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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was undertaken to assess the association between esophageal pH monitoring variables and signs such as regurgitation, vomiting, apnea, bradycardia, and cyanotic episodes attributable to gastroesophageal reflux (GER) in neonates. One hundred thirty-four infants with one or more of the above-described signs underwent 24-hour distal esophageal pH monitoring in the neonatal intensive care unit, and were divided into 2 groups by gestational age. Group 1 (preterm infant group) consisted of infants aged 25 to 36 weeks of gestation ( n = 45) and group 2 (term infant group) consisted of infants aged 37 to 42 weeks gestation ( n = 89). Esophageal pH monitoring variables were compared by gestational age group and within preterm infants by theophylline treatment and, separately, by nasogastric tube using the Mann-Whitney U test. Comparisons of nominal data were made using the chi square test. Logistic regression analysis was used to assess the net effect of each independent variable on the risk of developing GER. The prevalence of GER was not influenced by gestational age. The prevalence of gastrointestinal signs did not differ between groups. Cardiorespiratory signs attributed to GER were more frequent in preterm infants than in term infants. The number of episodes with pH < 4 in 24 hours was greater in the term compared with the preterm infant groups. Logistic regression analysis failed to detect an association between acid GER and gestational age, apnea, bradycardia, cyanotic episodes, vomiting, or regurgitation. Theophylline treatment and the presence of a nasogastric tube did not significantly affect the esophageal pH monitoring variables in preterm infants. Preterm infants have a smaller number of reflux episodes compared with term infants. In addition, treatment with theophylline for apnea of prematurity and the presence of a nasogastric tube in preterm infants did not significantly affect pH-monitoring variables in preterm infants.
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PMID:Esophageal pH study and symptomatology of gastroesophageal reflux in newborn infants. 1501 72

HELLP syndrome is a multi-organ disorder unique to pregnancy. It is characterized by hemolysis, elevated liver enzymes, and low platelets in patients with pre-eclampsia or eclampsia. In King Abdulaziz Oncology Center, Jeddah, seven patients with HELLP syndrome were admitted over a period of four years (1991-94). Retrospective analysis of data was done to study the clinical profile of HELLP syndrome. The incidence of HELLP syndrome in our institution was 1 per 2285 deliveries. One patient was Saudi and six were non-Saudis. The age range was 23 to 44 years, with a mean of 29 years. All patients were multipara. The disorder occurred between 24 to 33 weeks of gestational age, the average being 29 weeks. The most commonly encountered clinical feature was right upper quadrant/epigastric pain. Other features included nausea/vomiting, jaundice, hepatic encephalopathy, azotemia, hypotension and grand mal convulsions. All patients had severe pre-eclampsia pr eclampsia. Indirect hyperbilirubinemia was in the range of 2 to 8 mg/dL and elevated transaminases up to 229 U/L (n<40 U/L) were noted. Various degrees of peripheral thrombocytopenia (<150x10(9)/L) were present in seven patients. Four patients had elevated prothrombin and partial thromboplastin time with postive fibrinogen degradation products. Laboratory abnormalities returned to normal within 10 days following delivery. Four patients were delivered by cesarean section and three had vaginal deliveries. We had two maternal deaths (mortality 34%). One died of multi-organ failure and the other with adult respiratory distress syndrome. There was one stillbirth and the second baby died soon after birth due to prematurity (infant perinatal mortality 34%). We conclude that HELLP syndrome is rare among pregnant women in our institution. It should always be suspected in women with pre-eclampsia or eclampsia when they present with upper abdominal pain. Multipara seem to be more afflicted. Subclinical disseminated intravascular coagulation was detected in 55% of the patients. A majority of our patients presented late to the hospital.
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PMID:HELLP syndrome: Clinical profile of seven patients. 1737 23

Cholelithiasis is a rare finding in children, even though recent series show increased detection of this disease. A retrospective study was performed in children with a diagnosis of cholelithiasis between 1993 and 2005 in the Reina Sofia Hospital in Tudela (Spain). Eighteen patients with cholelithiasis and three with biliary sludge were detected. Predisposing factors for cholelithiasis were prematurity and parenteral nutrition (one patient), sepsis (two patients), obesity (one patient), and a family history of the disease (one patient). The disease was idiopathic in 11 patients. Gallstones were detected in two patients presenting with appendicular symptoms. One child with biliary sludge had received treatment with ceftriaxone as a predisposing factor. All patients were diagnosed by ultrasound. Plain abdominal X-ray detected lithiasis in 12 of the 15 patients (80 %) with cholelithiasis who underwent this procedure. The most frequent symptoms were abdominal pain (seven patients), abdominal pain and vomiting (five patients), and diarrhea (one patient). Two patients presented with appendicular symptoms. Fourteen patients underwent surgery (open cholecystectomy in two and laparoscopic cholecystectomy in 12). None of the patients required emergency surgery. Cholelithiasis in children is an unusual finding, but is not exceptional and is associated with nonspecific symptoms. Plain abdominal X-ray is useful in diagnosis but the main diagnostic technique is ultrasonography.
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PMID:[Childhood cholelithiasis in a district hospital]. 1758 24

