Caroline Rambaud

Blind protected specimen brush and bronchoalveolar lavage in ventilated children.

OBJECTIVE To determine whether nonbronchoscopic protected specimen brush (PSB) and bronchoalveolar lavage (BAL) are contributive for diagnosing ventilator-associated pneumonia in mechanically ventilated children. DESIGN Prospective study. SETTING Fifteen-bed pediatric intensive care unit in a university hospital. PATIENTS A total of 103 mechanically ventilated children, ranging in age from 7 days to 8.8 yrs, most with a high clinical suspicion for bacterial pneumonia. INTERVENTIONS All the children underwent nonbronchoscopic PSB and BAL. Nonbronchoscopic PSB was performed with a plugged double-sheathed brush and BAL with a double-lumen plugged catheter. Endotracheal secretions and blood cultures were also collected. Open-lung biopsy was performed for any child who died within 7 days after the inclusion in the study, according to the parental consent. MEASUREMENTS AND MAIN RESULTS The PSB specimens were submitted for bacteriologic quantitative culture (positive threshold, 10(3) colony-forming units [cfu]/mL). The BAL samples were processed for microscopic quantification of the polymorphonuclear cells containing intracellular bacteria (positive threshold, 1%) and quantitative culture (positive threshold, 10(4) cfu/mL). According to diagnostic categories based on clinical, biological, radiologic, and pathologic criteria, 29 children had bacterial pneumonia and 64 did not Ten children were classified as having an uncertain status. Of the 29 children with bacterial pneumonia, 26 (90%) met one of the following three criteria: a) PSB specimen culture, > or =10(3) cfu/mL; b) intracellular bacteria in cells retrieved by BAL, > or =1%; and c) BAL fluid culture, > or =10(4) cfu/mL. In contrast, 56 (88%) of the 64 patients without pneumonia did not. CONCLUSION The results of this study indicate the following: a) nonbronchoscopic PSB and BAL were feasible in a large population of mechanically ventilated children; b) nonbronchoscopic techniques were contributive for diagnosing ventilator-associated pneumonia in children; and c) a combined diagnostic approach, using nonbronchoscopic PSB and BAL, was superior to using either test alone.

Molecular identification of viruses in sudden infant death associated with myocarditis and pericarditis

A subset of infants dying suddenly and unexpectedly have myocarditis with or without pericarditis found at autopsy. To address whether viruses known to cause infantile myocarditis and pericarditis might be present in such infants, we examined myocardium, liver and skeletal muscle for the presence of genomic sequences from adenovirus, cytomegalovirus, enterovirus and echovirus 22/23 in infants enrolled in a comprehensive evaluation protocol. We studied eight infants who died suddenly and unexpectedly with histologic evidence of myocarditis and/or pericarditis detected at postmortem examination. One infant with myocarditis and pericarditis had adenovirus genome detected in the myocardium. In an additional infant with severe pericarditis alone, enterovirus genome was detected in the liver. Although echovirus 22/23 has been associated with myopericarditis in young infants, no previous studies have used molecular methods to search for the genomic sequences of these viruses in clinical samples. No echovirus 22/23 genome was detected in the patients reported here. The significance of enterovirus and adenovirus genome in the tissues of two patients dying suddenly and unexpectedly remains speculative but raises the possibility that pathogenic viruses may cause little or no clinical symptoms and yet be contributory to sudden death in young infants.

Cd1a-positive cells in bronchoalveolar lavage samples from children with Langerhans cell histiocytosis

We evaluated CD1a-positive cells in bronchoalveolar lavage samples from children with Langerhans cell histiocytosis (LCH). All children with multifocal LCH and pulmonary symptoms scored higher than 5% (30.6% +/- 7.2%), whereas those with other lung disorders scored much less than 5%. In children with multifocal LCH, bronchoalveolar lavage fluid abnormalities can precede pulmonary symptoms. During chemotherapy the CD1a-positive cell count lends to decrease.

Segregation of the G8993 mutant mitochondrial DNA through generations and embryonic tissues in a family at risk of leigh syndrome

We identified the T8993G mitochondrial mutation in a female infant who died of Leigh syndrome. The proportion of mutant mitochondrial DNA increased to near homoplasmy in three generations of the pedigree. A similarly high proportion of mutant mitochondrial DNA was found in the chorionic villi and in fetal tissues from a pregnancy interrupted because of the risk of Leigh syndrome. This study supports the concept that prenatal diagnosis can be used for Leigh syndrome with the T8993G mitochondrial DNA mutation.

