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.

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  Baby is spitting up often


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


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  Baby is growing poorly


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


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  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

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  Frequent vomiting


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  Persistent cough


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  Refusing to eat or difficulty in eating


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  Choking or gagging while feeding


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  Heartburn


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  Gas


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  Abdominal pain


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  Colic


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  Colicky behavior (frequent crying and fussiness)


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  Regurgitation


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  Re-swallowing


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  Poor growth


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  Breathing problems


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  Recurrent pneumonia

Cure For Gastroesophageal Reflux

For Babies:

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


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


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


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


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

For Older Children

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


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


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


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


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  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),>

Urine Blockage in Newborns

The urinary tract consists of:
two kidneys, which filter waste materials and excess water from the blood
two ureters, which carry urine from the kidneys to the bladder
the bladder, where urine is stored until it is released
the urethra, where urine flows out of the body
We rely on our kidneys and urinary system to keep fluids and natural chemicals in our bodies balanced. While a baby is developing in the mother’s womb, much of that balancing is handled by the mother’s placenta. The baby’s kidneys begin to produce urine at about 10 to 12 weeks after conception, but the mother’s placenta continues to do most of the work until the last few weeks of the pregnancy. Wastes and excess fluid are removed from the baby’s body through the umbilical cord. The baby’s urine is released into the amniotic sac and becomes part of the amniotic fluid. This fluid plays a role in the baby’s lung development.
Sometimes, a birth defect in the urinary tract will block the flow of urine in an unborn baby. As a result, urine backs up and causes the ureters and kidneys to swell. Swelling in the kidneys is called hydronephrosis. Swelling in the ureters is called hydroureter.

Normal urinary tract.
Swelling in the kidney is called hydronephrosis. Swelling in the ureter is called hydroureter.
Hydronephrosis is the most common problem found during ultrasound examination of babies in the womb. The swelling may be barely detectable or very noticeable. The results of hydronephrosis may be mild or severe, but the long-term outcome for the child’s health cannot always be judged by the severity of swelling. Urine blockage may damage the developing kidneys and reduce their ability to filter. The blockage may also raise the risk that the child will develop a urinary tract infection (UTI). Recurring UTIs can lead to more permanent kidney damage. In the most severe cases of urine blockage, the amniotic sac is so reduced that the lack of fluid threatens the baby’s lung development.

Types of Defects in the Urinary Tract:
Hydronephrosis can result from many types of defects in the urinary tract. Doctors use specific terms to describe the type and location of the blockage.

· Vesicoureteral reflux (VUR). The openings where the ureters empty urine into the bladder should work like valves to keep urine from backing up into the ureters. Sometimes the valve doesn’t work properly and urine flows back into the kidneys. The urine may flow only a short way back into the ureters, or it may go all the way back to the kidneys, causing the ureters and kidneys to swell. VUR may occur in only one ureter or in both. Kidneys with severe reflux may not develop normally, and after birth kidneys with reflux may be at risk for damage from infections.
· Ureteropelvic junction (UPJ) obstruction. The point where the ureter joins the kidney is called the ureteropelvic junction. If urine is blocked here, only the kidney swells. The ureter remains at a normal size. UPJ obstruction usually only occurs in one kidney.
· Bladder outlet obstruction (BOO). BOO describes any blockage in the urethra or at the opening of the bladder. The obstruction may occur in boys or girls. The most common form of BOO seen in newborns and during prenatal ultrasound examinations is posterior urethral valves (PUV). BOO caused by PUV occurs only in boys.

· Posterior urethral valves (PUV). In boys, sometimes an abnormal fold of tissue in the urethra keeps urine from flowing freely out of the bladder. This defect may cause swelling in the entire urinary tract, including the urethra, bladder, ureters, and kidneys.

· Ureterocele. If the end of the ureter does not develop normally, it can bulge, creating what is called a ureterocele. The ureterocele may obstruct part of the kidney or the bladder.
Ureterocele. The inset shows a cross-section of the ureter bulging into the interior of the bladder.

· Nerve dsease. Urination requires coordinated nerve signals between the bladder, spinal cord, and brain. Spina bifida and other birth defects that affect the spinal cord may interrupt nerve signals and lead to urine retention in newborns.
Ureteropelvic junction (UPJ) is the point where the ureter joins the kidney.

