Information
This is information I found online. I double and sometimes triple checked facts before posting them to make sure they are as up to date and realistic as I personally can find out for everyone.
Prematurity
10% of all babies are born prematurely each year in the USA. In Every 10 minutes 250 babies are born premature.
Preterm birth (commonly referred to as "prematurity") is the most important single cause of death in children under 1 year of age worldwide. A preterm birth is one that occurs before the 37th week of pregnancy. Every year more than 400,000 families are left grief-stricken across America as a result of this deadly medical occurrence. Sadly, one out of every ten women will experience a preterm birth. Many of those precious babies will not survive. Furthermore, some of the families whose babies do survive are left coping with life-long disabilities including:
The exact cause of preterm birth as well as premature rupture of fetal membranes (PROM) has yet to be positively identified and treated. Extensive studies over the last two decades indicate that contributing factors in preterm births include (but are not limited to):
In 2001, the preterm birth rate was 11.9%, reflecting more than 476,000 newborns and the highest rate ever reported for the U.S. This represents 1 in 8 babies in the U.S. born prematurely.
The rate of preterm birth increased 27% between 1981 and 2001 from 9.4% to 11.9%.
On an average day in the U.S., 1,305 babies are born preterm (before 37 weeks), 213 are born very preterm (before 32 weeks).
Women with periodontal disease are at three to five times greater risk of preterm birth than those who are periodontally healthy.
Among racial/ethnic subgroups, preterm birth rates were highest among infants born to black mothers (17.5%) in 2001.
Major risk factors associated with increasing rates of preterm delivery include multiple births, advanced maternal age, induced deliveries and additional factors as yet unknown.
Preterm labor/delivery is the number one obstetrical challenge in the U.S.
In 2000 prematurity/low birthweight was the leading cause of neonatal mortality in the U.S., accounting for 23% of deaths in the first month of life.
Preterm birth is a leading challenge in pediatrics, accounting for substantial long-term disabilities such as mental retardation, cerebral palsy, vision and hearing problems, and chronic lung disease.
Causes of nearly half of all preterm births are unknown.
Preterm labor can happen to any pregnant woman.
Preterm birth (commonly referred to as "prematurity") is the most important single cause of death in children under 1 year of age worldwide. A preterm birth is one that occurs before the 37th week of pregnancy. Every year more than 400,000 families are left grief-stricken across America as a result of this deadly medical occurrence. Sadly, one out of every ten women will experience a preterm birth. Many of those precious babies will not survive. Furthermore, some of the families whose babies do survive are left coping with life-long disabilities including:
- Mental retardation
- Increased risk of blindness and respiratory problems
- Physical impairments such as cerebral palsy
The exact cause of preterm birth as well as premature rupture of fetal membranes (PROM) has yet to be positively identified and treated. Extensive studies over the last two decades indicate that contributing factors in preterm births include (but are not limited to):
- Maternal infection in the uterus (known as chorioamnionitis), urinary tract infections
- Twin gestations, placental abruptions, fetal anomalies, placental previa
- Overwhelming Inflammatory Response.
In 2001, the preterm birth rate was 11.9%, reflecting more than 476,000 newborns and the highest rate ever reported for the U.S. This represents 1 in 8 babies in the U.S. born prematurely.
The rate of preterm birth increased 27% between 1981 and 2001 from 9.4% to 11.9%.
On an average day in the U.S., 1,305 babies are born preterm (before 37 weeks), 213 are born very preterm (before 32 weeks).
Women with periodontal disease are at three to five times greater risk of preterm birth than those who are periodontally healthy.
Among racial/ethnic subgroups, preterm birth rates were highest among infants born to black mothers (17.5%) in 2001.
Major risk factors associated with increasing rates of preterm delivery include multiple births, advanced maternal age, induced deliveries and additional factors as yet unknown.
Preterm labor/delivery is the number one obstetrical challenge in the U.S.
In 2000 prematurity/low birthweight was the leading cause of neonatal mortality in the U.S., accounting for 23% of deaths in the first month of life.
Preterm birth is a leading challenge in pediatrics, accounting for substantial long-term disabilities such as mental retardation, cerebral palsy, vision and hearing problems, and chronic lung disease.
Causes of nearly half of all preterm births are unknown.
Preterm labor can happen to any pregnant woman.
Congenital Heart Defects
About 35,000 infants (1 out of every 125) are born with heart defects each year in the United States. The defect may be so slight that the baby appears healthy for many years after birth, or so severe that his life is in immediate danger.
