C

Care of the Premature Infant

What is prematurity?
What is important to know prior to the birth of a premature infant?
What is the chance of survival for a premature infant?
What is the delivery room management of the premature infant?
What problems can be expected in the nursery?
What needs to happen for my baby to go home?
What is the outcome for survivors of the intensive care nursery?

by Adam A. Rosenberg, M.D.
Director of Newborn Services at University Hospital
Professor of Pediatrics at the University of Colorado School of Medicine
Denver, Colorado
What is prematurity?
Any infant born at less than 37 weeks gestation is by definition “premature.” Most infants born at 35 to 37 weeks gestation are relatively healthy, and they often have only brief hospital stays in normal newborn nurseries. The problems associated with premature infants occur with greater frequency in those of lower gestational age at birth, typically less than 35 weeks gestation.

What is important to know prior to the birth of a premature infant?
Some treatments may be used in mothers who are at risk of having their baby early. Anyone who has had a previous preterm infant is at a “high risk” of having another preterm infant. Therefore, prenatal care should be sought with a caregiver who is up to date and comfortable with the management of a mother who is at risk for a preterm delivery.
When a mother is in preterm labor, she should be admitted to the hospital and placed on drugs to slow the progress of labor. Although these drugs will not delay delivery for very long in many cases, they often allow enough time to receive a full course of steroids (betamethasone or dexamethasone) to accelerate the maturation of the fetus. Steroids have been shown to decrease the rate of death of preterm infants, as well as decrease the rate of lung, intestinal, and brain complications.
When there is a risk of delivering a baby early, it is appropriate to ask if the nursery at the hospital is able to take care of a preterm baby. If not-if it is safe for the mother and fetus-they should be transferred to a facility that is capable of caring for the baby after birth. In addition, an expectant mother should talk with the hospital staff members who will care for the baby after birth. Issues to discuss include a review of the problems associated with prematurity, chances of survival, and the anticipated long-term outcome.

What is the chance of survival for a premature infant?
The survival of premature infants is determined by gestational age at delivery and birth weight. Infants born after 28 weeks gestation and 1,000 grams, or 3 pounds 3 ounces (454 grams equals 1 pound), have more than a 90% chance of survival. The rate of survival at 27 weeks and 900 grams is 80% to 85%, at 26 weeks and 800 grams is 75% to 80%, and at 25 weeks and 700 grams is 60%. Rates of survival drop off rapidly at less than 25 weeks, and they vary quite a bit among different nurseries.
The long-term outcome also is dependent on gestational age and birth weight. For babies of 26 to 32 weeks gestation, the rate of severe neurodevelopmental problems among survivors is about 10%; at 23 to 26 weeks, the rate increases gradually to 25% of survivors. Other long-term complications, including lung problems, vision disturbances, and hearing loss, are more common in babies of lower gestational age at birth.

What is the delivery room management of the premature infant?
Staff members who are experienced in the management of premature infants should be present in the delivery room. The infant must be kept warm; provided with adequate oxygen; and helped with breathing, if necessary. Most infants who weigh less than 1,000 grams at birth will require a breathing tube in their airway.

What problems can be expected in the nursery?

