Pneumococcal subdural empyema in young infants.
We report three young infants including a neonate with fulminant pneumococcal subdural effusion.
Biomedical subjects
Publications and source records attributed to C Kirubakaran.
We report three young infants including a neonate with fulminant pneumococcal subdural effusion.
Screening for enteric pathogens in stool samples from 249 children under the age of 36 months, admitted to hospital for non-gastrointestinal disorders, was positive at admission in 41 (16.4 per cent) in a prospective study of enteric pathogen acquisition and diarrhoea in hospitalized children. Infection with multiple organisms was found in 31/41 (75.6 per cent) children who were positive when screened at admission. Of 194 children who had no enteric pathogens on admission and could be followed up for 3 days after discharge, clinical or laboratory data showed nosocomial enteric infections in 39 (20.1 per cent). Presumed nosocomial infection with more than one organism was seen in only two patients and no pathogens were isolated in 14 (35.8 per cent). Children presenting to hospital may asymptomatically carry enteric pathogens and potentially act as a source of nosocomial infections. One in five children admitted into hospital without an enteric infection is at risk of developing a nosocomial gastrointestinal infection, with rotavirus being the most common aetiological agent.
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Despite the well-known advantages of breast-feeding to both mother and infant, malnutrition of breastfed infants does occur. We report two term neonates who presented in the 3rd week of life with severe wasting, hypernatraemic dehydration and pre-renal failure while being exclusively breastfed. Breast-milk sodium levels were markedly elevated on admission. Both infants recovered following adequate hydration and showed excellent catch-up growth during follow-up while exclusive breast-feeding was maintained. The critical malnutrition in both cases was detected by the family physician during routine postnatal visits. Both mothers were well motivated toward breast-feeding and were unaware of the severity of the baby's illness.
We report pyknodysostosis presenting as extramedullary haematopoiesis in one of two siblings and as obstructive airway disease in the other. Visceral manifestations are rare and have been reported in only two cases in the Indian literature. They have often been mistaken for osteopetrosis, haemolytic anaemia and other osteochondrodystrophies. The cases we report illustrate that, though the physical characteristics may be similar, it is the radiological features that are typical and help establish the diagnosis.
OBJECTIVES: The aim of this study was to characterize the motor events responsible for gastroesophageal reflux (GER) and esophageal acid clearance in a cohort of healthy preterm infants. STUDY DESIGN: Esophageal motility was recorded for 2 to 3 hours after a feeding in 24 preterm infants, 31 to 38 weeks' postmenstrual age, by using a sleeveside hole micromanometric assembly incorporating a pH probe. RESULTS: Sixty acid GER episodes were recorded by pH probe, and 133 non-acid GER episodes were recorded manometrically by the presence of esophageal common cavities. Of the 193 GER episodes, 159 (82%) were associated with transient lower esophageal sphincter relaxation (TLESR). TLESRs were significantly longer in duration than single swallows (15.1 seconds vs 5.6 seconds, P < .001) and had lower nadir pressures (0.8 mm Hg vs 2.3 mm Hg, P < .001). A total of 3216 esophageal body pressure waves were analyzed; 70% of swallow-induced pressure waves were peristaltic in sequence compared with 5% of swallow-unrelated pressure waves. During periods of esophageal acidification (pH below 4), peristaltic esophageal body pressure wave sequences cleared acid refluxate more effectively than nonperistaltic pressure wave sequences. CONCLUSIONS: In healthy preterm infants, TLESRs are the predominant mechanism underlying GER, and esophageal clearance mechanisms are well developed by at least 31 weeks' postmenstrual age.
The aetiological contribution of viral agents in the causation of acute diarrhoea was studied prospectively in 915 infants and young children aged 1-35 months. This was a hospital-based study, selection being carried out by proportionate random sampling; 587 matched controls were also investigated simultaneously. Methods of detection included direct electron microscopy, ELISA for rotaviruses and immune electron microscopy. Rotaviruses emerged as the single most important cause with highest prevalence in the 6-11-month age group. The contribution of other agents was negligible. Electron microscopy, though a "catch-all' technique, is not a cost-effective diagnostic method for developing countries.