Children with genetic syndromes frequently have feeding problems and swallowing dysfunction as a result of the complex interactions between anatomical, medical, physiological, and behavioral factors. Feeding problems associated with genetic disorders may also cause feeding to be unpleasant, negative, or even painful because of choking, coughing, gagging, fatigue, or emesis, resulting in the child to stop eating and to develop behaviors that make it difficult, if not impossible, for a parent to feed their child. In addition, limited experiences with oral intake related to the medical or physical conditions, or other variables such as prematurity, often result in a failure of the child's oral motor skills to develop normally. For example, a child with Pierre Robin sequence may be unable to successfully feed orally, initially, due to micrognathia and glossoptosis. Oral-motor dysfunction may develop as a result of both anatomical problems, (e.g., cleft lip/palate), lack of experience (e.g., s/p. surgery), or oral motor abnormalities (e.g., brain malformation). Neuromotor coordination impairments such as those associated with Down syndrome (e.g., hypotonia, poor tongue control, and open mouth posture) frequently interfere with the acquisition of effective oral-motor skills and lead to feeding difficulties. Management of these phenomena is frequently possible, if an appropriate feeding plan exist that allows for three primary factors: (1) feeding program must be safe, (2) feeding program must support optimal growth, and (3) feeding program must be realistic. Researchers have demonstrated the utility of behavioral approaches in the treatment of feeding disorders, such as manipulations in the presentation of foods and drink and consequences for food refusal and acceptance (e.g., praise, extinction, contingent access to preferred foods). However, because a child's failure to eat is not frequently the result of a single cause, evaluation and treatment are typically conducted by an interdisciplinary team usually consisting of a behavioral psychologist, pediatric gastroenterologist, speech pathologist, nutrition, and sometimes other disciplines. This chapter provides an overview of some of the feeding difficulties experience by some of the more common genetic disorders including identification, interventions, and management.
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PMID:Feeding and swallowing dysfunction in genetic syndromes. 1864 13

Defined by the association of hemolysis, hepatic dysfunction and thrombocytopenia, the Hemolysis, Elevated Liver enzyme, Low Platelets (HELLP) syndrome can complicate preeclampsia and worsen maternal and fetal prognosis. It can be diagnosed in the immediate postpartum (30%) or in the absence of preeclampsia (10-20%). Clinical diagnosis can be difficult because there is no specific symptom. Abdominal pain or vomiting during the third trimester must lead to think about this diagnosis. Biological criteria are well defined: hemolysis by the presence of schistocytes, increased serum total bilirubin >12 mg/L or LDH >600 IU/L, hepatic dysfunction by increased transaminases and thrombocytopenia by a platelet count <100,000/microL. The evolution of those parameters is a major prognostic factor. With the HELLP syndrome, maternal morbidity is dramatically increased compared to isolated preeclampsia with complications such as eclampsia, placental abruptio, disseminated intravascular coagulation, pulmonary edema, acute renal insufficiency, subcapsular liver hematoma. The management of a HELLP syndrome requests level 3 hospital with intensive care units for neonate and mother. The treatment of this syndrome requires termination of the pregnancy as soon a possible, either by cesarean section or by vaginal delivery if cervical conditions are optimal (without any maternal or fetal complications). Before 32 weeks, a more expectative attitude could be acceptable with the prematurity permitting corticotherapy for fetal pulmonary maturation. This corticotherapy can improve temporary biological parameters but there are no proven benefits to consider improvement for long term maternal or fetal prognosis. During the postpartum, evolution is usually spontaneously favorable. Recurrences are not frequent.
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PMID:[Management of the HELLP syndrome]. 1900 44