Thermoregulation
Preterm infants are not able to maintain their body temperature without an external heat source. Initially, heat will be provided with an overhead warmer that responds to the baby’s temperature and provides adequate warmth to maintain a normal body temperature. The warmer provides easy access to the baby for necessary cares during the early, “unstable” period. When more stable, the baby will be moved into an incubator to maintain a warm environment. Most infants are able to move into an open crib at a weight of approximately 1,800 grams.
Nutrition
Initially, premature infants are given all the necessary fluid, calories, protein, sugar, and fat in their veins. When their condition stabilizes, a feeding tube into their stomachs can start. The amount of feeds starts at a very low level, and it is advanced slowly over 3 to 7 days to “full” feeds. At this point, the infant no longer needs fluids or nutrition into their veins. Once full feeds are achieved, anticipated rates of weight gain are 10 to 25 grams per day. Breast milk is the food of choice, but formulas developed for preterm infants are an acceptable substitute. A baby will be able to begin “nipple” feeding from a bottle at about 33 to 34 weeks post conception.
Monitoring
All babies in intensive care nurseries have their heart rates, breathing, and, in some cases, blood pressure monitored continuously. Blood oxygen also can be monitored with a pulse oximeter in infants with lung and heart problems. A pulse oximeter uses a light source, wrapped around the infant’s foot or hand, to measure the amount of oxygen carried by the hemoglobin in the red blood cells. At the start, a sick baby will usually have an indwelling tube in an artery (usually the umbilical artery in the cord that was connected to the placenta in the uterus) to sample blood for tests without having to draw blood from the infant. A tube also may be placed in the umbilical vein to give fluids and nutrition. These tubes are usually kept in the infant for 3 to 10 days depending on how sick they are.
Lung problems
Hyaline membrane disease (HMD) or respiratory distress syndrome (RDS). By 24 weeks gestation, there is adequate surface for gas exchange (bringing oxygen to the blood and removing carbon dioxide) in the lung; however, a necessary element for survival is missing. The natural tendency of a lung is to collapse when a person breathes out. Once collapsed, it is very difficult to reopen the lung. A chemical called surfactant is produced in the lungs to lower surface tension as the lungs get smaller during exhalation. This chemical prevents a total collapse of the lungs and allows easy re-expansion with inhalation.
Preterm babies have little or no surfactant in their lungs, and they would die from respiratory failure without intervention. The frequency of surfactant deficiency ranges from nearly 100% at 24 weeks gestation, to 60% at 28 weeks and 25% at 32 weeks. To treat this condition, babies are given surfactant substitutes through their breathing tubes into the lungs and to help them breathe with breathing machines called ventilators. Depending on their gestation at birth, premature infants will remain on the ventilator from a few days to up to about 6 weeks.
When babies are ready to come off the ventilator, they are “extubated” (removal of the breathing tube) to either nasal CPAP (provides low pressure through a device placed in the nose to help keep the lungs expanded) or to a bubble with extra oxygen placed over the head. Ultimately, supplemental oxygen can be delivered with a small hose under the nose called a nasal cannula.
Apnea and bradycardia (A&B spells). At the time of birth, preterm infants have an immature respiratory drive. This results in spells when they “forget” to breathe (apnea). If these spells are long enough, they result in a decrease in blood oxygen and then a slowing of the heart rate (bradycardia). Sometimes, these episodes resolve themselves, while, in other cases, the infants need to be stimulated to restart breathing. If the spells are bad enough or occur with a frequency of more than 6 to 10 times per day, they can be treated medically with caffeine (like in coffee) citrate.
In most infants, this is successful; however, if this treatment fails, it is sometimes necessary to place the infant back on nasal CPAP or the ventilator. Infants born beyond 28 weeks gestation generally outgrow these spells by 37 weeks post conception. In infants born at lower gestational ages, the spells may last longer.
Chronic lung disease (CLD) or bronchopulmonary dysplasia (BPD). The combination of prematurity, oxygen exposure, and mechanical ventilation can result in lung injury to preterm babies. The consequence of this lung injury is chronic lung disease. CLD can prolong ventilator courses in small preterm infants (less than 1,200 grams) and result in a long-term oxygen need that can sometimes extend to home care. The frequency of this complication is greatest in the least mature infants, and, in those infants less than 26 weeks gestation at birth, it can occur in over 75% of cases. However, the lungs still generate new gas exchange surface until adolescence so the vast majority of infants outgrow this problem.
Patent ductus arteriosus (PDA)
The major heart-related problem in premature infants is PDA. The ductus is a structure that is present in a fetus connecting the main blood vessel that goes to the lungs from the heart to the main blood vessel that goes to the rest of the body. In the fetus, very little blood goes to the lungs because the fetus does not breathe air. The ductus allows the majority of the blood that is headed from the heart to the lungs to cross to the circulation to the body, bypassing the lungs. At birth, it is supposed to close.
In preterm babies, this closure may not occur. After birth, if this vessel is open, too much blood ends up going to the lungs, making it harder for an infant to breathe or to be ventilated. To close this blood vessel, the medication indomethacin is used. This works over 75% of the time; however, if it fails, a surgical closure is needed. Fortunately, it is a brief procedure that can be done at the bedside with almost uniformly good results.
Necrotizing enterocolitis (NEC)
The most important intestinal complication in preterm babies is NEC. This disease is the result of periods of low blood flow to the intestine, intestinal immaturity, and infection. When a baby develops this problem, they cannot be fed into the intestine and require 10 to 21 days of nutrition in their veins. In addition, a large tube is placed in the stomach to keep air out, and antibiotics are given. Many of the cases respond to this treatment, but, in some cases, surgery is needed to remove parts of the intestine that have died.
Intraventricular hemorrhage (IVH)
The internal structures of the brain in a preterm infant are at risk for hemorrhage. The bleeding is usually the result of a previous period of low blood flow, and occurs in the first four days of life. Diagnosis of the bleeding is performed with bedside ultrasound exams. The degree of bleeding is graded from 1 to 4. Grade 1 and 2 bleeds are small, and they do not increase the infant’s risk of neurodevelopmental abnormalities, while 33% of the babies with grade 3 and 4 bleeds will suffer severe neurologic injury, and another 33% will suffer lesser deficits. The final neurologic complication in preterm babies is injury to the motor tracts in the brain called periventricular leukomalacia (PVL), which causes cerebral palsy-a movement disorder with spasms that can impair the ability to walk.
Retinopathy of prematurity
The retina of the preterm infant is not fully “vascularized”(i.e., the blood vessels are not fully developed) at birth. The infant is at risk for a process called ROP, which, in its worst form, can lead to detachment of the retina and blindness. In babies born at less than 28 weeks or 1,500 grams, an ophthalmologist will perform a screening exam at 6 weeks of age.
Follow-up exams will then be performed until any ROP resolves, and the retina is fully vascularized. ROP is graded from 1 to 5 for severity. The process resolves spontaneously in most infants, but those infants who reach an advanced stage 3 of disease are at a high risk for detachment of the retina. These infants require treatment with laser therapy, which often can save the vision in the affected eye(s).
Anemia of prematurity
Because of blood sampling for tests and conditions that cause blood loss, such as inventricular hemorrhage, many preterm babies will require red blood cell transfusions. To decrease the number of transfusions given and to minimize donor exposure, preterm babies can be treated with the hormone erythropoietin, which stimulates red blood cell production in the body.
Hyperbilirubinemia (jaundice)
Virtually all preterm babies will develop jaundice. Jaundice is caused by an accumulation of the yellow pigment “bilirubin,” which is the breakdown product of hemoglobin from the red blood cells. A preterm infant cannot effectively clear the bilirubin in the liver. If too much bilirubin accumulates in the blood, it can cause brain damage. To help these infants in clearing the bilirubin to prevent brain damage, they are placed under phototherapy (“bilirubin lights”).
Infection
Some preterm deliveries are the result of an infection in the uterus, which also can lead to an infection in the baby. In addition, infants in the intensive care nursery are at an increased risk for infection due to indwelling lines and tubes, as well as a compromised immune (“infection fighting”) system. Thus, the risk of infection is high. If there is concern that an infant might be infected or there is a proven infection, the infant is treated with antibiotics-an event that is likely to occur more than once during the nursery stay.

What needs to happen for my baby to go home?
Most preterm infants are ready for discharge at or a few weeks before their due date. The criteria for discharge include the ability to maintain body temperature in a crib, adequate oral intake to sustain consistent growth, and resolution of apneic and bradycardic spells. Occasionally, infants who are otherwise doing well may be sent home on partial tube feedings.
In addition, if A&B spells are not completely resolved, but are not felt to be life threatening, some physicians will send a baby home on a heart monitor. If an infant needs supplemental oxygen at discharge, a test needs to be performed prior to going home to be sure if the oxygen were to fall off that the blood oxygen does not drop to dangerously low levels.

What is the outcome for survivors of the intensive care nursery?
Neurodevelopmental handicaps may occur in survivors of the intensive care nursery. These handicaps include cerebral palsy, which can be severe enough to prevent a child from walking, and cognitive deficits, which can be severe enough to prevent a child from learning to talk or read. Fortunately, deficits this severe occur in the minority of survivors, but others may have lesser deficits that cause delayed motor development, learning disabilities, and behavioral disorders, such as attention deficit disorder (hyperactivity).
The rates of abnormalities are higher in babies of lower gestational age at birth, particularly those born at 25 weeks or less. Although ROP rarely causes blindness, vision problems may still occur. The frequency of hearing loss is increased compared to term infants. The consequences of chronic lung disease are an increased rate of hospital readmission during the first two years of life, a continued oxygen need, and an increased incidence of asthma-like symptoms.
Finally, preterm infants are at an increased risk for poor weight gain, and they may require nutritional supplements or special formulas. Most premature infants who “graduate” from an intensive care nursery do quite well; however, coordinated follow-up to address all of their needs is of paramount importance.

