Tag: Infant

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Laryngomalacia

A labeled anatomical diagram of the vocal fold...
A labeled anatomical diagram of the vocal folds or cords. (Photo credit: Wikipedia)

Definition:
Laryngomalacia is a softening of the tissues of the larynx (voice box) above the vocal cords. This softening causes the tissues to become floppy, and they may fall over the airway opening and partially block it.

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Laryngomalacia (literally, “soft larynx”) is a very common condition of infancy, in which the soft, immature cartilage of the upper larynx collapses inward during inhalation, causing airway obstruction. It can also be seen in older patients, especially those with neuromuscular conditions resulting in weakness of the muscles of the throat. However, the infantile form is much more common.

There are several types – the mildest may cause no problems, while the most severe can be associated with other abnormalities of the respiratory tract, and with neuromuscular and gastroenterological problems.

Symptoms:
Until the larynx becomes stronger, problems can arise for several reasons:

•The soft limp tissues of the larynx can collapse as the baby breathes in. This interrupts the flow of air and causes noisy breathing, with a sound called stridor, which is a sign of obstructed air flow – in fact laryngomalacia is the commonest cause of stridor in babies. It may be worse if the baby has a respiratory infection.

•In some children, laryngomalacia can interfere with feeding. The effort required to draw air in through the obstructed airway can cause reflux of food from the stomach back up into the oesophagus or gullet.

•There may be other ear, nose and throat problems, and rarely problems with the lungs. Low oxygen levels may disrupt normal growth.

Common symptoms are :-
*Nosy breathing (stridor) – An audible wheeze when your baby breathes in. It is often worse when the baby is agitated, feeding, *crying or sleeping on the back
*High pitched sound
*Difficulty feeding
*Poor weight gain
*Choking while feeding
*Apnea — Breathing stoppage
*Pulling in neck and check with each breath
*Cyanosis — Turning blue
*Gastroesophageal reflux — Spitting, vomiting and regurgitation
*Aspiration – Inhalation of food into the lungs

Causes:
Laryngomalacia is thought to be the result of abnormally slow maturation of the tissues of the larynx, possibly because of genetic factors. This simply means that at birth the baby’s respiratory tract isn’t developed and string enough to cope with the mechanical demands of drawing breath.

Although doctors believe there’s a link between laryngomalacia and gastro-oesophageal reflu, there isn’t a single common mechanism to link these two problems, so several theories exist. In some patients with laryngomalacia, reflux may be the primary cause of their airway problems. In others, it’s an additional factor on top of neurological or anatomical abnormalities.

Reflux is common in babies less than one year old, because the muscular valve at the entrance to the stomach (which holds food in the stomach) may be weak in small infants.

Research suggests that a very large number, if not all, of babies with laryngomalacia also have reflux of gastric acid and digestive enzymes up to the pharynx (back of the throat). This may have detrimental effects on the larynx and tracheobronchial tree (air passages into the lungs). This may cause persistent swelling (oedema) of the larynx lining, which is common in children with laryngomalacia.

There’s no consensus yet about managing this link, but it makes sense to think simple treatments to control reflux could help resolve the laryngomalacia more quickly, too. More interventional treatments such as surgery, with all their inherent risks, are best avoided if possible.

Although laryngomalacia is not associated with a specific gene, there is evidence that some cases may be inherited.

Diagnosis:
Your doctor will ask you some questions about your baby’s health problems and may recommend a test called a flexible laryngoscopy (lar ring os co pee) to further evaluate your baby’s condition.

During this test, done in your doctor’s office, a tiny camera that looks like a strand of spaghetti with a light on the end is passed through your baby’s nostril and into the lower part of the throat where the larynx is. This allows your doctor to see your baby’s voicebox.

After the diagnosis — additional tests:
If laryngomalacia is diagnosed, the doctor may want to do other diagnostic tests to evaluate the extent of your child’s problems and to see whether the lower airway is affected. These tests may include:

X-ray of the neck;
A neck X-ray is done to make sure that your baby does not have other problems below the voice box (in the subglottis, trachea or chest). These are areas that the doctor cannot see during the flexible laryngoscopy.

Airway fluoroscopy;
The doctor may also order a motion picture X-ray of the trachea to make sure that there are no other problems.