In addition to ten children with Wilson's disease and one with Indian childhood cirrhosis, nine Indian children, aged from 4 to 15 years, with cryptogenic cirrhosis had significant deposits of stainable copper in their hepatocytes. These nine children had normal or elevated serum caeruloplasmin levels, absence of Kayser-Fleischer rings and a history of sibling death owing to liver disease in four cases. Histologically, fatty change was absent from all the biopsies but Mallory's hyaline, pericellular fibrosis and ballooning of hepatocytes were present in some. Since these children did not conform to the accepted clinical or histological definitions of either Indian childhood cirrhosis or Wilson's disease, they were designated as having atypical copper cirrhosis. The relationship of this group of cases to other types of copper cirrhosis is unknown.
The aim of this study was to determine the reasons for admission, charges made, and causes of death in a tertiary referral neonatal unit in India. Records of the Christian Medical College Hospital, Vellore, Tamil Nadu, India, were reviewed for the period 1 January-31 December 1992. The principal cause of death was ascertained with reference to predetermined diagnostic criteria. There were 5592 livebirths, 138 stillbirths and 1809 admissions to the nurseries (1603 inborn, 206 outborn). Suspected sepsis accounted for 24 per cent of admissions, 14 per cent required preterm care, 13 per cent phototherapy and 8 per cent were full term low birth weight babies admitted for observation. There were 87 early neonatal deaths, 4 per cent (49) of inborn admissions and 18 per cent (38) of outborn admissions. A further 11 babies were discharged to receive terminal care at home and nine were discharged, critically ill, against medical advice. Causes of death were respiratory problems of prematurity (49 per cent), lethal congenital malformations (22 per cent), complications of asphyxia (20 per cent) and sepsis (5 per cent). The median duration of nursery care was 2 days (range 1-21) and the median charge made Rs 714 (range 122-5036). Although the pattern of admissions and deaths still reflects the substantial problems of suspected sepsis, asphyxia, and congenital malformations, problems of immaturity may be on the increase. We caution against hospital-based statistics that fail to take account of babies who are discharged alive in the knowledge that death is imminent. Considered strategies for the provision or selective provision, of neonatal care in India, are called for.
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This report describes an epidemic of dengue haemorrhagic fever/dengue shock syndrome (DHF/DSS) in the North Arcot Ambedkar district and the adjoining districts in Tamil Nadu and Andhra Pradesh. Nineteen children who fulfilled the clinical criteria for the diagnosis of DHF/DSS were admitted to the Christian Medical College Hospital, Vellore, during June through November, 1990. The clinical presentation was similar to that described in South-east Asian children and the case fatality rate was 26.3 per cent. Serology was confirmatory or suggestive of recent dengue virus infection in 16 children, uninterpretable in 2 and not consistent with recent dengue virus infection in 1 child. All children over 1 yr of age had very high antibody titres suggesting a secondary response whereas infants had lower titres consistent with primary response. The occurrence of recurrent epidemics in this region in the last few years with associated high case fatality emphasizes the urgent need for public health measures to curtail further epidemics.
We report the pattern of childhood liver disease revealed by a study of 134 biopsies obtained from 128 infants and children below the age of 16 years seen in this hospital during a 3-year period. The most common histological diagnoses were neonatal hepatitis syndrome in 23, storage disorders in 11, and cirrhosis in 26 children. Less common diagnoses included Reye's syndrome in four, fatty liver in seven, granulomas in four, and chronic active hepatitis, fulminant hepatitis, congenital hepatic fibrosis and neoplasms in two children each. Miscellaneous specific diagnoses were made in 16 cases. Twenty-three per cent of the liver biopsies were non-diagnostic. The study has provided background information on the occurrence of specific histological diagnoses in liver biopsies in infants and children in this tropical region and identifies a group with cirrhosis and copper deposition which was not typical of either Indian childhood cirrhosis or Wilson's disease.
A case of focal seizures with right hemiparesis in a 6-year-old Indian girl is presented. CT scan showed four ring-enhancing lesions in the left cortex. She was treated with phenytoin and a course of praziquantel. The hemiparesis recovered in 3 weeks and a repeat CT scan after 2 months was normal. Arbitrary use of anti-tuberculous therapy in Indian children with focal lesions in the brain is not recommended as the lesions are often due to cysticercosis.