Heart defects are among the most common birth defects and are the leading cause of birth defect-related deaths. However, advances in diagnosis and surgical treatment have led to dramatic increases in survival for children with serious heart defects. In the United States, about 1.4 million children and adults live with congenital heart defects today. Almost all are able to lead active, productive lives.
A congenital heart defect is an abnormality in any part of the heart that is present at birth. Heart defects originate in the early weeks of pregnancy when the heart is forming.
Some babies and children with heart defects experience no symptoms. The heart defect may be diagnosed if the health care provider hears an abnormal sound, called a murmur. Children with normal hearts also can have heart murmurs, called innocent or functional murmurs. A provider may suggest tests to rule out a heart defect.
What are some of the most common heart defects, and how are they treated?
Patent ductus arteriosus (PDA): Before birth, a large artery (ductus arteriosus) lets the blood bypass the lungs because the fetus gets its oxygen through the placenta. The ductus normally closes soon after birth so that blood can travel to the lungs and pick up oxygen. If it doesn’t close, the baby may develop heart failure. This problem occurs most frequently in premature babies. Treatment with medicine during the early days of life often can close the ductus. If that doesn't work, surgery is needed. Septal defect: This is a hole in the wall (septum) that divides the right and left sides of the heart. A hole in the wall between the heart’s two upper chambers is called an atrial septal defect, while a hole between the lower chambers is called a ventricular septal defect. These defects can cause the blood to circulate improperly, so the heart has to work harder. Some atrial septal defects can be repaired without surgery by inserting a thin, flexible tube into the heart and then releasing a device that plugs the hole. A surgeon also can close an atrial or ventricular septal defect by sewing or patching the hole. Small holes may heal by themselves or not need repair at all. Coarctation of the aorta: Part of the aorta, the large artery that sends blood from the heart to the rest of the body, may be too narrow for the blood to flow evenly. A surgeon can cut away the narrow part and sew the open ends together, replace the constricted section with man-made material, or patch it with part of a blood vessel taken from elsewhere in the body. Sometimes, this narrowed area can be widened by inflating a balloon on the tip of a catheter (tube) inserted through an artery. Heart valve abnormalities: Some babies are born with heart valves that do not close normally or are narrowed or blocked, so blood can’t flow smoothly. Surgeons usually can repair the valves or replace them with man-made ones. Balloons on catheters also are frequently used to fix faulty valves. Tetralogy of Fallot: This combination of four heart defects keeps some blood from getting to the lungs. As a result, the blood that is pumped to the body may not have enough oxygen. Affected babies have episodes of cyanosis and may grow poorly. This defect is usually surgically repaired in the early months of life. Transposition of the great arteries: Transposition occurs when the positions of the two major arteries leaving the heart are reversed, so that each arises from the wrong pumping chamber. Affected newborns suffer from severe cyanosis due to a lack of oxygen in the blood. Recent surgical advances make it possible to correct this serious defect in the newborn period. Hypoplastic left heart syndrome: This combination of defects results in a left ventricle (the heart’s main pumping chamber) that is too small to support life. Without treatment, this defect is usually fatal in the first few weeks of life. However, over the last 25 years, survival rates have dramatically improved with new surgical procedures and, less frequently, heart transplants.
Heart defects are among the most common birth defects and are the leading cause of birth defect-related deaths. However, advances in diagnosis and surgical treatment have led to dramatic increases in survival for children with serious heart defects. In the United States, about 1.4 million children and adults live with congenital heart defects today. Almost all are able to lead active, productive lives.
A congenital heart defect is an abnormality in any part of the heart that is present at birth. Heart defects originate in the early weeks of pregnancy when the heart is forming.
Some babies and children with heart defects experience no symptoms. The heart defect may be diagnosed if the health care provider hears an abnormal sound, called a murmur. Children with normal hearts also can have heart murmurs, called innocent or functional murmurs. A provider may suggest tests to rule out a heart defect.
What are some of the most common heart defects, and how are they treated?
Congenital Diaphragmatic Hernia (CDH)
Congenital diaphragmatic hernia (CDH) is the absence of the diaphragm, or a hole in the diaphragm. This can occur on either the left or right side, but is most common on the left.
The contents of the abdomen, including the stomach, intestines, liver and spleen, may go through the hole and into the chest. The contents prevent the normal development of the lung (pulmonary hypoplasia) on that side, and may affect the growth of the other lung. After birth the infant will have difficulty breathing if the lungs are not developed enough.