Microlaryngoscopy (my crow lar ring os co pee)and bronchoscopy (brawn cos co pee), also known as MLB
This test is done when a neck X-ray shows additional problems in the lower airway. Your child is taken to the operating room and given anesthesia. Then the doctor passes a tiny camera through your child’s mouth and down past the vocal cords (larynx) to look at the area below the vocal folds that may be contributing to the stridor (noisy breathing). The surgeon will take some pictures and will review the results with you afterward.

EGD or esophagogastroduodenoscopy pH probe
This test will be done if your child’s doctor suspects that there may be a more severe problem.

Treatment :
In almost all cases (99 percent), laryngomalacia resolves without treatment by the time your child is 18 to 20 months of age. However, if the laryngomalacia is severe, your child’s treatment may include medication or surgery.

Medication:
Your child’s GI doctor may prescribe an anti-reflux medication to help manage the gastroesophageal reflux (GERD). This is important because your child’s chronic neck and chest retractions from the laryngomalacia can worsen GERD. Also, the acid reflux can cause swelling above the vocal cords and worsen the noisy breathing.

Surgery:
Surgery is the treatment of choice if your child’s condition is severe. Symptoms that signal the need for surgery include:

*Life-threatening apneas (stoppages of breathing)

*Significant blue spells

*Failure to gain weight with feeding

*Significant chest and neck retractions

*Need for extra oxygen to breathe

*Heart or lung issues related to your child’s inability to get enough oxygen

Supraglottoplasty:
In this surgery, extra tissue above the vocal cords is trimmed in the operating room. Your child will be under general anesthesia while the surgeon does a thorough evaluation of the airway and removes the tissue. After surgery, your child will be taken to the pediatric intensive care unit (PICU) and will spend one night with a breathing tube in the nose. If there is not much swelling in this area, and if the surgeon feels it will be safe, the breathing tube will be removed the next day in the PICU. Your child will then be observed for another day to ensure that the airway is safe, and that your child is getting enough oxygen and is drinking normally.

This surgery may not completely eliminate the noisy breathing but it should help to:

*Reduce the severity of the symptoms

*Lessen the apneas (breathing stoppages)

*Reduce the extra oxygen requirements

*Improve swallowing

*Help your child gain weight.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://en.wikipedia.org/wiki/Laryngomalacia
http://www.chop.edu/service/airway-disorders/conditions-we-treat/laryngomalacia.html
http://www.bbc.co.uk/health/physical_health/conditions/laryngomalacia.shtml

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Ailmemts & Remedies Pediatric

Infant jaundice

Definition:
Infant jaundice is a yellow discoloration in a newborn baby’s skin and eyes. Infant jaundice occurs because the baby’s blood contains an excess of bilirubin (bil-ih-ROO-bin), a yellow-colored pigment of red blood cells. Jaundice isn’t a disease itself but the name given to the yellow appearance of skin and the conjunctiva (whites) of the eyes.

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Infant jaundice is a common condition, particularly in babies born before 38 weeks gestation (preterm babies) and breast-fed babies. Infant jaundice usually occurs because a baby’s liver isn’t mature enough to get rid of bilirubin in the bloodstream. In some cases, an underlying disease may cause jaundice.

Infant jaundice can be concerning as although the majority of causes are easily treated, some rarer causes are very serious. Also, high levels of unconjugated bilirubin can cause brain damage. This is virtually never seen now due to treatment with UVB light, but it means that it is very important that the baby receives proper treatment.

Types of Infant jaundice:
The most common types of jaundice are:

Physiological (normal) jaundice: occurring in most newborns, this mild jaundice is due to the immaturity of the baby’s liver, which leads to a slow processing of bilirubin. It generally appears at 2 to 4 days of age and disappears by 1 to 2 weeks of age.

Jaundice of prematurity: occurs frequently in premature babies since they are even less ready to excrete bilirubin effectively. Jaundice in premature babies needs to be treated at a lower bilirubin level than in full term babies in order to avoid complications.

Breastfeeding jaundice: jaundice can occur when a breastfeeding baby is not getting enough breast milk because of difficulty with breastfeeding or because the mother’s milk isn’t in yet. This is not caused by a problem with the breast milk itself, but by the baby not getting enough to drink.