References
Fanaroff A.A., Martin R.J. (editors): Neonatal-Perinatal Medicine. Diseases of the Fetus and Infant, 6th ed., Mosby, 1997.
Zaichkin J.: Newborn Intensive Care. What Every Parent Needs to Know. NICU Ink, 1996.
About the Author
Dr. Rosenberg graduated from Vanderbilt Medical School in 1976. His Pediatric Residency was at the University of Colorado and his Neonatal Fellowship was fulfilled at Johns Hopkins University. He is the Director of Newborn Services at University Hospital in Denver and Professor of Pediatrics at the University of Colorado School of Medicine.
His professional interests include newborn brain injury and long-term follow up of high-risk newborns. Some of his personal interests include tennis, skiing and youth sports programs.
Copyright 2012 Adam A. Rosenberg, M.D., All Rights Reserved

Celiac Disease

What is celiac disease?
Who gets celiac disease?
How does celiac disease cause disease?
What are the common findings of celiac disease?
How is celiac disease diagnosed?
How is celiac disease treated?
How do you prevent celiac disease?
What research is being done?
Are there other links to more information?

Edward J. Hoffenberg, M.D.
Associate Professor of Pediatrics
University of Colorado Health Sciences Center
Denver, Colorado

What is celiac disease?
Celiac disease, also called “sprue” and “gluten-sensitive enteropathy,” is a chronic, lifelong condition in which certain cereal proteins in the diet lead to injury of the lining of the small intestine, or bowel. Gluten is an insoluble protein found in wheat, rye, and other grains. The cause of celiac disease is not clearly understood. A complex interaction between genetic and environmental factors causes celiac disease to develop in susceptible people who include wheat, rye, and barley cereals in their diet. An unknown third factor, possibly an infection or other triggering stimulus, may be required since many people with similar risk factors do not develop celiac disease.

Who gets celiac disease?
Celiac disease affects all ethnic groups. Most frequently affected are Caucasians, then Blacks, and, only rarely, Orientals. Based on blood tests, about 1% of the European population has evidence of celiac disease, and preliminary data suggests the same is true in the United States. Most people with celiac disease have a certain genetic type, which can be detected by screening. Although present in about 35% of the general U.S. population, over 90% of patients with celiac disease have this genetic type. How this genetic type predisposes individuals to developing celiac disease is unclear. Groups at risk for celiac disease include those with:
type 1 diabetes (5% to 10% have celiac disease),
a first-degree relative with type 1 diabetes or celiac disease (2% to 7% have celiac disease),
Down syndrome,
dermatitis herpetiformis (a skin rash),
IgA deficiency (a lack of the chief antibody in the mucous membranes of the gastrointestinal tract),
thyroid disease, and
other autoimmune deficiencies.

How does celiac disease cause disease?
Illness from celiac disease generally comes from two processes: injury to the intestine and from chronic inflammation. Upon biopsy (i.e., the removal of a small amount of tissue and/or fluid from a living body and its examination to confirm the presence of a disease), the small bowel injury has a typical appearance. White blood cells (lymphocytes) enter the lining of the small bowel. The usual ridges, like tall mountains and valleys, may become blunted, like small hills, or even flat, like the plains. The injured small bowel may lead to diarrhea and impaired absorption. Over time, nutritional deficiencies may develop, leading to poor growth; weight loss; short stature; delayed puberty; anemia; and a lack of “micronutrients,” including vitamins A, E, and K; iron; zinc; and folic acid.
The second mechanism, chronic inflammation, may lead to a long-lasting ill feeling, with poor appetite, and possibly bone thinning and easy fractures, called osteoporosis. An eventual loss of regulation over the immune response has been thought to play a role in the increased risk for small bowel lymphoma noted in untreated celiac disease.
A similar inflammatory reaction may occur in the skin causing an itchy, scaly rash, called dermatitis herpetiformis, and is a non-intestinal indication of gluten sensitivity.

What are the common findings of celiac disease?
Celiac disease can be thought of as occurring in two forms: “symptomatic” and “silent.” Both have positive blood tests for celiac disease-associated antibodies, and both have a typical injury on biopsy of the small intestine. In the symptomatic form, typical signs and symptoms are present. The most information about celiac disease is known from this type. Common findings include abdominal pain, chronic diarrhea with poor fat absorption (characterized as oily or greasy stools), vomiting, and nutritional deficiencies (iron deficiency anemia, bleeding due to vitamin K deficiency, and deficiencies of folic acid and zinc). Other findings include poor weight gain, weight loss, short stature, delayed puberty, abdominal distention and gas, and, in toddlers, irritability and edema (swelling of the feet, eyelids, and other soft tissues).
In contrast, affected individuals with the silent type feel fine, have mild or no symptoms, and do not know they have celiac disease. Less is known about silent celiac disease; although, it is about six times more common than symptomatic celiac disease. Whether silent celiac disease is a risk for the long-term complications seen in symptomatic celiac disease is unknown.

How is celiac disease diagnosed?
Most experts agree that if both the blood test and the small intestine biopsy are positive, then the diagnosis of celiac disease is made. The available blood tests include anti-endomyseal antibody, anti-gliadin antibody, and, the newest one, anti-transglutaminase antibody. These tests may be used separately or together, and are highly accurate in screening individuals for celiac disease. However, rarely, the antibody tests can be negative, especially in individuals with IgA deficiency and in young children.
A key in the proper diagnosis of celiac disease is improvement after starting a gluten-free diet. Symptoms should resolve, the antibody tests should become negative after 6 to 12 months of a strict gluten-free diet, and the small bowel injury should resolve completely. In difficult diagnostic cases, screening for DQ-2, the genetic marker of celiac disease, may be helpful. Previously, rechallenging the body with gluten to show a reappearance of the symptoms was required to diagnose celiac disease; but, now, it is rarely needed.

How is celiac disease treated?
Treatment for celiac disease first involves replacing deficient nutrients and choosing a gluten-free diet. If patients-especially toddlers-are severely ill, a short course of prednisone improves symptoms quickly. A lifelong gluten-free diet is the treatment for celiac disease. A gluten-free diet means avoiding foods containing wheat, rye, and barley proteins. Pure oats is probably allowable. Following a gluten-free diet is quite challenging, as these products are widespread in Western diet. However, within one week of the diet, irritability resolves, and appetite and energy level improve. Many people with silent celiac disease report feeling healthy for the first time, even though they never before complained of symptoms. If a gluten-free diet is not followed, celiac disease will always recur; however, it may take weeks to months.