There are two types of diaphragmatic hernia:
- Bochdalek hernia: This type involves an opening on the back side of the diaphragm. The stomach, intestines and liver or spleen usually move up into the chest cavity.
- Morgagni hernia: This type is rare and involves an opening in the front of the diaphragm, just behind the breast bone. The liver or intestines may move up into the chest cavity.
As a fetus grows in its mother's uterus before birth, different organ systems are developing and maturing. The diaphragm forms between the 7th and 10th week of pregnancy. The esophagus (the tube that leads from the throat to the stomach), the stomach, and the intestines are also developing at this time. In a Bochdalek hernia, the diaphragm may not develop properly, or the intestine may become trapped in the chest cavity as the diaphragm is forming. At times, the tendon that should develop in the middle of the diaphragm does not develop properly. In both cases, normal development of the diaphragm and the digestive tract does not occur.
Diaphragmatic hernia is a multifactorial condition, which means that "many factors," both genetic and environmental, are involved. It is thought that multiple genes from both parents, as well as a number of environmental factors that scientists do not yet fully understand, contribute to diaphragmatic hernia.
How often does a diaphragmatic hernia occur?
CDH occurs in about 1 in every 2,500 births. Bochdalek hernias make up about ninety percent of all cases. Why is a diaphragmatic hernia of concern? The lungs are developing at the same time as the diaphragm and the digestive system. A diaphragmatic hernia allows abdominal organs to move into the chest cavity, instead of remaining in the abdomen as they are developing. With the heart, lungs, and abdominal organs all taking up space in the chest cavity, the lungs do not have space to develop properly. This underdevelopment of the lungs is called pulmonary hypoplasia. A diaphragmatic hernia is a life-threatening illness. When the lungs do not develop properly during pregnancy, it can be difficult for the baby to breathe after birth. Healthy lungs have millions of small air sacs (alveoli), which resemble a balloon filled with air. With pulmonary hypoplasia:
- There are fewer air sacs than normal.
- The air sacs that are present are only able to partially fill with air.
- The air sacs deflate easily due to a lack of a lubricating fluid called surfactant.
What if a diaphragmatic hernia is suspected during pregnancy?
During routine prenatal care at around 18 weeks, an ultrasound may reveal the existence of a diaphragmatic hernia, or what is suspected to be CDH. A more detailed diagnosis, using more sophisticated testing including fetal MRI, is essential to confirm the presence of CDH, and to show more specifically the details of its severity.
What are the symptoms of a diaphragmatic hernia in babies?
When CDH is not diagnosed prenatally, the symptoms of a Bochdalek diaphragmatic hernia are often observable soon after the baby is born. The following are the most common symptoms of a Bochdalek diaphragmatic hernia. However, each child may experience symptoms differently. Symptoms may include:
- difficulty breathing
- fast breathing
- fast heart rate
- cyanosis (blue color of the skin)
- abnormal chest development, with one side being larger than the other
- abdomen that appears caved in (concave).
How is congenital diaphragmatic hernia diagnosed after birth?
After birth, your baby's physician will perform a physical examination. A chest X-ray is done to look at the abnormalities of the lungs, diaphragm, and intestine. A blood test known as an arterial blood gas is often performed to evaluate the baby's breathing ability. Other tests that may be performed include:
- blood test for chromosomes (to determine if there is a genetic problem)
- ultrasound of the heart (echocardiogram).
Parents who have had one child with a diaphragmatic hernia are at increased risk to have another child with the same problem. In cases where it is the only health problem in a baby, the chance for diaphragmatic hernia to happen again in a future pregnancy is 2 percent, or two in 100 chances. Morgagni hernia is more common in girls than boys, whereas Bochdalek hernia is slightly more common in boys than girls. Babies with the Bochdalek type of diaphragmatic hernia are more likely to have another birth defect. Almost twenty percent have a congenital heart defect. Between 5 to 16 percent have a chromosomal abnormality
Taybi-Linder dwarfism
Note: Also referred to as microcephalic osteodysplastic primordial dwarfism
Taybi-Linder is an extremely rare and horrible syndrome. There are only 34 reported cases since it was identified 40 years ago. Most children die before one year of age. My nephew Drake who's on the Angel Page 1 was one of these children. There is VERY little information out there about Taybi-Linder Dwarfism so I will just post what I could find.
Definition: These syndromes associate growth retardation with microcephaly and various facial anomalies. The number of reported case is small and the difference between the subtypes probably not identifiable by prenatal ultrasound, which is the reason they are lumped them altogether.