Breast milk jaundice: in 1% to 2% of breastfed babies, jaundice may be caused by substances produced in their mother’s breast milk that can cause the bilirubin level to rise. These can prevent the excretion of bilirubin through the intestines. It starts after the first 3 to 5 days and slowly improves over 3 to 12 weeks.

Symptoms:
The main symptom of jaundice is yellow colouring of the skin and conjunctiva of the eyes. Jaundice can also make babies sleepy which can lead to poor feeding. Poor feeding can make jaundice worse as the baby can become dehydrated.

If a baby has conjugated jaundice, it may have white chalky stool (poo) and urine that is darker than normal. (The bilirubin that normally colours the stool is excreted in the urine.)

Medical advise should be sought urgently if:
•Jaundice is present in the first 24 hours of life
•Jaundice is present when the baby is 10 days old
•The baby has problems feeding or is very sleepy
•The stools are pale or the urine is very dark

Causes:
The main cause of jaundice is:
Excess bilirubin (hyperbilirubinemia). Bilirubin is the substance that causes the yellow color of jaundice. It’s a normal part of the waste produced when “used” red blood cells are broken down. Normally, the liver filters bilirubin from the bloodstream and releases it into the intestinal tract. Before birth, a mother’s liver removes bilirubin from the baby’s blood. The liver of a newborn is immature and often can’t remove bilirubin quickly enough, causing an excess of bilirubin. Jaundice due to these normal newborn conditions is called physiologic jaundice, and it typically appears on the second or third day of life.Other causes

A baby may have an underlying disorder that is causing jaundice. In these cases, jaundice often appears much earlier or much later than physiologic jaundice.

Diseases or conditions that can cause jaundice include:
*Internal bleeding (hemorrhage)
*An infection in your baby’s blood (sepsis)
*Other viral or bacterial infections
*An incompatibility between the mother’s blood and the baby’s blood
*A liver malfunction
*An enzyme deficiency
*An abnormality of your baby’s red blood cells

Risk Factors:
Problems with the blood may lead to a rapid breakdown of cells (haemolysis) – if the mother’s blood type isn’t compatible with her baby’s. For example, she may make antibodies that attack and destroy her baby’s red blood cells.

Hormone deficiencies such as low levels of thyroid hormone (hypothyroidism) or pituitary gland hormones (hypopituitarism) can trigger jaundice.

There may be inherited genetic problems with the enzymes that convert or break down bilirubin – these include rare conditions such as Crigler-Najjar syndrome, Gilbert’s syndrome, galactosaemia and tyrosinaemia.

There may be problems with the liver, such as biliary atresia, in which the tubes that drain bile from the liver are blocked. If spotted early, an operation can prevent long-term damage (which is why it is important to investigate jaundice that is still there at 10 days).

Diagnosis:
Doctors, nurses, and family members will watch for signs of jaundice at the hospital, and after the newborn goes home.

Any infant who appears jaundiced should have bilirubin levels measured right away. This can be done with a blood test.

Many hospitals check total bilirubin levels on all babies at about 24 hours of age. Hospitals use probes that can estimate the bilirubin level just by touching the skin. High readings need to be confirmed with blood tests.

Tests that will likely be done include:
•Complete blood count
•Coomb’s test
•Reticulocyte count
Further testing may be needed for babies who need treatment or whose total bilirubin levels are rising more quickly than expected.

Treatment:
Treatment is usually not needed.

When determining treatment, the doctor must consider:

•The baby’s bilirubin level
•How fast the level has been rising
•Whether the baby was born early (babies born early are more likely to be treated at lower bilirubin levels)
•How old the baby is now
Your child will need treatment if the bilirubin level is too high or is rising too quickly.

Keep the baby well hydrated with breast milk or formula. Frequent feedings (up to 12 times a day) encourage frequent bowel movements, which help remove bilirubin through the stools. Ask your doctor before giving your newborn extra formula.

Some newborns need to be treated before they leave the hospital. Others may need to go back to the hospital when they are a few days old. Treatment in the hospital usually lasts 1 to 2 days.

Sometimes special blue lights are used on infants whose levels are very high. This is called phototherapy. These lights work by helping to break down bilirubin in the skin.