How do you prevent celiac disease?
Currently, celiac disease cannot be prevented

What research is being done?
Current research includes: identifying risk groups for celiac disease; understanding the genetic predisposition and environmental triggers for developing celiac disease; and determining how silent celiac disease is similar to and different from symptomatic celiac disease, especially regarding growth, osteoporosis, and intestinal malignancy.

Are there other links to more information?
Celiac Sprue Association of the United States of America, Inc., P.O. Box 31700, Omaha, NE 68131-0700, phone number: (402) 558-0600. The Web site, of interest.
The Web site for the North American Society for Pediatric Gastroenterology and Nutrition, www.naspgn.org/disease_information.htm, provides information from pediatric gastroenterologists with sections for parents and for children. There is a nice section on foods that are “gluten-free”
Gluten Intolerance Group of North America, P.O. Box 23053, Seattle, WA 98102-0353, phone number: (206) 325-6980. Information provided includes newsletters, fact sheets, cookbooks, diet instructions, and videotapes.
Celiac Disease Foundation, P.O. Box 1265, Studio City, CA 91614-0265, phone number: (213) 654-4085.
About the Author
Dr. Hoffenberg is on staff at the Children’s Hospital in Denver, the University of Colorado School of Medicine, and is the Director at the Center for Pediatric Inflammatory Bowel Diseases. His areas of specialty include Inflammatory Bowel Disease, Celiac Disease and Polyps.
Copyright 2012 Edward J. Hoffenberg, M.D., All Rights Reserved

Chickenpox

What is varicella (or chickenpox)?
What causes varicella (or chickenpox)?
Who gets varicella (or chickenpox)?
How does the varicella-zoster virus cause disease?
What are the common findings?
How is varicella (or chickenpox) diagnosed?
How is varicella (or chickenpox) treated?
What are the complications?
How is varicella (or chickenpox) prevented?
What research is being done?
Links to other information

by Philip Alfred Brunell, M.D.
Senior Attending Physician
Clinical Center, National Institute of Health
Bethesda, Maryland
What is varicella (or chickenpox)?
Varicella, commonly referred to as chickenpox, is an infectious disease that is caused by a virus. The infection produces a rash with fluid-filled “vesicles,” or lesions, on the face and body.

What causes varicella (or chickenpox)?
The disease is caused by the varicella-zoster virus, or VZV, a member of the herpes family of viruses. As the name implies, it causes varicella, or chickenpox, as well as “zoster,” or shingles. After a recovery from varicella, the virus remains in some of the body’s nerve cells in an inactive, or “latent,” state. After many decades, the virus may become active again, travel down the nerve cells, and produce a rash on the skin. This rash is similar to the rash produced by varicella; however, the rash in zoster occurs in one segment of the skin, on one side of the body, rather than all over the body, as in varicella. Occasionally, zoster occurs in children, but it most commonly occurs in older adults.

Who gets varicella (or chickenpox)?
Varicella occurs in children. Fewer than two percent of the cases occur in adults. About half of all children will have had varicella by the time that they enter school. Varicella can occur early in infancy, and it can occur in a newborn if the mother had chickenpox just before delivery. Varicella is very contagious. If there is a case of it in a household, there is only a 1 in 25 chance that individuals in the house who are susceptible to varicella will not be infected.

How does the varicella-zoster virus cause disease?
Varicella occurs following close contact with a person who has the disease. Children are contagious the day before the rash, which suggests that they are able to spread the disease from their respiratory tract. The virus is inhaled, and then multiplies in the newly infected person. It is transported in certain blood cells to the skin, where it multiplies and causes the skin lesions, or vesicles.

What are the common findings?
The most common finding of varicella is the fluid-filled skin vesicles, usually no more than an eighth of an inch in diameter, which may have a slight redness around them. They start centrally on the body, and then spread to the arms and the legs. Often, vesicles can be felt on the scalp before they can be seen on the skin. Scabbed or crusted lesions, or a flat or slightly raised red rash, may occur at the same time as the vesicles. Often, scratch marks will result from the scratching of a very itchy rash.
The temperature is generally 100oF to 102oF. There is a cause for concern if a temperature is greater than 103oF. Fussiness may occur, caused mainly by the itching. Respiratory and gastrointestinal symptoms are not usually associated with varicella.

How is varicella (or chickenpox) diagnosed?
Varicella is diagnosed simply by looking. Laboratory testing is rarely required; although, there are tests that can be performed. Chickenpox can be confused with insect bites, hand-foot-and-mouth disease, and rickettsialpox. A history of exposure to a person with either chickenpox or shingles about two weeks previously is helpful in making an accurate diagnosis.

How is varicella (or chickenpox) treated?
Medication to treat the fever rarely is required. Aspirin or aspirin-containing medications (look for “salicylate” on the label) should never be given to children with varicella, because it has been associated with Reye’s syndrome. Acetaminophen may prolong the itching. Ibuprofen has been associated with a severe, complicated streptococcal disease, but this drug may have been given for relief of the complication, rather than for treatment of varicella; therefore, it cannot be causally related.
The itching may require treatment. Calomine lotion may be applied to the skin, or the child may bathe in an oatmeal bath (Aveno). The drying of the oatmeal on the skin after the bath may offer relief. Oral medications, such as Benadryl, also are available. Since it may cause sleepiness, Benadryl is best used at bedtime. Your doctor may recommend other oral medications, if necessary.
It is very important to keep the skin clean. Daily showers or baths, preferably with an antibacterial soap, is recommended. Phisohex is excellent, but it may be too drying. Bathing will not cause the rash to spread on the skin. The scratch marks on the skin of patients with varicella do not have vesicles, meaning that an individual cannot spread the virus by inoculating it into the skin or by bathing. It is best to prevent scratch marks by trimming a child’s nails.
Although acyclovir-a specific antiviral drug that inhibits the growth of VZV-has been approved for use in children, there has been little enthusiasm for it. It must be given within 24 hours after the onset of the rash to be effective. The effect on a person’s symptoms is minimal; however, they are statistically significant when compared to the symptoms of a person who has not had the drug. In adolescents and adults who have more severe chickenpox than children, acyclovir may be useful. The drug may be more effective in second cases in a family, where acyclovir can be obtained at the time of the first child’s illness, and treatment can be started on the other children as soon as a rash appears. Second cases tend to be more severe than the first case in a family.

