were found among the three groups. Study patients more often had a history of pica or ingestion of a poison than control patients from the medical clinic. Inner-city children with foreign bodies have increased lead exposure and may have an increased risk for lead poisoning. In areas of high prevalence of lead poisoning, children with foreign bodies should be screened for lead poisoning in the emergency department. General lead screening in the emergency department may be justified for high-risk, inner-city populations.
The comprehensive drug screen has serious limitations when used as the sole study for diagnosing intoxication. A careful history and physical examination in the poisoned patient can provide important clues that point to possible toxins. Ancillary studies help differentiate the most likely poison and guide treatment. Fortunately, most poison victims do well with supportive care alone. However, the clinician should be aware of agents that can cause significant harm to patients if not detected and treated quickly. Iron and carbon monoxide are good examples of lethal agents that need a high index of clinical suspicion for early recognition and require specific therapy to ensure a good outcome. Patients who overdose with clonidine, calcium-channel blockers, beta-adrenergic blockers, or albuterol must be managed expectantly and according to their clinical presentation because rapid laboratory verification is not available for these poisons. In all situations, the clinician must integrate information from history, physical examination, and laboratory to render the best care.
We reviewed 47 consecutive inpatient records to determine the clinical course, role of supportive measures, and response to naloxone in children with clonidine poisoning. Severity of illness was assigned by means of the "pediatric risk of mortality" (PRISM) score. The children's ages ranged from 9 to 84 months. Central nervous system effects were noted in 44 patients; bradycardia occurred in 25, and apnea or depressed respiration was seen in 18. Thirty-four patients had symptoms within 1 hour of presentation, but no patient had further clinical deterioration more than 4 hours after presentation. Six patients required endotracheal intubation and mechanical ventilation. There was no difference in PRISM score or duration of symptoms between those patients who received naloxone and those who did not. More patients receiving naloxone required intubation, and only three patients had definite improvement after naloxone administration. We conclude that (1) young children who ingest clonidine have a wide spectrum of serious findings, (2) delayed progression of symptoms after clonidine poisoning is unlikely in a young child with normal renal function, and (3) naloxone is an inconsistent antidote for clonidine poisoning.
Mammalian bites account for a large number of emergency department and doctor's visits. Children are the victims in more than half of reported cases. Dogs account for the majority of wounds, and almost all fatalities in these cases are due to dog bites. Human bites and cat bites account for the majority of infected wounds. Basic wound care, combined with appropriate antibiotic coverage in high risk wounds, is the most important principle of management.
We report a case of subgaleal abscess formation in a 16-year-old boy with varicella and minor head trauma. He presented four weeks after injury with left-sided scalp swelling and periorbital edema. There was no break in the skin over the involved area. Diagnosis was made on the basis of prolonged swelling, an elevated erythrocyte sedimentation rate, and computed tomography that showed a subgaleal fluid collection. Aspirated material grew Group A beta-hemolytic Streptococcus. Subgaleal abscess formation without an overlying wound is previously unreported. Management of subgaleal abscess usually requires operative debridement and IV antibiotics. However, in our patient, needle aspiration and oral antibiotics sufficed.
The purpose of this study is to compare a revised rule of thumb with the Harriet Lane and Behrman's formulas for predicting haematocrit rise following packed red blood cell (PRBC) transfusion in premature neonates. Pre- and post-transfusion, equilibrated central haematocrits were obtained within 24 h of transfusion in 12 premature neonates undergoing 18 transfusions. Iatrogenic blood loss between pre- and post-transfusion haematocrit determinations was measured for each transfusion event, and infants with detectable, non-iatrogenic blood loss were excluded. Expected haematocrit rise was calculated three different ways using the Behrman, Harriet Lane, and proposed formulas (see text). The Harriet Lane formula predicted haematocrit rise with a correlation, r = 0.66 and slope m = 0.43. The Behrman's formula predicted haematocrit rise with a correlation r = 0.81 and slope m = 0.60. The proposed formula predicted haematocrit rise with a correlation r = 0.79 and slope m = 0.56. On the basis of these findings, we propose the following formula: Quantity PRBC transfused (ml) = 4/3 X desired haematocrit rise X weight (Kg) This formula takes into account the higher blood volume per kilogram body weight seen in premature infants while estimating PRBC unit haematocrit as 0.75 to obviate the need of measurement before each transfusion and, therefore, is an accurate, practical, and simple replacement for the Harriet Lane and Behrman's formulas.
Changes in serum potassium in premature neonates undergoing transfusion from CPDA-1 triple satellite PRBC paediatric packs cannot be predicted solely on the basis of potassium dose and estimated plasma volume. Despite significant potassium loading during PRBC transfusion, the actual serum potassium change is much less than predicted in neonates with good renal status. These findings indicate that special washing procedures to reduce potassium concentrations in PRBC units for transfusion in neonates is not warranted although exclusion of units older than 5 days for transfusion in premature infants seems to be a reasonable policy.
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