The infant is placed under artificial light in a warm, enclosed bed to maintain constant temperature. The baby will wear only a diaper and special eye shades to protect the eyes. The American Academy of Pediatrics recommends that breastfeeding be continued through phototherapy, if possible. Rarely, the baby may have an intravenous (IV) line to deliver fluids.

If the bilirubin level is not too high or is not rising quickly, you can do phototherapy at home with a fiberoptic blanket, which has tiny bright lights in it. You may also use a bed that shines light up from the mattress.

•You must keep the light therapy on your child’s skin and feed your child every 2 to 3 hours (10 to 12 times a day).
•A nurse will come to your home to teach you how to use the blanket or bed, and to check on your child.
•The nurse will return daily to check your child’s weight, feedings, skin, and bilirubin levels.
•You will be asked to count the number of wet and dirty diapers.
In the most severe cases of jaundice, an exchange transfusion is required. In this procedure, the baby’s blood is replaced with fresh blood. Treating severely jaundiced babies with intravenous immunoglobulin may also be very effective at reducing bilirubin levels.

Prognosis:
Usually newborn jaundice is not harmful. For most babies, jaundice usually gets better without treatment within 1 to 2 weeks.

Very high levels of bilirubin can damage the brain. This is called kernicterus. However, the condition is almost always diagnosed before levels become high enough to cause this damage.

For babies who need treatment, the treatment is usually effective

Possible Complications:–
Rare, but serious, complications from high bilirubin levels include:

•Cerebral palsy
•Deafness
•Kernicterus — brain damage from very high bilirubin levels

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/001559.htm
http://www.mayoclinic.com/health/infant-jaundice/DS00107
http://www.bbc.co.uk/health/physical_health/conditions/jaundice2.shtml

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Group B Streptococcus (GBS) Infection

Definition:
Infection with Group B Streptococcus (GBS), also known as ‘Streptococcus agalactiae’ and more colloquially as Strep B and group B Strep, can cause serious illness and sometimes death, especially in newborn infants, the elderly, and patients with compromised immune systems. Group B streptococci are also prominent veterinary pathogens, because they can cause bovine mastitis (inflammation of the udder) in dairy cows. The species name “agalactiae” meaning “no milk”, alludes to this.

Streptococcus is a genus of spherical, Gram-positive bacteria of the phylum Firmicutes. Streptococcus agalactiae is a gram-positive streptococcus characterized by the presence of Group B Lancefield antigen, and so takes the name Group B Streptococcus.

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This type of bacteria (not to be confused with group A strep which causes “strep throat”) is commonly found in the human body, and it usually does not cause any symptoms. However, in certain cases it can be a dangerous cause of various infections that affect pregnant women & their newborns .

Group B streptococcal infections affect one in 2,000 babies born every year in the UK and Ireland. About 340 babies a year will develop group B streptococcal infection within seven days of birth (early group B streptococcus disease).

Causes:
The bacteria is found living harmlessly in the vaginal and gastrointestinal tracts of up to 50 per cent of healthy women (and in many men too). It may be passed on to a baby either while the baby is still in the womb or during delivery. Although about 50 per cent of babies born to mothers carrying group B streptococcus pick up the micro-organism, only about one to two per cent of these newborns then go on to develop severe group B streptococcal disease.

Group B streptococcal sepsis is most likely to develop when the baby is premature or if there has been prolonged rupture of the membranes, with many hours passing before the baby is born, or if the baby has no antibodies to group B streptococci.

In the last 30 years it’s been show to be a cause of serious infection in non-pregnant adults too. It’s extremely rare in healthy people and is almost always associated with underlying problems such as diabetes or cancer, or less often, problems with:

•Heart and blood vessels
•Genitourinary system
•Liver disease
•Kidney disease

About five per cent of affected adults will eventually experience a second episode of group B streptococcal disease.

How is group B strep transmitted?
In newborns, GBS infection is acquired through direct contact with the bacteria while in the uterus or during delivery; thus the infection is transmitted from the colonized mother to her newborn. However, not every baby born to a colonized mother will develop GBS infection. Statistics show that about one of every 100-200 babies born to a GBS-colonized mother will develop GBS infection.

