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This study was conducted to determine the efficacy of procainamide therapy for rapid rate control of postoperative junctional tachycardia (JT). Postoperative JT is one of the most difficult forms of tachycardia to manage. Reported success with a variety of treatments of JT in infants and children has been inconsistent and limited. Rate control using procainamide was achieved in 17 children having rapid JT (heart rate >200 beats/min) between 1986 and 1997. In the first 5 patients (protocol A), following a loading dose of 3 mg/kg over 20 minutes, a continuous procainamide infusion was initiated at a rate of 20 microg/kg/min. The infusion dose was increased in 10 microg/kg steps every 30 minutes to 40-120 microg/kg/min until the heart rate decreased below the target rate of 180 beats/min. In the other 12 patients (protocol B), after a higher loading dose of 10 mg/kg the infusion rate was increased every 10-15 minutes until the heart rate decreased below the target rate of 180 beats/min. Procainamide decreased JT rates in all patients but the response was significantly faster in protocol B. In the patients treated with protocol A, pretreatment JT rates ranged from 203 to 240 (213+/-17) beats/min and decreased to 195+/-10 beats/min at 2 hours (p = ns), 186+/-8.8 at 4 hours (p<0.02), and 179+/-8 at 6 hour postinitiation of PA. In protocol B, pretreatment JT rates ranged from 201 to 240 (218+/-17) beats/min and decreased to 183+/-20 beats/min at 2 hours (p<0.001) and 171+/-12 at 4 hours after starting the procainamide therapy. The mean duration to decrease JT rates below the target rate of 180 beats/min was 3.2+/-1.1 hours in protocol B compared to 6.4+/-3.8 hours in protocol A (p<0.02). Eight of 12 patients in protocol B achieved rate control below the target rate of 180 beats/min within 4 hours despite remaining on significant inotropic support. The procainamide infusion rates to maintain heart rates below 180 beats/min were 40-120 (68.4+/-22.1) microg/kg/min. No proarrhythmia, bradycardia, or significant hypotension was observed. In this series procainamide provided safe, effective, and rapid rate control of JT occurring in the immediate postoperative period.

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OBJECTIVE: To detect the presence and source of calciotropic activity in the serum of children with juvenile rheumatoid arthritis (JRA). METHODS: Metabolic evaluation of an adolescent with polyarticular JRA and hypercalcemia/hypercalciuria included testing with a bone disc bioassay. The bioassay detects calciotropic activity (increased bone resorption or reduced bone formation) in serum. Interleukin 1 receptor antagonist (IL-1RA) was added to patient sera to test the role of IL-1beta. The results in this index case prompted additional study in 9 children with JRA. Correlation of calciotropic activity with disease activity score, erythrocyte sedimentation rate (ESR), and urinary calcium excretion was by Spearman rank correlation. RESULTS: Calciotropic activity was found in 2 consecutive samples from the index patient. This activity was eliminated by addition of IL-1RA (p < 0.001 compared to serum alone). Testing of the other 9 children showed calciotropic activity at least once in 7/9 and 10/15 samples studied. Addition of IL-1RA completely (6/8) or partially (2/8) neutralized calciotropic activity (p < 0.001 compared to serum alone) in the specimens available for testing. Calciotropic activity did not significantly correlate with disease activity score, ESR, or urine calcium. CONCLUSION: Our data indicate the presence of IL-1beta mediated calciotropic activity in the sera of children with JRA, and suggest a role for IL-1beta in JRA associated osteopenia.

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BACKGROUND: Complications of Epstein-Barr virus (EBV) infection are diverse and include a number of neurologic manifestations such as meningitis, meningoencephalitis, cerebellitis, cranial neuritis and others. In general encephalitis caused by EBV in pediatric patients has been considered a self-limited illness with few or no sequelae. METHODS: Charts were reviewed from all patients < 18 years of age admitted to or discharged from the State University of New York Health Science Center at Syracuse between 1982 and 1992 with a diagnosis of encephalitis or meningo-encephalitis. Eleven cases of EBV encephalitis diagnosed during a 10-year period were reviewed to characterize the clinical and laboratory findings in the acute setting and the extent of neurologic sequelae on follow-up. RESULTS: Acute neurologic manifestations were diverse and included combative behavior (55%), seizures (36%), headache (36%) and evidence of focal involvement (27%). Classic findings of infectious mononucleosis were noted infrequently; 18% each had pharyngitis, adenopathy, positive heterophile antibody tests or atypical lymphocytosis. Two patients (18%) had abnormal neuroimaging studies, one in the acute stage and the other at the time of follow-up. Seven patients (64%) had abnormal electroencephalograms (EEGs) in the acute setting; of these three had persistent abnormalities on follow-up. Forty percent developed persistent neurologic abnormalities including global impairment, perseverative autistic-like behavior and persistent left upper extremity paresis. CONCLUSIONS: Classic signs, symptoms and laboratory findings in infectious mononucleosis may be absent in Epstein-Barr virus encephalitis. Neurologic sequelae occur in a substantial number of patients.

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A prospective study was performed to determine whether excess morbidity occurred in critically ill and injured pediatric patients during interhospital transport compared with morbidity in a control group. Control observations were made during the first 2 hours of pediatric intensive care unit (PICU) care of patients emergently admitted from within the same institution and not requiring interhospital transport. The first 2 PICU hours of control patients corresponded to the interval of transport in those who required interhospital transfer. Transport care was provided by nonspecialized teams from referring hospitals. Morbidity occurred in 20.9% of 177 transported patients, exceeding the morbidity rate of 11.3% in 195 control patients (P < .05). The difference in morbidity was due to intensive care-related adverse events (eg, plugged or dislodged endotracheal tubes, loss of intravenous access) in 15.3% and 3.6% of transported and control patients, respectively (P < .05). Physiologic deterioration occurred at similar rates of 7.9% and 8.7% in transported and control patients, respectively (P > .05). Slightly greater pre-ICU severity of illness in transported than control patients (median Pediatric Risk of Mortality Score = 10 and 7, respectively, P < .05) and greater pre-ICU therapy relative to severity (P < .05) in control patients are potential confounding sources of the morbidity differences. If patients are stratified into subgroups of similar pre-ICU severity, an excess of intensive care-related adverse events in transported patients remains evident in the severe subgroup (P < .05). Further investigation is warranted to determine whether specialized transport teams can reduce the excess morbidity associated with interhospital transport of critically ill and injured pediatric patients.

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