Iron overload in children receiving prolonged parenteral nutrition

This study was carried out to evaluate the iron status of 30 children aged 1 to 18 years who had been receiving total parenteral nutrition (TPN) for an average of 43 months with iron intakes of 100 micrograms/kg per day. Iron status was assessed by assaying the serum iron and ferritin levels and the transferrin saturation coefficient as a function of iron intake. Liver biopsy specimens were taken from 13 children. Twelve children had serum ferritin levels greater than 300 ng/ml, and 8 had levels greater than 800 ng/ml. The serum ferritin level and the transferrin saturation coefficient were positively correlated (r = 0.81; p < 0.01). The serum ferritin level was positively correlated with TPN duration and with the total iron intake (r = 0.68; p < 0.01). Of the 13 liver biopsy specimens, six showed signs of iron deposition. We conclude that there is a risk of iron overload in children receiving 100 micrograms iron per kilogram of body weight per day by TPN, indicating that intake should be reduced.

Cot death and myocarditis

We have investigated the hearts from 153 infants found dead in their cots at ages ranging from one month to one year. The deaths occurred over a period of five years (January 1986 to December 1990) and were studied in a center for the study of the sudden infant death syndrome located in Paris. The epidemiological characteristics of this group are:male predominance (sex ratio 1.43), age less than four months (82%), and a predominance of winter deaths. These are the characteristic features ofthe sudden infant death syndrome. Ofthe 143 children studied with the permission of their parents, 24 (16.8%–12 girls and 12 boys) had histological lesions consistentwith myocarditis according to the Dallas criteria. The histological diagnosis of myocarditis is based on the association of cellular necrosis with a mononuclear or mixed inflammatory infiltrate. Cytoplasmic vacuolization, the presence of inflammatory cells in myocytes, and rupture of the cell walls of myocardial fibres are the equivalent histological signs of cellular necrosis. Myocarditis was diversely associated with respiratory, hepatic, muscular, gastrointestinal and/or neurological involvement. Twelve infants had previously been ill. Two died during the course of a serious illness. In only four cases was a viral association demonstrated. This incidence of myocardial involvement, similar to thatdescribed elsewhere in the literature, suggests that myocarditis could be a pathogenic explanation of some deaths thought on general autopsy investigation to be sudden and unexplained.

Fatal Rhabdomyolysis in 2 Children with LPIN1 Mutations

We report 2 cases of fatal rhabdomyolysis in children carrying an LPIN1 mutations preceded by similar electrocardiogram changes, including diffuse symmetrical high-amplitude T waves. Our report underlines the severity of this disease and the need for active management of episodes of rhabdomyolysis in a pediatric intensive care unit.

Fatal parvovirus B19 myocarditis in children and possible dysimmune mechanism.

We report 2 cases of previously healthy children, who developed, after a common parvovirus B19 infection, a sudden inflammatory response, involving predominantly T cell, directed against myocardium and leading to fatal outcome. These cases and several published case reports further our understanding of fulminating parvovirus myocarditis in children.

P468 - Myocardites fulminantes à parvovirus B19 : un mécanisme dysimmun ?

L’infection a Parvovirus B19 (PB19) est une maladie infantile benigne et frequente. De rares cas de myocardites fatales ont ete rapportes, dont la physiopathologie demeure incertaine. Nous rapportons deux nouveaux cas de myocardites fulminantes a PB 19 : 2 enfants sains qui, quelques jours suivant l’apparition de symptomes evoquant une infection banale a PB19, sont brutalement decedes d’incompetence myocardique. Le virus a ete isole dans le serum des 2 patients par PCR ; les serologies confirmaient l’infection recente a PB 19. L’analyse histologique post-mortem complete du tissu cardiaque a permis le diagnostic de myocardite fulminante en montrant un infiltrat inflammatoire majeur. Ces constatations sont en accord avec les hypotheses actuelles qui ecartent un role cytopathogene du virus et privilegient une atteinte indirecte du myocarde. La myocardite aigue grave a PB19 de l’enfant, probablement de nature inflammatoire ou post-infectieuse, serait due a une dysregulation de la reponse immune de l’hote : elle serait disproportionnee et responsable de lesions myocardiques massives. Aucun critere clinique ne peut malheureusement a l’heure actuelle predire l’evolution bien que tres rarement dramatique de cette infection banale.