There are maternal risk factors, however, that increase the chance of transmitting the disease to the newborn:

•labor or membrane rupture before 37 weeks
•membrane rupture more than 18 hours before delivery
•urinary tract infection with GBS during pregnancy
•previous baby with GBS infection
•fever during labor
•positive culture for GBS colonization at 35-37 weeks
.
Group B strep infection is not a sexually transmitted disease (STD).

Symptoms :
If a pregnant woman is carrying (or ‘colonised with’) group B streptococcus, there is a chance she could pass it to her unborn baby. Most babies will not be harmed and will simply carry the bacteria themselves, but it can cause:

•Early birth
•Stillbirth
•Late miscarriage and complications
Group B streptococcal disease in newborns is divided into early and late disease. Early group B streptococcal neonatal sepsis appears within 24 hours of delivery (and up to seven days afterwards) and accounts for over 80 per cent of cases. Typically it causes signs of pneumonia (breathing problems) or, less often, meningitis. Most of these babies will make a full recovery.

Late group B streptococcal neonatal sepsis appears between one week and three months after birth, and is more likely to cause meningitis. One in ten infected babies will die of blood poisoning, pneumonia or meningitis, while one in five will be affected permanently by cerebral palsy, blindness, deafness or serious learning difficulties.

Once a baby has reached three months of age, group B streptococcal infection is extremely rare.

In vulnerable adults, group B streptococcus can cause a range of different infections at different sites in the body.

Diagnosis:
In pregnant women, routine screening for colonization with GBS is recommended. This test is generally performed between 35-37 weeks of gestation. The test involves using a swab to collect a sample from both the vaginal and rectal area, and results are usually available within 24-72 hours.

In newborns, GBS infection can be diagnosed with blood tests and/or spinal-fluid analysis. Similar testing may be used to diagnose the disease in adults.

Treatment:
For women who test positive for GBS during pregnancy and for those with certain risk factors for developing or transmitting GBS infection during pregnancy, intravenous antibiotics are generally recommended at the time of labor (before delivery). The administration of antibiotics has been shown to significantly decrease GBS infection in newborns. If a pregnant carrier of GBS receives intravenous antibiotics prior to delivery, her baby has a one in 4,000 chance of developing GBS infection. Without antibiotics, her baby has a one in 200 chance of developing GBS infection.

In adults who develop GBS infection, whether they are pregnant women or individuals with chronic medical conditions, intravenous(IV) antibiotics are also recommended.

At this point in time, the best treatment for GBS infection is prevention through routine screening during pregnancy. This testing has served to decrease the overall number of GBS infections in newborns, and there is currently research underway to develop a GBS vaccine.

Should all at-risk women be treated?
Some women prefer not to receive antibiotics if their risk is only slightly increased. Experts advise that the risk of infection in the baby must be balanced against the wishes and beliefs of the woman in labour and against her risk of an adverse reaction to the antibiotics. If a group B streptococcus carrying woman had a healthy baby in a previous pregnancy, she is unlikely to be at greater risk with following pregnancies.

Scientists are trying to develop a vaccine for group B streptococcus, but technical problems mean that it’s likely to be some years before one is available.

Prevention:
Through collaborative efforts clinicians, researchers, professional organizations, parent advocacy groups, and the public health community developed recommendations for intrapartum prophylaxis to prevent perinatal GBS disease. Many organizations have developed perinatal GBS disease prevention and education programs to reduce the incidence of the disease. Information about the recommendations and the prevention programs can be found in medical journals and on the internet. Simple anti-septic wipes do not prevent mother-to-child transmission

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.medicinenet.com/group_b_strep/article.htm
http://www.bbc.co.uk/health/physical_health/conditions/group_b_streptococcus_infection.shtml
http://en.wikipedia.org/wiki/Group_B_streptococcal_infection
http://www.trying-to-conceive.com/pregnancy/preventing-group-b-strep-%E2%80%93-is-it-possible/
http://www.medicaldaily.com/news/20110211/5422/third-trimester-group-b-streptococcus-test-doesnt-accurately-predict-presence-during-labor.htm

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Feeding Problems

Definition:–
Feeding problem of infancy or early childhood is characterized by the failure of an infant or child under six years of age to eat enough food to gain weight and grow normally over a period of one month or more. The disorder can also be characterized by the loss of a significant amount of weight over one month. Feeding disorder is similar to failure to thrive, except that no medical or physiological condition can explain the low food intake or lack of growth.
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Infants and children with a feeding disorder fail to grow adequately, or even lose weight with no underlying medical explanation. They do not eat enough energy or nutrients to support growth and may be irritable or apathetic. Factors that contribute to development of a feeding disorder include lack of nurturing, failure to read the child’s hunger and satiety cues accurately, poverty, or parental mental illness. Successful treatment involves dietary, behavioral, social, and psychological intervention by a multidisciplinary

Feeding problems are common throughout childhood and affect both boys and girls.