What are the complications?
Most cases of varicella are mild, and can be treated by applying ointment to the skin; however, some cases may require antibiotics. Rarely, cases are very severe. If your child develops a skin infection following varicella, us should evaluate it.
The most common complication of varicella is a bacterial infection of the skin. This can occur when the fever rises after several days of illness or redness appears on the skin. The skin also may be warm and tender. In a severe infection, pain may be a prominent symptom. In recent years, streptococcal skin infections have become more frequent, and require prompt attention.
Neurologic complications do occur with varicella. The most common complication occurs 1 in about 4,000 cases, and is characterized by difficulty with balance. Although this is frightening to the child and the parents, it generally gets better by itself with time. Loss of consciousness and convulsions with fever, headache, and vomiting may indicate encephalitis. This complication occurs 1 in about 40,000 cases, but it may be life threatening. In the past, before the warning about aspirin, similar symptoms were seen in Reye’s syndrome. In any of these situations, your physician should be contacted.
There are a number of less common complications that include, among others, bleeding disorders, joint involvement, and kidney problems.

How is varicella (or chickenpox) prevented?
Avoiding contact with those individuals who are affected with chickenpox can prevent it; however, this is very difficult. Many children are not even aware that they have been exposed. Protecting children from varicella is cumbersome, as they must be kept from school and other activities.
Immunization is the only practical way to prevent varicella. A live attenuated (weakened) varicella vaccine is recommended for all children who have passed their first birthday and have not had chickenpox. Children under 12 years of age require only a single injection; adolescents and adults are given two injections. The vaccine has few side effects; tenderness or pain at the injection site is the most common. Occasionally, a child may have a few chickenpox lesions on the injection side or over the trunk. The vaccine is effective in preventing or modifying varicella. In persons who have had the vaccine and still developed varicella, their cases have been extremely mild.
There are two concerns about the vaccine: how long immunity will last, and whether zoster will be a greater problem later in life in vaccinated children than in children who actually had chickenpox. There is no reason to suspect that zoster will be a problem since children who have had the vaccine do not seem to get it more frequently, and children with leukemia who were vaccinated had zoster less frequently.
Chickenpox is a much more severe disease in adults than in children. Most children will be immunized during childhood, and it is anticipated that there will be fewer cases of varicella. Therefore, children who are not immunized during childhood will have a decreased chance of contracting chickenpox as an adult. However, children who are not vaccinated will be susceptible adults, and, if infected, may get a severe case of chickenpox. If vaccine immunity should decrease, it is likely that there may be partial immunity, which will modify the severity of chickenpox in an adult who was immunized as a child. At the present time, there is no evidence to suggest that the protection produced by the vaccine will be lost.
In persons who are exposed to varicella, the antiviral drug, acyclovir, may be given. An injection of Varicella-Zoster Immune Globulin (VZIG) is used to protect adults and children who have compromised immune systems (e.g., those receiving high doses of steroids or children with leukemia), if they are exposed to chickenpox. This injection is very expensive (about $500), and it provides protection for only a few weeks. Thus, it is necessary to give it at the time of each exposure. However, many individuals will get chickenpox following an exposure of which they were unaware.

What research is being done?
Efforts continue to find better drugs to treat varicella. In addition, basic research is being conducted to better understand why the virus becomes latent and why it becomes activated to cause zoster. Currently, there is a study, which eventually will have 37,000 participants, to determine whether a stronger varicella vaccine can prevent shingles in people over 60 years of age.

Links to other information
http://www.cdc.gov/vaccines/pubs/vis/downloads/vis-varicella.pdf

References
Brunell, P.A. Varicella-Zoster (Chickenpox) in Rudolph’s Pediatrics, 20th ed., Appleton and Lange, Stamford, CT, 1996.
Report of the Committee on Infectious Diseases, American Academy of Pediatrics, Elk Grove Village, IL, 1997.
Copyright 2012 Philip Alfred Brunell, M.D., All Rights Reserved

Coarctation of the Aorta

What is coarctation of the aorta?
Who gets coarctation of the aorta?
What are the effects of this defect on my child’s health?
How is this problem diagnosed?
How is coarctation of the aorta treated?
Why treat children with coarctation of the aorta?
What is the outlook for children with coarctation of the aorta?

Albert P. Rocchini, M.D.
Professor of Pediatrics
University of Michigan
What is coarctation of the aorta?
Coarctation of the aorta is a narrowing of the aorta that causes a blockage to blood flow. Most coarctations are congenital (meaning they are present at birth) and usually are discovered in infancy; however, some coarctations can develop over time. The narrowing may be discrete or may extend over a long segment. Most coarctations are located in the chest, and rarely they can occur in the abdomen. “Simple” is the term used to describe coarctations that are isolated; “complex” is the term used to describe coarctations that are associated with other congenital heart disease. Types of congenital heart disease associated with coarctation include ventricular septal defect (an abnormal hole between the two ventricles), atrioventricular canal (an abnormal connection between the atrium and the ventricle), and double outlet right ventricle (two exit vessels from the ventricle, rather than one).

Who gets coarctation of the aorta?
Coarctation of the aorta is one of the more common forms of congenital heart disease. It is twice as common in boy as in girls. Coarctation rarely runs in families. The only syndrome that has a strong association with coarctation is Turner’s syndrome, a condition in which a girl has only one instead of two X chromosomes.

What are the effects of this defect on my child’s health?
Infants with coarctation frequently have congestive heart failure (the heart cannot keep up with its workload, so it starts to fail). A narrowing of the aorta results in a selective elevation in blood pressure in the upper extremity blood vessels and, ultimately, in an increase in heart work. In some newborns with coarctation, closure of the ductus arteriosus results in an acute increase in heart work. If the coarctation is severe, the increased heart work results in the development of congestive heart failure. In infants with milder degrees of coarctation, the heart adapts to the increase in work, and heart failure does not occur.
The cardiovascular system has two ways to respond to the increased work produced by coarctation of the aorta. The first way the body compensates for the increased cardiac workload is to develop extra heart muscle (myocardial hypertrophy). The second way is to develop collateral vessels to bypass the aortic obstruction. As the child develops these alternate blood channels, the blood pressure and the cardiac work are reduced, and there is an improvement in blood supply to the abdominal organs, such as the liver, the gastrointestinal tract, and the kidneys.
Cardiovascular lesions can aggravate the heart’s burden associated with coarctation. The presence of a coarctation will increase the amount of blood flow across a ventricular septal defect, making a small hole act (as far as the heart is concerned) as if it were a large hole.