Syndromes That May Affect the Urinary Tract:
In addition to defects that occur in a single spot in the urinary tract, some babies are born with genetic conditions that affect several different systems in the body. A condition that includes multiple, seemingly unrelated problems, is called a syndrome.
Prune belly syndrome (PBS). Occurring only in boys, PBS causes a baby to have an enlarged abdomen because the normal abdominal wall muscles are missing or very weak. The entire urinary tract is enlarged, and both testicles remain inside the body instead of descending into the scrotum. The skin over the abdomen is wrinkled, giving the appearance of a prune. Most children with PBS have hydronephrosis and VUR.

Esophageal atresia (EA). EA is a birth defect in which the esophagus is incomplete. The esophagus is the tube that carries food from the mouth to the stomach. About 30 percent of babies born with EA will have problems in other body systems, such as the heart or urinary tract.
Congenital heart defects. Heart defects range from mild to life threatening. Children born with heart defects also have a higher rate of problems in the urinary tract than children in the general population, suggesting that some types of heart and urinary defects may have a common genetic cause.

Diagnosis:
Birth defects and other problems of the urinary tract may be discovered before the baby is born, at the time of birth, or later, when the child is brought to the doctor for a urinary tract infection or urination problem.
Prenatal Screening
Tests during pregnancy can help determine if the baby is developing normally in the womb.
Ultrasound. Ultrasound uses sound waves to produce a picture on a television screen. A wand gliding on the mother’s abdomen directs harmless sound waves into the womb. The sound waves bounce off the baby and back into the wand to create a black-and-white image on the screen. Ultrasound images can even display internal organs within the baby, so enlarged kidneys, ureters, or bladder may be visible.
Amniocentesis. In amniocentesis, the doctor inserts a needle through the mother’s skin into the amniotic sac to collect about an ounce of amniotic fluid. The fluid contains genetic material from the baby that can be analyzed for signs of defects.

Ultrasound allows evaluation of a baby’s internal organs, even before birth.

Chorionic villus sampling (CVS). In CVS, the doctor collects a small piece of tissue from the placenta using a needle passed through the mother’s vagina and cervix. The placenta has the same genetic makeup as the baby.Most healthy women do not need all the tests. Ultrasound examinations during pregnancy are routine, although they are not always required and rarely influence treatment decisions. Amniocentesis and CVS are recommended only when a risk of genetic problems exists because of family history or something detected during an ultrasound. Amniocentesis and CVS carry a slight risk of harming the baby and mother, or ending the pregnancy in miscarriage, so those risks should be weighed carefully against the potential benefits of learning about the baby’s condition.

Examination of Newborn:
Sometimes a newborn does not urinate as expected, even though prenatal testing showed no sign of urine blockage. The baby may urinate only small amounts or not at all. An enlarged kidney may be felt during the newborn examination as well. Different imaging techniques are available to determine the cause of the problem.

Ultrasound. Once the baby is born, ultrasound can be used to view the baby’s urinary tract directly for a clearer image than could be achieved while the baby was in the womb.
Voiding cystourethrogram (VCUG). If the doctor suspects that urine is backing up into the ureters or that the bladder outlet is obstructed, a VCUG may be needed. In this test, a catheter is used to fill the child’s bladder with warm liquid containing iodine to make it visible on an x ray. A video records the x-ray images of the bladder as it is filled and as the child urinates. The video will reveal reflux if the liquid enters the ureters and blockage of the bladder in the case of an obstruction, such as PUV.

Nuclear scan. A nuclear scan involves injecting a very small amount of radioactive material, just enough to show up using a camera that captures gamma rays. The amount of radioactive substance used is determined by the child’s weight. The liquid is injected into the child’s bloodstream and eventually passes through the kidneys, where it is filtered from the blood and directed down the ureters to the bladder. The camera may be mounted above or below a table where the patient lies. The camera passes over or under the urinary tract as the child lies on the table.

