RESUMO
Febrile neutropenic children with cancer were eligible for outpatient management with intravenous ceftriaxone therapy if they displayed selected low-risk criteria. Nineteen children were enrolled. All patients had sterile blood cultures, and only one of them was hospitalized because of persistent fever. This pilot study suggests that selected children with febrile neutropenia might be successfully managed without hospitalization.
Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Bacteriemia/tratamento farmacológico , Ceftriaxona/uso terapêutico , Cefalosporinas/uso terapêutico , Febre de Causa Desconhecida/tratamento farmacológico , Neoplasias/tratamento farmacológico , Neutropenia/induzido quimicamente , Adolescente , Assistência Ambulatorial , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Bacteriemia/etiologia , Ceftriaxona/efeitos adversos , Cefalosporinas/efeitos adversos , Criança , Pré-Escolar , Feminino , Febre de Causa Desconhecida/etiologia , Humanos , Lactente , Infusões Intravenosas , Contagem de Leucócitos/efeitos dos fármacos , Masculino , Neutropenia/tratamento farmacológico , Neutrófilos/efeitos dos fármacos , Contagem de Plaquetas/efeitos dos fármacos , Resultado do TratamentoRESUMO
A 2-year-old boy with sickle cell anemia had a massive, fatal hemolytic reaction after administration of an intravenous dose of ceftriaxone. Laboratory studies demonstrated the presence of an IgM antibody against ceftriaxone, binding to and destroying the patient's erythrocytes by an immune complex mechanism. This rare complication should be considered in the differential diagnosis when hemoglobinuria develops in a child after administration of ceftriaxone or a similar agent.
Assuntos
Anemia Hemolítica Autoimune/induzido quimicamente , Anemia Falciforme/tratamento farmacológico , Ceftriaxona/efeitos adversos , Hemoglobinúria/induzido quimicamente , Anemia Hemolítica Autoimune/sangue , Anemia Hemolítica Autoimune/imunologia , Ceftriaxona/uso terapêutico , Pré-Escolar , Evolução Fatal , Hemoglobinúria/sangue , Hemólise , Humanos , Imunoglobulina M/sangue , MasculinoRESUMO
We reviewed our experience with gram-negative enteric bacillary meningitis in neonates and infants from 1969 through 1989. Ninety-eight patients were identified. Their ages were from 1 day to 2 years with a median of 10 days. In 25 patients (26%), predisposing factors were identified, the most common of which were neural tube defects and urinary tract anomalies. The causative agents were Escherichia coli (53%), Klebsiella-Enterobacter species (16%), Citrobacter diversus (9%), Salmonella species (9%), Proteus mirabilis (4%), Serratia marcescens (3%), Bacteroides fragilis (3%), and Aeromonas species (2%). At the time of diagnosis, Gram-stained smears of cerebrospinal fluid revealed gram-negative bacilli in 61% of patients. The causative organism was cultured from blood obtained from 55% of patients, and 21% had positive urine culture results. The cerebrospinal fluid leukocyte counts ranged from 0 to 80,600 cells/mm3, and the cerebrospinal fluid/serum glucose concentration ratio was less than 0.5 in 72% of patients. Antimicrobial regimens varied greatly. After initiation of antibiotic therapy, an average of 3 days was needed for eradication of bacteria from cerebrospinal fluid. The case-fatality rate was 17%, and 61% of survivors had long-term sequelae that included seizure disorders, hydrocephalus, physical disability, developmental delay, and hearing loss.
Assuntos
Infecções por Enterobacteriaceae/epidemiologia , Meningites Bacterianas/epidemiologia , Antibacterianos , Quimioterapia Combinada , Infecções por Enterobacteriaceae/líquido cefalorraquidiano , Infecções por Enterobacteriaceae/complicações , Infecções por Enterobacteriaceae/tratamento farmacológico , Infecções por Enterobacteriaceae/fisiopatologia , Infecções por Escherichia coli/epidemiologia , Humanos , Hidrocefalia/etiologia , Lactente , Recém-Nascido , Deficiência Intelectual/etiologia , Meningites Bacterianas/líquido cefalorraquidiano , Meningites Bacterianas/complicações , Meningites Bacterianas/tratamento farmacológico , Meningites Bacterianas/fisiopatologia , Espasticidade Muscular/etiologia , Paralisia/etiologia , Complicações Pós-Operatórias/epidemiologia , Complicações Pós-Operatórias/microbiologia , Recidiva , Fatores de Risco , Convulsões/etiologia , Taxa de Sobrevida , Texas/epidemiologia , Resultado do TratamentoRESUMO
Because interleukin-1 beta (IL-1 beta) and cachectin (tumor necrosis factor) are thought to mediate the body's response to microbial invasion, we measured IL-1 beta and tumor necrosis factor concentrations in paired cerebrospinal fluid (CSF) samples (on admission to the hospital, CSF1; 18 to 30 hours later, CSF2) from 106 infants and children with bacterial meningitis. In CSF1, IL-1 beta was detected in 95% of samples; the mean (+/- 1 SD) concentration was 944 +/- 1293 pg/ml. Patients with CSF1 IL-1 beta concentrations greater than or equal to 500 pg/ml were more likely to have neurologic sequelae (p = 0.001). Tumor necrosis factor was present in 75% of CSF1 samples; the mean concentration was 787 +/- 3358 pg/ml. In CSF2 the mean IL-1 beta concentration was 135 +/- 343 pg/ml, and IL-1 beta concentrations correlated significantly with CSF2 leukocyte count, with glucose, lactate, protein, and tumor necrosis factor concentrations, and with neurologic sequelae. Tumor necrosis factor was detected in CSF2 specimens of 53 of 106 patients, with a mean concentration of 21 +/- 65 pg/ml. Of the 106 patients, 47 received dexamethasone therapy at the time of diagnosis. These patients had significantly lower concentrations of IL-1 beta and higher glucose and lower lactate concentrations in CSF2, and they had a significantly shorter duration of fever compared with the values in patients not treated with steroids (p less than or equal to 0.002). Our data suggest a possible role of IL-1 beta and tumor necrosis factor as mediators of meningeal inflammation in patients with bacterial meningitis, and might explain, in part, the beneficial effect of dexamethasone as adjunctive treatment in this disease.