How is this problem diagnosed?
Clinical features of coarctation
Most children with coarctation have no symptoms. In older children, if symptoms are present, they are usually nonspecific and relate either to high blood pressure (hypertension) in the upper part of the body, causing headaches or frequent nose bleeds, or to reduced blood supply to the lower extremities (e.g., exercise-induced leg pain, claudication).
In infancy, coarctation can be associated with congestive heart failure. Although heart failure can develop in an infant at any time during the first six months, it typically develops during the first six weeks. The major features associated with heart failure are a rapid heart and respiratory rate and poor weight gain. The infant in heart failure needs to be diagnosed and treated immediately, since the infant rapidly can develop shock that can result in death.
Physical findings in coarctation
The hallmarks of coarctation of the aorta are absent leg pulses and a difference in blood pressure between the arms and the legs (i.e., high blood pressure in the arms and low to normal blood pressure in the legs). The typical heart murmur associated with a coarctation is a systolic murmur that is loudest in the back below the left shoulder blade (scapula). If a prominent back murmur is not heard and the child has a blood pressure difference between the arms and the legs, a coarctation located in the abdomen should be considered.
Laboratory findings in coarctation
The chest x-ray can be very helpful in suggesting the presence of coarctation of the aorta. However, the diagnosis usually is confirmed by an echocardiogram (a specialized ultrasound of the heart). A heart catheterization is performed only if the coarctation cannot be adequately documented by the echocardiogram or to treat the coarctation with the use of a balloon angioplasty.

How is coarctation of the aorta treated?
Management of a patient with coarctation of the aorta must be individualized. In children without symptoms, in whom a coarctation is diagnosed on routine examination, repair of the coarctation-either surgically or using balloon angioplasty at a cardiac catheterization-is not recommended before 18 to 24 months of age.
In the newborn or infant with coarctation who presents in congestive heart failure, initial treatment consists of stabilizing the infant with medications. These medications include agents that increase the strength of the heartbeat, inotropic agents, and agents that help the body remove excess fluids, diuretics. If the infant is less than two weeks of age, a medicine (prostaglandin E1) will be administered to keep open the ductus arteriosus. The most critically ill babies will require the use of a ventilator to assist with breathing. After a brief period of stabilization, all infants with coarctation and congestive heart failure require surgical repair.
Surgical repair involves removal of the narrowed segment of aorta. In some children, it is necessary to place a piece of artifical material (e.g., Dacron, Gore-Tex) to enlarge the area of narrowing or to bypass the area of narrowing. A balloon angioplasty is performed at the time of a heart catheterization. The angioplasty involves the placement of a special balloon catheter across the narrowed area and then inflating the balloon, thereby stretching open the aorta.

Why treat children with coarctation of the aorta?
Untreated coarctation of the aorta significantly reduces life expectancy, with death frequently occurring within a patient’s fourth to fifth decade. Causes of death in individuals with unoperated coarctation of the aorta include congestive heart failure, aortic rupture (the aorta bursts), bacterial endocarditis (an infection of the heart), and stroke.

What is the outlook for children with coarctation of the aorta?
The long-term outlook for children who have had their coarctation repaired, either with surgery or angioplasty, is excellent. Children who have successful repair of coarctation usually can live full and productive lives. Women usually can become pregnant safely. However, medical problems can occur after repair.
Recoarctation
Recoarctation is the redevelopment of a narrowing in the aorta. This problem occurs more commonly in children who have had their coarctation repaired during the first year of life. Recoarctation occurs in approximately 10% to 20% of children who have had their repair in infancy, and in less than 3% of children who have had their repair after 3 years of age. Treatment of recoarctation of the aorta usually is with a balloon angioplasty.
High blood pressure
High blood pressure is one of the most common medical problems seen in patients after successful repair of coarctation. Approximately 60% of people who have had their coarctation repaired will require medication to treat high blood pressure in adulthood.
Other medical problems
Other medical problems, which are seen rarely in people after successful repair of coarctation, include the development of aneurysms in the aorta, the early development of coronary artery disease, the development of disease to the aortic valve, and the development of a stroke.

References
Beekman R, Rocchini A. Coarctation of the aorta and interruption of the aortic arch. In: Moller J, Neal W, eds. Fetal, neonatal, and infant cardiac disease. Norwalk, CT: Appleton and Lange, 1990:497-521.
Keith J. Coarctation of the aorta. In: Keith J, Rowe R, Valad P, eds. Heart disease in infancy and children. New York: MacMillan, 1978.
About the Author
Dr. Rocchini received both his bachelor of science degree in chemical engineering and his medical degree from the University of Pittsburgh. He completed his pediatric residency at the University of Minnesota and his pediatric cardiology fellowship at the Children’s Hospital of Boston. Dr. Rocchini is currently a professor of pediatrics and serves as director of pediatric cardiology at the University of Michigan. His research interests include interventional cardiac catheterization and obesity-induced hypertension.
Copyright 2012 Albert P. Rocchini, M.D., All Rights Reserved

Congenital Hip Dysplasia

What is Developmental Dysplasia of the Hip?
What Causes Developmental Dysplasia of the Hip?
Who gets Developmental Dysplasia of the Hip?
What are the Symptoms of Developmental Dysplasia of the Hip?
How is Developmental Dysplasia of the Hip Diagnosed?
How is Developmental Dysplasia of the Hip Treated?
What are the Complications of Developmental Dysplasia of the Hip?