Causes:–
The kind of feeding problem may depend on the age of the child.

Some new mothers take a while to get the hang of breastfeeding and may worry they’re not producing sufficient milk or their baby isn’t satisfied. But as long as the baby is gaining weight at the normal rate, there’s no need for concern.

Occasionally, early feeding problems are due to anatomical difficulties (for example, a severe cleft palate or oesophageal atresia) or more general illness, but these are usually quickly identified.

Minor infections, such as a cold, can interrupt established feeding patterns, but rarely for long.

Gastro-oesophageal reflux disease (GORD) can also make feeding difficult, affect weight gain and cause great stress for parents.

More serious conditions can interfere with the absorption of food and weight gain, including coeliac disease, cystic fibrosis, inflammatory bowel disease and food intolerance.

In toddlers and older children, emotional and social factors can cause feeding problems. Older children, especially girls, are more likely to develop eating disorders such as anorexia nervosa and bulimia.

Symptoms:–
The symptoms of feeding disorders can vary, but common symptoms include:

•Refusing food
•Lack of appetite
•Colic
•Crying before or after food
•Failing to gain weight normally
•Regurgitating or vomiting
•Diarrhoea
•Abdominal pain
•Constipation
•Behavioural problems

Diagnosis :–
Between 25% and 35% of normal children experience minor feeding problems. In infants born prematurely, 40% to 70% experience some type of feeding problem. For a child to be diagnosed with feeding disorder of infancy or early childhood, the disorder must be severe enough to affect growth for a significant period of time. Generally, growth failure is considered to be below the fifth percentile of weight and height.

Feeding disorder of infancy or early childhood is diagnosed if all four of the following criteria are present:

•Failure to eat adequately over one month or more, with resultant weight loss or failure to gain weight.
•Inadequate eating and lack of growth not explained by any general medical or physiological condition, such as gastrointestinal problems, nervous system abnormalities, or anatomical deformations.
•The feeding disorder cannot be better explained by lack of food or by another mental disorder, such as rumination disorder.
•The inadequate eating and weight loss or failure to gain weight occurs before the age of six years. If feeding behavior or weight gain improves when another person feeds and cares for the child, the existence of a true feeding disorder, rather than some underlying medical condition, is more likely.

Treatments :-
Successful treatment of feeding disorders requires a multidisciplinary team approach to assess the child’s needs and to provide recommendations and education to improve feeding skills, behavior, and nutrient intake. The multidisciplinary team for treatment of feeding disorders in childhood usually includes physicians specializing in problems of the gastrointestinal tract or of the ear, nose, and throat; a dietitian, a psychologist , a speech pathologist, and an occupational therapist. Support from social workers and physicians in related areas of medicine is also helpful.

An initial evaluation should focus on feeding history, including detailed information on type and timing of food intake, feeding position, meal duration, energy and nutrient intake, and behavioral and parental factors that influence the feeding experience. Actual observation of a feeding session can give valuable insight into the cause of the feeding disorder and appropriate treatments. A medical examination should also be conducted to rule out any potential medical problems or physical causes of the feeding disorder.

After a thorough history is taken and assessment completed, dietary and behavioral therapy is started. The goal of diet therapy is to gradually increase energy and nutrient intake as tolerated by the child to allow for catch up growth. Depending on the diet history, energy and nutrient content of the diet may be kept lower initially to avoid vomiting and diarrhea. As the infant or child is able to tolerate more food, energy and nutrient intake is gradually increased over a period of one to two weeks, or more. Eventually, the diet should provide about 50% more than normal nutritional needs of infants or children of similar age and size.

