Thursday, April 16, 2009

Gastro-esophageal Reflux Disease (GERD) In Newborns

Gastro-esophageal Reflux Disease, more popularly abbreviated as GERD, can be described as the ailment in which the gas or liquid in the stomach of the baby goes up the esophagus. The result is that that baby 'spits up'. It is not unusual for babies to suffer from the problem, mainly because their muscles, which are involved in opening and closing the top of the stomach, are quite relaxed. If, and when, they get relaxed after the consumption of food, the gas and fluid manage to escape from the stomach and go up the esophagus. While having reflux is common, it is only when it becomes severe that it takes the shape of Gastro-esophageal Reflux Disease, making the baby spit up too much, not get enough nourishment from food and even suffer from breathing problems.

Need For TreatmentIt is common for newborn babies and infants to suffer from Gastroesophageal Reflux Disease (GERD). However, it is only in the following conditions that you need to visit a doctor.



  • Baby is spitting up often


  • Baby has apnea (breathing stops for 15-20 seconds at a time)


  • Baby is growing poorly


  • Baby gets pneumonia or breathing difficulties from aspirating spit-up liquid


  • Causes Of Gastroesophageal Reflux One of the main reasons of Gastro-esophageal Reflux

Disease in children comprises of a poorly coordinated gastrointestinal tract. The immature digestive system results in unnecessary opening of the stomach, after eating food, as a result of which gas and fluid manage to escape to the esophagus. This leads to reflex in children. It has been seen that majority of the infants grow out of GERD by the time they are one year old.


Symptoms of Gastroesophageal Reflux




  • Frequent vomiting


  • Persistent cough


  • Refusing to eat or difficulty in eating


  • Choking or gagging while feeding


  • Heartburn


  • Gas


  • Abdominal pain


  • Colic


  • Colicky behavior (frequent crying and fussiness)


  • Regurgitation


  • Re-swallowing


  • Poor growth


  • Breathing problems


  • Recurrent pneumonia

Cure For Gastroesophageal Reflux


For Babies:




  • Try to keep the head of the baby's crib or bassinet elevated, as much as you can.


  • Every time you feed baby, hold him/her upright for the next 30 minutes


  • You can make the bottle feeds a bit thicker by adding some cereal. However, it is advisable to consult a doctor before doing this.


  • Try to bring some changes in the feeding schedule of the baby.


  • You can try giving some solid food to the baby, though with the doctor's approval.

For Older Children




  • Try to keep the head of your child's bed elevated, as much as you can


  • Instead of giving your baby three large meals in a day, give him/her several small meals spaced at small, but regular intervals.


  • Keep a track of the foods and beverages worsen your child's reflux and limit their consumption.


  • Encourage your child to indulge in exercise, on a regular basis.


  • For at least two hours after your child takes a meal, make sure to keep him/her upright.

Anemia in newborns


Anemia is a disorder in which there are too few red blood cells in the blood.
Normally, the newborn's bone marrow does not produce new red blood cells between birth and 3 or 4 weeks of age. Anemia can occur when red blood cells are broken down too rapidly, too much blood is lost, or more than one of these processes occurs at the same time.
Any process that leads to red blood cell destruction, if sufficiently severe, results in anemia and high levels of bilirubin (hyperbilirubinemia). Hemolytic disease of the newborn may cause the newborn's red blood cells to be destroyed rapidly. The red blood cells may also be rapidly destroyed if the newborn has a hereditary abnormality of the red blood cells. An example is hereditary spherocytosis, in which the red blood cells appear small and spherical in shape when viewed under a microscope.
Infections acquired before birth, such as toxoplasmosis, rubella, cytomegalovirus, herpes simplex, or syphilis, may also rapidly destroy red blood cells, as can bacterial infections of the newborn acquired during or following birth.
Another cause of anemia is blood loss. Blood loss can occur in many ways, for example, if there is a large transfusion of the fetal blood across the placenta and into the mother's circulation (fetal-maternal transfusion) or if too much blood gets trapped in the placenta at delivery, when the umbilical cord is clamped. The placenta may separate from the uterine wall before delivery (placental abruption), leading to hemorrhage of the fetal blood. Rarely, anemia may result from a failure of the fetal bone marrow to produce red blood cells. One example of this is a genetic disorder called Fanconi's anemia. Another rare example is that due to exposure of the mother and fetus to certain drugs used during pregnancy.
Symptoms and Treatment
A newborn who has suddenly lost a large amount of blood during labor or delivery may appear pale and have a rapid heart rate and low blood pressure, along with rapid, shallow breathing. Milder anemia may result in lethargy, poor feeding, or no symptoms. When the anemia is a result of rapid breakdown of red blood cells, there is also increased production of bilirubin, and the newborn's skin and the whites of the eyes appear yellow (jaundice).
A newborn who has rapidly lost a large amount of blood, often during labor and delivery, is treated with intravenous fluids followed by a blood transfusion. Very severe anemia caused by hemolytic disease may also require a blood transfusion, but the anemia is more often treated with an exchange blood transfusion, in which part of the newborn's blood is gradually removed and replaced with equal volumes of fresh donor blood. The exchange transfusion also removes bilirubin in the circulation and thus treats the hyperbilirubinemia.