Later Diagnosis
Sometimes urine blockage is not apparent until the child develops the symptoms of a urinary tract infection. These symptoms include
fever
irritability
poor appetite
vomiting
unusual smelling urine
dark urine
If these symptoms persist, the child should be seen by a doctor. For any fever in the first 2 months of life, the child should be seen by a doctor immediately. The doctor will ask for a urine sample to test for bacteria. The doctor may also recommend imaging tests including ultrasound, VCUG, or nuclear scan.

Treatment:
Treatment for urine blockage depends on the cause and severity of the blockage. Hydronephrosis discovered before the baby is born will rarely require immediate action, especially if it is only on one side. Often the condition goes away without any treatment before birth or sometimes after. The doctor will keep track of the condition with frequent ultrasounds. With few exceptions, treatment can wait until the baby is born.

Prenatal Shunt
If the urine blockage threatens the life of the unborn baby, the doctor may recommend a procedure to insert a small tube, called a shunt, into the baby’s bladder to release urine into the amniotic sac. The placement of the shunt is similar to an amniocentesis, in that a needle is inserted through the mother’s abdomen. Ultrasound guides the placing of the shunt. This fetal surgery carries many risks, so it is performed only in special circumstances, such as when the amniotic fluid is absent and the baby’s lungs aren’t developing or when the kidneys are very severely damaged.

Antibiotics
Antibiotics are medicines that kill bacteria. A newborn with possible urine blockage or VUR may be given antibiotics to prevent urinary tract infections from developing until the urinary defect corrects itself or is surgically corrected.

Surgery
If the urinary defect doesn’t correct itself and the child continues to have urine blockage, surgery may be needed. The decision to operate depends upon the degree of blockage. The surgeon will remove the obstruction to restore urine flow. A small tube, called a stent, may be placed in the ureter or urethra to keep it open temporarily while healing occurs.
Intermittent Catheterization
If the child has urine retention because of nerve disease, the condition may be treated with intermittent catheterization. The parent, and later the child, will be taught to drain the bladder by inserting a thin tube, called a catheter, through the urethra to the bladder. Emptying the bladder in this way helps prevent kidney damage, overflow incontinence, and urinary tract infections.

Hope through Research
Researchers from universities and government agencies are working to understand the causes of urinary birth defects and to find more effective treatments. Through its Pediatric Urology Program, the National Institute of Diabetes and Digestive and Kidney Diseases funds research into bladder and urinary tract development, prenatal interventions for urinary tract disorders, and bladder abnormalities associated with spina bifida. Additionally, the Eunice Kennedy Shriver National Institute of Child Health and Human Development has established the Birth Defects Initiative to study the genetic and molecular mechanisms underlying developmental processes of the fetus.

Vitamin K and hemorrhagic disease of newborns.

First described by Charles Townsend in 1894, (1) hemorrhagic disease of newborns (HDN HDN Hemolytic disease of the newborn, see there ) is undoubtedly linked to vitamin K deficiencyVitamin K Deficiency Definition
Vitamin K deficiency exists when chronic failure to eat sufficient amounts of vitamin K results in a tendency for spontaneous bleeding or in prolonged and excessive bleeding with trauma or injury. ..... and can cause bleeding in infants in the first few weeks of life. It is one of the causes of acquired hemostatic hemostatic /he·mo·stat·ic/ (he?mo-stat´ik)1. causing hemostasis, or an agent that so acts.
2. due to or characterized by stasis of the blood.
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he·mo·stat·icadj. disorder in early infancy. Vitamin K is a cofactor cofactor
An atom, organic molecule, or molecular group that is necessary for the catalytic activity (see catalysis) of many enzymes. A cofactor may be tightly bound to the protein portion of an enzyme and thus be an integral part of its functional structure, or it may for the hepatic carboxylationcarboxylation /car·box·y·la·tion/ (kahr-bok?si-la´shun) the addition of carbon dioxide or bicarbonate to form a carboxyl group, as to pyruvate to form oxaloacetate. --------------------------------------------------------------------------------
car·box·yl·a·tionn. ..... . of glutamic acid residues in a number of proteins, including the procoagulantprocoagulant /pro·co·ag·u·lant/ (-ko-ag´ul-int)1. tending to promote coagulation.
2. a precursor of a natural substance necessary to coagulation of the blood. factors II, VII, IX and X.