Behavioral therapy can help the parent and child overcome conditioned feeding problems and food aversions. Parents must be educated to recognize their child’s hunger and satiety cues accurately and to promote a pleasant, positive feeding environment. Changing the texture of foods, the pace and timing of feedings, the position of the body, and even feeding utensils can help the child overcome aversions to eating. If poverty, abuse, or parental mental illness contribute to the feeding disorder, these issues must also be addressed.

Prognosis :-
If left untreated, infants and children with feeding disorders can have permanent physical, mental, and behavioral damage. However, most children with feeding disorders show significant improvements after treatment, particularly if the child and parent receive intensive nutritional, psychological, and social intervention.

Prevention :-
Providing balanced, age-appropriate foods at regular intervals—for example, three meals and two or three snacks daily for toddlers—can help to establish healthy eating patterns. If a child is allowed to fill up on soft drinks, juice, chips, or other snacks prior to meals, appetite for other, more nutritious foods will decrease.

Positive infant and childhood feeding experiences require the child to communicate hunger and satiety effectively and the parent or caregiver to interpret these signals accurately. This set of events requires a nurturing environment and an attentive, caring adult. Efforts should be made to establish feeding as a positive, pleasant experience. Further, forcing a child to eat or punishing a child for not eating should be avoided.

You may click to see :

*Feeding Problems in Infants and Children…
*Problems feeding your baby?

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/feedingproblems2.shtml
http://www.minddisorders.com/Del-Fi/Feeding-disorder-of-infancy-or-early-childhood.html

http://www.brighttomorrowstoday.com/behavior-feeding-therapy.html

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Ailmemts & Remedies Pediatric

Tetralogy of Fallot

Definition:
Tetralogy of Fallot (TOF) is an abnormality of the heart and major blood vessels, which may be found in babies.

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It’s one of the most complex heart problems, as there are four different abnormalities (hence the term ‘tetralogy’):

•A large ventricular septal defect – one of the more serious types of hole in the heart, in which there is a connection between the two main pumping chambers of the heart (ventricles)

•Narrowing of the pulmonary valve (pulmonary stenosis) – this means the heart has to work harder to pump blood into the lungs to collect oxygen

•Right ventricular hypertrophy – thickening of the muscle wall of the right ventricle

•A displaced aorta – the major blood vessel that takes blood out of the heart and directs it around the body

Although these are the main problems, every child is different and there may be all sorts of other abnormalities.

Tetralogy of Fallot occurs in approximately 400 per million live births.

It was described in 1672 by Niels Stensen, in 1773 by Edward Sandifort, and in 1888 by the French physician Étienne-Louis Arthur Fallot, for whom it is named.

Symptoms:
Tetralogy of Fallot symptoms vary, depending on the extent of obstruction of blood flow out of the right ventricle and into the lungs. Signs and symptoms may include:

click to see the pictures

You may click to see different pictures of  Tetralogy of Fallot

*A bluish coloration of the skin caused by blood low in oxygen (cyanosis)

*Shortness of breath and rapid breathing, especially during feeding

*Loss of consciousness (fainting)

*Clubbing of fingers and toes — an abnormal, rounded shape of the nail bed

*Poor weight gain

*Tiring easily during play

*Irritability

*Prolonged crying

*A heart murmur

Tet spells
Sometimes, babies with tetralogy of Fallot will suddenly develop deep blue skin, nails and lips after crying, feeding, having a bowel movement, or kicking his or her legs upon awakening. These episodes are called “Tet spells” and are caused by a rapid drop in the amount of oxygen in the blood. Toddlers or older children may instinctively squat when they are short of breath. Squatting increases blood flow to the lungs. Tet spells are more common in young infants, around 2 to 4 months old.

Seek medical help if you notice that your baby has the following symptoms:

*Difficulty breathing

*Bluish discoloration of the skin

*Passing out or seizures

*Weakness

*Unusual irritability

If your baby becomes blue (cyanotic), immediately place your child on his or her side and pull the knees up to the chest. This helps increase blood flow to the lungs.

Causes:–
The cause of TOF isn’t fully understood. While a baby is in the womb, something interferes with the development of the heart and major blood vessels.

Its cause is thought to be due to environmental or genetic factors or a combination. It is associated with chromosome 22 deletions and DiGeorge syndrome.

Specific genetic associations include:

JAG1[4]
NKX2-5[5]
ZFPM2[6]
VEGF[7]
It occurs slightly more often in males than in females.