Among the 157 children with culture proven pyogenic meningitis who were admitted during 1987-1991, in the Department of Child Health at the Christian Medical College and Hospital, Vellore, 40 had H. influenzae type b (HIB) meningitis; 17 of these had multiantimicrobial resistant HIB (MRHIB) and 23 others had usual susceptibility HIB (USHIB) meningitis. The two groups were compared. Children with MRHIB meningitis who received optimal treatment with cefotaxime had excellent recovery. When cefotaxime therapy was delayed, mortality was noted in all except one child who survived with severe neurological sequelae. MRHIB meningitis treated with drugs other than cefotaxime had 100 per cent mortality. Cefotaxime is therefore recommended in children below 3 yr of age presenting with purulent meningitis, as MRHIB is a possible causative agent in this group.
Bacterial, viral and parasitic enteric pathogens were detected in 692 of 916 children below 36 months of age with acute diarrhoea and in 289 of 587 matched controls. The rates of identification of only four groups of pathogens, rotavirus, Shigellae, Salmonella typhimurium and enterotoxigenic E. coli, were significantly higher in the patients. The prevalence of a variety of other enteric pathogens was similar in controls of patients. Shigellosis had a characteristic clinical profile but none of the other agents could be suspected on clinical grounds. The high prevalence of pathogens in controls suggested that the population may be partially protected against a variety of enteric pathogens and that final common pathways leading to diarrhoea may be activated by changes in the microbial ecology of the gut lumen.
More than 80% of patients with cystic fibrosis have poor pancreatic function, and have large daily faecal bile acid losses. This has been postulated to lower luminal bile acid concentrations and adversely affect fat absorption. We studied, for the first time, quantitative individual conjugated duodenal bile acid secretion rates into the duodenum during cholecystokinin/secretin infusion in 55 cystic fibrosis patients and six controls, using a quantitative non-absorbable marker technique. We were able to show adequate duodenal total bile acid concentrations and normal secretion rates in these children. The bile acid secretion pattern in cystic fibrosis patients showed a marked increase in bile acid concentration during cholecystokinin/secretin infusion, to levels which were above the critical micellar concentration indicating that the gall bladder is a functional organ in this disease. The subsequent fall in secretion rate was similar to controls. We have documented a significantly raised glycine/taurine bile acid conjugation ration in duodenal juice from cystic fibrosis patients and suggest that the combined effects of lowered ileal pH and increased glycine conjugated proportion of bile acids may cause precipitation of bile acids leading to decreased fat absorption and large faecal bile acid losses. To further investigate bile acid secretion in children with cystic fibrosis, we modified the high performance thin layer chromatography/densitometry method to enable measurement of individual glycine and taurine conjugates in serum. In comparing cystic fibrosis patients and controls, we were able to determine a group of 18 (36%) with bile acid evidence of liver damage who also showed reduced bile acid secretion into the duodenum. We were unable to study changes in serum bile acids during cholecystokinin/secretin infusion because of the high level of bile acid contamination in Boots Secretin. Some patients showed raised fasting serum bile acid concentrations more than two years before changes in conventional liver function tests or clinically evident liver disease. We have shown fasting serum bile acids to be a sensitive measure of liver dysfunction in cystic fibrosis and postulate that raised proportions of glycine conjugated bile acids may be responsible for the high incidence of liver disease in cystic fibrosis.
During a 12-month period, we tested faecal samples from 386 children with acute enteritis and 332 controls by light and electron microscopy, and by bacterial and viral culture for pathogens, especially to assess the importance of campylobacter. Campylobacter alone was responsible for the illness in 17 patients (5%), and was second to salmonella among the bacterial agents, which were predominant in summer. Overall, rotavirus was the commonest identifiable cause of acute enteritis and was especially important in winter (with a rate of 49% in August). Thirty-five patients showed two or more agents. In 117 patients (30%) no pathogen was isolated or identified, suggesting that there are as yet unidentified agents in acute enteritis.