One hundred and fifty exchange transfusions, using citrated donor blood, were investigated to determine the mortality rate from the procedure. One infant died during manipulation of the catheter in the umbilical vein. Four infants died of combined causes including anemia, prematurity and elevated potassium in the donor blood. Sixty-two exchange transfusions were investigated in detail to determine the incidence of clinical disturbances. Vomiting, retching, respiratory distress, convulsions or tetany developed during 23 exchanges. A rapid rate of exchange, elevated potassium in the donor blood, and failure to administer calcium during the exchange were major factors contributing to these disturbances. Exchange transfusion with citrated blood can be safeguarded by (1) using donor blood less than five days old, (2) employing a rate of exchange of 2 ml./kg./min. and (3) injecting calcium gluconate during the exchange.
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PMID:Mortality and Morbidity of Exchange Transfusion. 2032 33

Temporary brittle bone disease has been described since 1990. It is a syndrome characterised by multiple unexplained fractures in early childhood. There is growing evidence that it has natural causes and does not represent inflicted trauma. We report the clinical and laboratory features of 104 patients investigated personally between 1985 and 2000. These patients had in aggregate 976 fractures or fracture-like lesions. Our patients included disproportionate numbers of infants born preterm or as a result of multiple pregnancy. The fractures were mainly identified in the first 6 months of life and entirely within the first year of life. Most fractures were asymptomatic, particularly the many rib fractures and metaphyseal lesions. Few patients had evidence of bruising at presentation; none had clinical evidence of inflicted injury commensurate with the fractures found. In 22 patients the fractures were found in the course of investigation for unrelated symptoms. In several cases fractures took place while the children were in hospital. Unexplained bruising and sub-conjunctival haemorrhages also occurred in hospital, suggesting collagen defects. Hernias were recorded; in most these resolved spontaneously, again suggesting transient collagen defects. Among the unexplained symptoms of the patients was a history of vomiting, often projectile vomiting. Some patients had unusually blue or grey sclerae for the child's age. Many patients had abnormally large anterior fontanelles. Laboratory findings included anaemia, neutropenia and an exceptionally high serum alkaline phosphatase. Our findings reinforce the view that children with temporary brittle bone disease have a distinctive and identifiable syndrome which probably includes osteopathy of prematurity. These patients do not have osteogenesis imperfecta and are not the victims of non-accidental injury. While the causes of this syndrome remain uncertain, its distinctive features should now be more readily recognised.
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PMID:Clinical and laboratory features of temporary brittle bone disease. 2395 May 68

Term infants with hypertrophic pyloric stenosis (HPS) typically present between 4 and 6 weeks. There is limited consensus, however, regarding age of presentation of premature infants. We aim to determine if there is an association between the degree of prematurity and chronological age of presentation of HPS. A total of 2988 infants who had undergone a pyloromyotomy for HPS were identified from the 2012 and 2013 NSQIP-P Participant Use Files. Two hundred seventeen infants (7.3%) were born prematurely. A greater degree of prematurity was associated with an older chronological age of presentation ( P < .0001). Prematurity was significantly associated with an increase in overall postoperative morbidity, reintubation, readmission, and postoperative length of stay. When clinicians evaluate an infant with nonbilious emesis with a history of prematurity, they should consider pyloric stenosis if the calculated postconceptional age is between 44 and 50 weeks. When counseling families of premature infants, surgeons should discuss the increased incidence of postpyloromyotomy morbidity.
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PMID:Prematurity Affects Age of Presentation of Pyloric Stenosis. 2714 87

Bilious vomiting is synonymous with intestinal obstruction, be it functional or anatomical. In the neonate it may be due to congenital malformations of the gastrointestinal tract or develop due to acquired conditions, particularly intestinal complications associated with prematurity. This review considers the congenital malformations that may present with bilious vomiting and explores the diagnostic dilemmas faced in the preterm infant. The difficult issue of the need to exclude malrotation in term infants with bilious vomiting and the consequences of time-critical transfer is discussed.
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PMID:The management of bilious vomiting in the neonate. 2763 37

Antenatal Bartter syndrome is a rare condition that can present with different clinical features. These features include early onset maternal polyhydramnios, failure to thrive, prematurity and nephrocalcinosis.We are presenting this 20-day-old girl who had an antenatal history of polyhydramnios. She developed persistent non-bilious vomiting that was associated with constipation soon after birth. She presented with failure to thrive and features suggestive of intestinal obstruction. On the initial evaluation, she was noted to have hypokalaemic, hyponatraemic metabolic alkalosis. The initial work-up was done to exclude surgical and renal causes of her presentation, and the diagnosis was confirmed by gene analysis to be type III-classic Bartter syndrome. She was closely monitored for her growth and development with the appropriate salt replacement therapy.
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PMID:Antenatal Bartter syndrome presenting with vomiting and constipation mimicking subacute intestinal obstruction in a 20-day-old neonate. 2914 24


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