Synonyms: Osteodysplastic primordial dwarfism, type I, brachymelic primordial dwarfism, Taybi-Linder syndrome, cephaloskeletal dysplasia, low-birth-weight dwarfism with skeletal dysplasia.
Incidence: Less than 50 cases have been reported.
Etiology: Sporadic with possible autosomal recessive inheritance.
Diagnosis: The findings include growth retardation with microcephaly, micrencephaly, lissencephaly, micrognathia and moderately short limbs. Type II-III may have platyspondyly.
Associated anomalies: Include beaked nose, large eyes, dysplastic ears, clinodactyly, dysgenesis of the corpus callosum, focal renal medullary dysplasia, small iliac wings with flat acetabular angles, coxa vara, V-shaped distal femoral metaphyses, triangular distal femoral epiphyses, pseudoepiphyses of metacarpals, short first metacarpals, and brachymesophalangy of the fifth digit.
Differential diagnosis: Aneuploidies (trisomy 13, 18).
Prognosis: Not known. Most children have died within the first year.
Management: Termination of pregnancy can be offered before viability, otherwise no alteration of prenatal care are suggested
Microcephalic and osteodysplastic primordial dwarfism (MODP) types I, II, and III were defined by Majewski et al. in 1982. This group of syndromes was characterized by intrauterine growth retardation, microcephaly, and typical facial appearance with prominent nose and micrognathia. Type II was clearly different, both clinically and radiologically, whereas types I and III shared manifestations. Distinction between the latter two was established on the basis of subtle radiological differences. In 1967, Taybi and Linder described another syndrome with microcephalic congenital dwarfism. There is a consensus that MODP type I and III and Taybi-Linder cephaloskeletal dysplasia represent the same disorder. We report on four patients with MODP type Taybi-Linder syndromes, two of whom were born to unrelated but consanguineous parents, while the other two were sibs. Second-trimester prenatal detection by ultrasonography was possible in one case. Consanguinity in two cases and recurrence among sibs are consistent with autosomal recessive inheritance.
Taybi-Linder is an extremely rare and horrible syndrome. There are only 34 reported cases since it was identified 40 years ago. Most children die before one year of age. My nephew Drake who's on the Angel Page 1 was one of these children. There is VERY little information out there about Taybi-Linder Dwarfism so I will just post what I could find.
Definition: These syndromes associate growth retardation with microcephaly and various facial anomalies. The number of reported case is small and the difference between the subtypes probably not identifiable by prenatal ultrasound, which is the reason they are lumped them altogether.
Synonyms: Osteodysplastic primordial dwarfism, type I, brachymelic primordial dwarfism, Taybi-Linder syndrome, cephaloskeletal dysplasia, low-birth-weight dwarfism with skeletal dysplasia.
Incidence: Less than 50 cases have been reported.
Etiology: Sporadic with possible autosomal recessive inheritance.
Diagnosis: The findings include growth retardation with microcephaly, micrencephaly, lissencephaly, micrognathia and moderately short limbs. Type II-III may have platyspondyly.
Associated anomalies: Include beaked nose, large eyes, dysplastic ears, clinodactyly, dysgenesis of the corpus callosum, focal renal medullary dysplasia, small iliac wings with flat acetabular angles, coxa vara, V-shaped distal femoral metaphyses, triangular distal femoral epiphyses, pseudoepiphyses of metacarpals, short first metacarpals, and brachymesophalangy of the fifth digit.
Differential diagnosis: Aneuploidies (trisomy 13, 18).
Prognosis: Not known. Most children have died within the first year.
Management: Termination of pregnancy can be offered before viability, otherwise no alteration of prenatal care are suggested
Microcephalic and osteodysplastic primordial dwarfism (MODP) types I, II, and III were defined by Majewski et al. in 1982. This group of syndromes was characterized by intrauterine growth retardation, microcephaly, and typical facial appearance with prominent nose and micrognathia. Type II was clearly different, both clinically and radiologically, whereas types I and III shared manifestations. Distinction between the latter two was established on the basis of subtle radiological differences. In 1967, Taybi and Linder described another syndrome with microcephalic congenital dwarfism. There is a consensus that MODP type I and III and Taybi-Linder cephaloskeletal dysplasia represent the same disorder. We report on four patients with MODP type Taybi-Linder syndromes, two of whom were born to unrelated but consanguineous parents, while the other two were sibs. Second-trimester prenatal detection by ultrasonography was possible in one case. Consanguinity in two cases and recurrence among sibs are consistent with autosomal recessive inheritance.