What is Developmental Dysplasia of the Hip?
Developmental dysplasia of the hip (aka Congenital Hip Dysplasia) is generally identified in the newborn period. The term describes a spectrum of hip problems that ranges from mild movement of the femur (upper leg bone) in the acetabulum (cartilaginous lining of the hip) to complete dislocation of the femur from the acetabulum. The femur is dependent on the proper formation of the acetabulum to help keep the femur in a stable environment. Instability (movement or subluxation) in the hip of a newborn can lead to abnormal development of the hip joint.
What Causes Developmental Dysplasia of the Hip?
Multiple factors may result in the development of an unstable hip joint. Children who have been in a breech position prior to delivery are at a higher risk of developing this condition. Low amniotic fluid (oligohydramnios) or a small uterus (in a first born child) may result in improper positioning of the femurs in respect to the hip joint.
Who gets Developmental Dysplasia of the Hip?
First-born female newborns are more prone to developing this condition. It generally occurs in 0.5 – 2% of all live births. The presence of a breech position or a positive family history are other factors that will increase the risk.
What are the Symptoms of Developmental Dysplasia of the Hip?
Your child’s health care provider will examine your infant at birth or at the two week visit for certain signs of a dysplastic hip. At times, the provider may identify a click with movement of the femur. This should not be mistaken for instability of the hip for 10% of normal newborns will have a click. As a child gets older, she or he may develop a limp, hip pain or, rarely, some degenerative disease in the hip if the condition is not treated properly.
How is Developmental Dysplasia of the Hip Diagnosed?
The Ortalani and Barlow maneuvers will be done by your child’s health practitioner to detect mild or significant subluxation of the hips. The symmetry of the gluteal fold (the fold of skin below each buttocks) is closely examined (although normal children can have an asymmetric fold). When your child’s practitioner is suspicious of dyplasia, an ultrasound of the hips will be obtained to look for abnormalities of the hip as well as subluxation.
How is Developmental Dysplasia of the Hip Treated?
A Pavlik harness can be used to align the femur and acetabulum so that proper growth and development of the hip joint can take place. This harness is effective 95% of the time if it is used prior to 6 months of age. The harness bends the legs at the knee, as well as bends the hip at approximately 90 degrees, placing the femur in an ideal location within the acetabular space. The harness is worn 24 hours a day for a minimum of 6 weeks.
A plain x-ray of the hip may occasionally be required to monitor the progress of the hip.
What are the complications of Developmental Dysplasia of the Hip?
In rare circumstances, a child will require surgery to repair the hip joint. Poor vascularization of the head of the femur is a rare complication.
References
American Academy of Pediatrics. Clinical Practice Guideline: Early Detection of Developmental Dysplasia of the Hip.
Reviewed by: Daniel J. Feiten MD
This Article contains the comments, views and opinions of the Author at the time of its writing and may not necessarily reflect the views of Pediatric Web, Inc., its officers, directors, affiliates or agents. No claim is made by Pediatric Web, the Author, or the Author’s medical practice regarding the effectiveness and reliability of the statements contained herein and such individuals and entities disclaim any and all liability for the comments and statements contained in this Article and for any use or misuse of the statements made in this article in any specific medical situations. Further, this Article is intended to be general in nature and shall not be considered medical advice. The statements made are not to be utilized to diagnose and/or treat any individual’s medical symptoms. If you or someone you know has symptoms which you believe are similar to this Article, you should discuss such symptoms with your personal physician or other qualified medical practitioner.

Coxsackie A16

http://children.webmd.com/hand-foot-and-mouth-disease-directory

 

Cyclic Vomiting Syndrome (CVS)

What is cyclic vomiting syndrome?
What causes cyclic vomiting syndrome?
Who gets cyclic vomiting syndrome?
What are the common findings?
How is cyclic vomiting syndrome diagnosed?
How is cyclic vomiting syndrome treated?
What are the complications?
How can cyclic vomiting syndrome be prevented?
What research is being done?
Links to other information?

B U.K. Li, M.D.
Director of Pediatric Gastroenterology
Children’s Memorial Hospital
Chicago, IL
What is cyclic vomiting syndrome?
Cyclic vomiting syndrome, or CVS, is a disorder characterized by recurrent and severe episodes of vomiting. Because its cause is unknown and there is not a laboratory test for it, this condition is considered a syndrome, rather than a disease.

What causes cyclic vomiting syndrome?
Currently, there is no known cause of CVS. The main theory to its cause is that CVS may be related to migraine headaches. It also is suspected that it is a “brain-gut” disorder in which a trigger within the brain signals the gut to begin vomiting. Other theories to its cause also are being investigated (see the What research is being done? section).

Who gets cyclic vomiting syndrome?
Children between the ages of 4 and 11 years most often are affected with CVS; however, newborns and adults can develop it. Slightly more girls than boys experience this syndrome.

What are the common findings?
The main symptom is relentless vomiting, often three to six times per hour at the peak of the worst episode. Many children state that the unremitting nausea is the worst symptom because they do not experience momentary relief from the vomiting.
Other common gastrointestinal symptoms include loss of appetite, nausea, dry heaving, and abdominal pain. Diarrhea occurs in one-third of the children who have CVS. Common general symptoms include paleness and listlessness.
Fever occurs in one-third of the children. Typical symptoms of migraine headaches and sensitivity to lights occur in less than one-half of those children who experience CVS. During these episodes, children are sicker than if they had the stomach flu.
There is a timing pattern to this syndrome. The episodes most often occur in the early morning hours, between 2 a.m. and 4 a.m., or upon awakening; however, they can occur at any time of the day.
The term “cyclic” refers to the predictable period between episodes. However, only one-half of the children have predictable intervals, most commonly every two or four weeks, and one-half of the children have attacks that occur at irregular intervals. Episodes rarely occur more than twice a week, and they can be as infrequent as 6 to 12 months apart.
The episodes can be triggered by various life events. The most common include viral infections, such as colds and sinusitis, and psychological stress that occurs at school or even during holidays, vacations, and birthdays.
Dietary cheese, chocolate and monosodium glutamate, long car rides, physical exhaustion, and allergies also trigger cause it. In teenage girls, menstruation can precipitate episodes.
Fortunately, CVS usually resolves itself as the child enters adolescence; however, it can persist into adulthood. In some cases, it begins in adulthood. For those children in whom it ss completely, one-third of them develop typical migraine headaches.