Vitamin K is transmitted poorly across the placental barrier, and at birth, vitamin K levels are often below the detection limit of 0.02 ng/mL. The clotting system of the newborn is essentially intact except for a deficiency in vitamin K dependent clotting factors. Failure to provide vitamin K at birth poses a risk for the development of hemorrhagic HemorrhagicA condition resulting in massive, difficult-to-control bleeding.
Mentioned in: Hantavirus Infections
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hemorrhagic
pertaining to or characterized by hemorrhage. disease in the neonatal period. HDN is exceedingly rare in the United States because of the routine administration of prophylactic vitamin K shortly after birth.
HDN is classically defined as early or late, depending on the time of onset related to birth. The classic form of HDN usually presents on days 2 to 7 of life in healthy, breastfed, full-term infants. The common bleeding sites are gastrointestinal, cutaneous cutaneous /cu·ta·ne·ous/ (ku-ta´ne-us) pertaining to the skin. --------------------------------------------------------------------------------
cu·ta·ne·ousadj.Of, relating to, or affecting the skin.
--------------------------------------------------------------------------------CutaneousPertaining to the skin. , nasal and from the site of circumcision. Late HDN presents between weeks 2 and 12 of life, and is related to conditions that interfere with the vitamin K supply. It may present with intracranial hemorrhage. This form of vitamin K deficiency is mainly due to inadequate vitamin K intake in exclusively breastfed infants. Late hemorrhagic disease of the newbornhemorrhagic disease of the newborn A neonatal condition caused by vitamin K deficiency, the combined result of a lack of unbound maternal vitamin K, immaturity of the fetal liver and lack of vitamin K-producing bacteria in the infant colon Clinical Abrupt early . rarely occurs in formula-fed infants because of formula supplementation with vitamin K (approximately 4-100 [micro]g/L).

HDN is still an important cause of mortality and morbidity in developing countries where vitamin K prophylaxis is not routinely practiced. Studies from these countries showed a higher incidence of late onset vitamin K deficiency bleeding.
(2) Since hemorrhagic disease of the newborn can lead to significant morbidity and mortalityMorbidity and Mortality can refer to: Morbidity & Mortality, a term used in medicine Morbidity and Mortality Weekly Report, a medical publication See also
Morbidity, a medical term Mortality, a medical term
., it should be prevented by providing vitamin K prophylaxis to all newborns.
Does vitamin K prophylaxis prevent HDN? The answer is yes, and the data in this country support the efficacy of neonatal vitamin K prophylaxis for the prevention of HDN. The American Academy of PediatricsThe American Academy of Pediatrics ("AAP") is an organization of pediatricians, physicians trained to deal with the medical care of infants, children, and adolescents. Its motto is: "Dedicated to the Health of All Children.recommends vitamin [K.sub.1] prophylaxis to all newborns as a single, IM dose of 0.5 to 1 mg.
(3) A single IM injection of vitamin K, designed to prevent early vitamin K deficiency bleeding, may protect against late deficiency bleeding,
(4) but this has not been tested in randomizedran·dom·ize tr.v. ran·dom·ized, ran·dom·iz·ing, ran·dom·iz·esTo make random in arrangement, especially in order to control the variables in an experiment.trials with respect to its effect on late HDN.
(5) However, one study showed a significant decline in the incidence of the late form of vitamin K deficiency bleeding.
(6) In this issue of the Southern Medical Journal, a review of two infants with intracranial hemorrhage due to hemorrhagic disease of the newborn is presented. Both were secondary to failure of vitamin K administration at birth. The infants in this report were born at home, did not receive vitamin K prophylaxis and developed intracranial hemorrhage at five weeks of age. The author concluded that late onset hemorrhagic disease of the newborn might occur when prophylactic vitamin K is not administered at birth and can have serious and even devastating consequences. This article emphasizes the association between failure of administration of vitamin K and risk of development of hemorrhagic disease of the newborn. In conclusion, HDN, although uncommon, does still occur and has the potential for severe consequences. Therefore, vitamin K prophylaxis at birth is a priority and should be provided to all newborns to prevent HDN and its associated complications, including intracranial hemorrhage.