'Silent' Chagas disease killing newborns


BUENOS AIRES] For every newborn detected with Chagas disease in Argentina, another six to twelve cases are not even diagnosed, with potentially fatal consequences, according to researchers there. Chagas disease — caused by the parasite Trypanosoma cruzi — affects around 17 million people worldwide. Transmission of the disease is generally associated with a blood-sucking insect known as the ‘assassin bug’, which lives in cracks and crevices of poor-quality houses, particularly in rural areas.But while the number of vector-transmitted infections is now under control in Argentina — for example through insecticide spraying, housing improvement and education — 'vertical' (i.e. mother-to-child) transmission is becoming an even greater threat, according to a study published last month in the journal Emerging Infectious Diseases. "The congenital transmission of [Chagas] appears to be a sizeable public health problem in Argentina, where it has already surpassed the number of vector-mediated acute cases by a factor of ten," say the study's authors. Cases of newborns with Chagas disease can remain undetected because the infection has a period in which no symptoms are present. “A lot of pregnant women cannot access prenatal diagnosis because they live in rural areas, or the maternity hospitals do not have the facilities to diagnose Chagas disease,” explains lead author Ricardo Gürtler, a researcher at the University of Buenos Aires.And although vertical transmission is not preventable, early detection and treatment of congenital infection can achieve cure rates close to 100 per cent. The authors call for improved diagnosis of pregnant women, treatment of infected newborns, and greater awareness of the problem among medical practitioners.

Abnormal brain development in newborns with congenital heart disease

Department of Neurology, University of California at San Francisco, San Francisco, USA. smiller6@cw.bc.ca
BACKGROUND: Congenital heart disease in newborns is associated with global impairment in development. We characterized brain metabolism and microstructure, as measures of brain maturation, in newborns with congenital heart disease before they underwent heart surgery. METHODS: We studied 41 term newborns with congenital heart disease--29 who had transposition of the great arteries and 12 who had single-ventricle physiology--with the use of magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) before cardiac surgery. We calculated the ratio of N-acetylaspartate to choline (which increases with brain maturation), the ratio of lactate to choline (which decreases with maturation), average diffusivity (which decreases with maturation), and fractional anisotropy of white-matter tracts (which increases with maturation). We compared these findings with those in 16 control newborns of a similar gestational age. RESULTS: As compared with control newborns, those with congenital heart disease had a decrease of 10% in the ratio of N-acetylaspartate to choline (P=0.003), an increase of 28% in the ratio of lactate to choline (P=0.08), an increase of 4% in average diffusivity (P<0.001), and a decrease of 12% in white-matter fractional anisotropy (P<0.001). Preoperative brain injury, as seen on MRI, was not significantly associated with findings on MRS or DTI. White-matter injury was observed in 13 newborns with congenital heart disease (32%) and in no control newborns. CONCLUSIONS: Term newborns with congenital heart disease have widespread brain abnormalities before they undergo cardiac surgery. The imaging findings in such newborns are similar to those in premature newborns and may reflect abnormal brain development in utero. Copyright 2007 Massachusetts Medical Society. PMID: 17989385 [PubMed - indexed for MEDLINE]BACKGROUND: Congenital heart disease in newborns is associated with global impairment in development. We characterized brain metabolism and microstructure, as measures of brain maturation, in newborns with congenital heart disease before they underwent heart surgery. METHODS: We studied 41 term newborns with congenital heart disease--29 who had transposition of the great arteries and 12 who had single-ventricle physiology--with the use of magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) before cardiac surgery. We calculated the ratio of N-acetylaspartate to choline (which increases with brain maturation), the ratio of lactate to choline (which decreases with maturation), average diffusivity (which decreases with maturation), and fractional anisotropy of white-matter tracts (which increases with maturation). We compared these findings with those in 16 control newborns of a similar gestational age. RESULTS: As compared with control newborns, those with congenital heart disease had a decrease of 10% in the ratio of N-acetylaspartate to choline (P=0.003), an increase of 28% in the ratio of lactate to choline (P=0.08), an increase of 4% in average diffusivity (P<0.001), and a decrease of 12% in white-matter fractional anisotropy (P<0.001). Preoperative brain injury, as seen on MRI, was not significantly associated with findings on MRS or DTI. White-matter injury was observed in 13 newborns with congenital heart disease (32%) and in no control newborns. CONCLUSIONS: Term newborns with congenital heart disease have widespread brain abnormalities before they undergo cardiac surgery. The imaging findings in such newborns are similar to those in premature newborns and may reflect abnormal brain development in utero. Copyright 2007 Massachusetts Medical Society. PMID: 17989385 [PubMed - indexed for MEDLINE]
BACKGROUND: Congenital heart disease in newborns is associated with global impairment in development. We characterized brain metabolism and microstructure, as measures of brain maturation, in newborns with congenital heart disease before they underwent heart surgery. METHODS: We studied 41 term newborns with congenital heart disease--29 who had transposition of the great arteries and 12 who had single-ventricle physiology--with the use of magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) before cardiac surgery. We calculated the ratio of N-acetylaspartate to choline (which increases with brain maturation), the ratio of lactate to choline (which decreases with maturation), average diffusivity (which decreases with maturation), and fractional anisotropy of white-matter tracts (which increases with maturation). We compared these findings with those in 16 control newborns of a similar gestational age. RESULTS: As compared with control newborns, those with congenital heart disease had a decrease of 10% in the ratio of N-acetylaspartate to choline (P=0.003), an increase of 28% in the ratio of lactate to choline (P=0.08), an increase of 4% in average diffusivity (P<0.001),>