How is cyclic vomiting syndrome diagnosed?
A test to diagnose CVS is not available. At the first international symposium on CVS in 1994, an international committee developed its diagnostic criteria.
The three main criteria included are:
Recurrent, severe episodes of vomiting
Normal health between episodes
No cause of vomiting found on testing
The four supportive criteria included:
Each episode is similar to the other episodes
Episodes resolve if they are left untreated
Associated symptoms of nausea, abdominal pain, headache, motion sickness, and sensitivity to lights
Associated signs of fever, paleness, diarrhea, dehydration, and excess salivation
Most often, cyclic vomiting syndrome is confused with stomach flu or viral gastroenteritis. The symptoms of vomiting, when combined with fever and diarrhea, can be indistinguishable from those with the stomach flu. In addition, the physician often does not appreciate the overall pattern of recurrence.
Several serious disorders can be confused with CVS, including malrotation with volvulus (twisted and kinked small intestine), brain tumors, acute hydronephrosis (swelling of the kidneys), Addison’s disease (lack of cortisol hormone), various metabolic disorders (problems processing nutrition or waste products), and psychological disturbances.
Although a diagnostic test for CVS is not available, laboratory testing (blood and urine), x-rays (intestines, kidney, and brain), and endoscopic (stomach) testing can be used to exclude the most serious disorders. For example, if a twisted, or malrotated, intestine appears to be the cause of the vomiting, a child would be diagnosed with malrotation, not CVS.
A family physician, a pediatrician, a pediatric gastroenterologist, or a pediatric neurologist may arrange the specific tests. The amount of testing that is requested is up to the doctor’s best judgment.
How is cyclic vomiting syndrome treated?
Because there have not been definitive studies on treatment, there is not a standard recommended therapy for CVS. However, there are effective medications. Five approaches are used in treating CVS, including care during the episode itself, medicines to break the attack once it starts, avoidance of known triggers, medicines used to prevent the next episode, and family support.
The first two treatment approaches are discussed in this section. The second two treatment approaches are discussed in the How can cyclic vomiting syndrome be prevented? section. The final treatment approach is discussed in the Links to other information section.
Care during the episode
Intravenous sugar (dextrose) and fluids often help to correct dehydration. Although the pain can be severe, it usually does not require narcotic drugs. Although the vomiting can be lessened by medications, the nausea often persists. Sometimes, sedation with diphenhydramine, lorazepam, or chlorpromazine is the only way to lessen the nausea.
Medicines to break the attack
Medications used to break an attack are given at the start of the episode. They include anti-vomiting medicines, such as ondansetron and granisetron, which are administered intravenously, and promethazine and prochlorperazine, which are administered rectally or by shot.
Although widely used, the latter two drugs are not very effective in treating CVS. Anti-migraine medications can also be used. Oral agents, such as Midrin, are often ineffective because they are expelled by vomiting. Oral and nasal sumatriptan have been used in a few children with CVS, but they have not been studied for proper dosage, safety, or effectiveness.

What are the complications?
Fortunately, there does not appear to be serious long-term complications associated with CVS. However, despite being sick only intermittently, children miss 2 to 4 weeks of school and require intravenous fluids at the hospital 50% of the time. Unfortunately, the correct diagnosis of CVS typically is not made for two and one-half years.

How can cyclic vomiting syndrome be prevented?
Avoidance of known triggers
In a few cases, known triggers of CVS can be avoided to prevent episodes, e.g., having the parents eliminate chocolate and/or cheese from the child’s diet.
Medicines used to prevent episodes
To prevent episodes of CVS, migraine (propranolol, cyproheptadine, and amitriptyline), seizure (phenobarbital and phenytoin), or stomach (ranitidine, erythromycin, and cisapride) medications can be taken daily. Most of these medications have been studied in children, and they are widely used.
A physician should choose the appropriate medication, with the least amount of side effects, for a child. Although none of the medications are 100% effective, most of them reduce the severity of CVS in half of the children.

What research is being done?
The cause of CVS is unknown; it is not known whether it is a disorder of the brain, the gut, or another organ. There are several new theories about how CVS is caused, and research is being conducted on each theory. Many children with CVS may have an underlying, but atypical, migraine disorder that primarily causes vomiting and abdominal pain rather than headache.
Some children are thought to have a mitochondrial disorder (energy factory for each cell) that affects respiratory chain or fatty acid metabolism. Other children are thought to have a disorder of the hypothalamus (brain thermostat) that produces excess stress hormones.
Some children are thought to have a dysmotility (pumping disorder) of the intestinal tract. New medications to treat both vomiting and stress-induced disorders are being developed by pharmaceutical companies.

Links to other information?
Family support
Often, parents are stressed by this repetitive, unpredictable, and disruptive illness. They watch their child become ill and hospitalized, they do not know what is causing the illness, they miss work, and physicians often do not take the recurrent illness seriously. The parents and the child can benefit from the support of other families with the same illness.
Mailing Address:
Cyclic Vomiting Syndrome Association
Ms. Debra Waites, Administrator
3585 Cedar Hill Rd, NW
Canal Winchester, Ohio 43110
Phone: (614) 837-2586
Web Site: http://www.cvsaonline.org/
Listserv: majordomo@jatek.net

References
Fleisher DR, Matar M. The cyclic vomiting syndrome: a report of 71 cases and literature review. J Pediatr Gastroenterol Nutr 1993 Nov;17(4):361-9.
Li BUK, ed. Proceedings of the International Symposium on Cyclic Vomiting Syndrome J Pediatr Gastroenterol Nutr 1995;21(Suppl.):S1-S62.
Li BUK, Issenman RM, Sarna SK, eds. Proceedings of the 2nd International Symposium on Cyclic Vomiting Syndrome Dig Dis Sci 1999;44(Suppl.):1S-120S.
Li BUK, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Heterogeneity of diagnoses presenting as cyclic vomiting. Pediatrics 1998 Sep;102(3):583-7.
Li BUK, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Is cyclic vomiting syndrome related to migraine? J Pediatr 1999 May;134(5):567-72.
Author’s Biography
Fleisher DR, Matar M. The cyclic vomiting syndrome: a report of 71 cases and literature review. J Pediatr Gastroenterol Nutr 1993 Nov;17(4):361-9.
Li BUK, ed. Proceedings of the International Symposium on Cyclic Vomiting Syndrome J Pediatr Gastroenterol Nutr 1995;21(Suppl.):S1-S62.
Li BUK, Issenman RM, Sarna SK, eds. Proceedings of the 2nd International Symposium on Cyclic Vomiting Syndrome Dig Dis Sci 1999;44(Suppl.):1S-120S.
Li BUK, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Heterogeneity of diagnoses presenting as cyclic vomiting. Pediatrics 1998 Sep;102(3):583-7.
About the Author
Dr. Li is the Director of Gastroenterology at Children’s Memorial Hospital in Chicago, IL. He is Professor of Pediatrics at Northwestern University. His primary research interests are in Cyclic Vomiting Syndrome and outcomes in H. Pylori Gastritis. He is a fitness buff and a soccer dad on the side.
Copyright 2012 B U.K. Li, M.D., All Rights Reserved