Embryology studies show that it is a result of anterior malalignment of the aorticopulmonary septum, resulting in the clinical combination of a VSD, pulmonary stenosis, and an overriding aorta. Right ventricular hypertrophy results from this combination, which causes resistance to blood flow from the right ventricle.

Although no specific single genetic abnormality has yet been found to explain every case, genetics often do play a part in these types of malformations (known as conotruncal abnormalities). In some children, a particular genetic problem can be identified, such as DiGeorge syndrome, where a small piece of chromosome 22 is lost or deleted.

Some researchers have suggested that TOF is caused by an autosomal recessive gene that has yet to be identified and which has variable penetrance (that is, it doesn’t always cause disease).

However, this is far from proven and TOF has also been linked to environmental factors such as certain medications or alcohol taken by the mother while pregnant.

Whatever the cause, in those families who have a child with TOF, the risk of a second child being born with the condition is only increased very slightly.

Risk factors:-
While the exact cause of tetralogy of Fallot is unknown, several factors may increase the risk of a baby being born with this condition. These include:

*A viral illness in the mother, such as rubella (German measles), during pregnancy

*Maternal alcoholism

*Poor nutrition

*A mother older than 40

*A parent with tetralogy of Fallot

*Babies who are also born with Down syndrome or DiGeorge syndrome

Diagnosis:-
The abnormal “coeur-en-sabot” (boot-like) appearance of a heart with tetralogy of Fallot is easily visible via chest x-ray, and before more sophisticated techniques became available, this was the definitive method of diagnosis. Congenital heart defects are now diagnosed with echocardiography, which is quick, involves no radiation, is very specific, and can be done prenatally.

Treatment:-
Emergency management of tet spells:

Prior to corrective surgery, children with tetralogy of Fallot may be prone to consequential acute hypoxia (tet spells), characterized by sudden cyanosis and syncope. These may be treated with beta-blockers such as propranolol, but acute episodes may require rapid intervention with morphine to reduce ventilatory drive and a vasopressor such as epinephrine, phenylephrine, or norepinephrine to increase blood pressure. Oxygen is effective in treating spells because it is a potent pulmonary vasodilator and systemic vasoconstrictor. This allows more blood flow to the lungs. There are also simple procedures such as squatting and the knee chest position which increases aortic wave reflection, increasing pressure on the left side of the heart, decreasing the right to left shunt thus decreasing the amount of deoxygenated blood entering the systemic circulation.

Palliative surgery:
The condition was initially thought untreatable until surgeon Alfred Blalock, cardiologist Helen B. Taussig, and lab assistant Vivien Thomas at Johns Hopkins University developed a palliative surgical procedure, which involved forming an anastomosis between the subclavian artery and the pulmonary artery (See movie “Something the Lord Made”).  It was actually Helen Taussig who convinced Alfred Blalock that the shunt was going to work. This redirected a large portion of the partially oxygenated blood leaving the heart for the body into the lungs, increasing flow through the pulmonary circuit, and greatly relieving symptoms in patients. The first Blalock-Thomas-Taussig shunt surgery was performed on 15-month old Eileen Saxon on November 29, 1944 with dramatic results.

The Potts shunt  and the Waterston-Cooley shunt  are other shunt procedures which were developed for the same purpose. These are no longer used.

Currently, Blalock-Thomas-Taussig shunts are not normally performed on infants with TOF except for severe variants such as TOF with pulmonary atresia (pseudotruncus arteriosus).

…

Total surgical repair:
The Blalock-Thomas-Taussig procedure, initially the only surgical treatment available for Tetralogy of Fallot, was palliative but not curative. The first total repair of Tetralogy of Fallot was done by a team led by C. Walton Lillehei at the University of Minnesota in 1954 on a 11-year-old boy. Total repair on infants has had success from 1981, with research indicating that it has a comparatively low mortality rate.

Total repair of Tetralogy of Fallot initially carried a high mortality risk. This risk has gone down steadily over the years. Surgery is now often carried out in infants one year of age or younger with less than 5% perioperative mortality. The open-heart surgery is designed (1) to relieve the right ventricular outflow tract stenosis by careful resection of muscle and (2) to repair the VSD with a Gore-Tex patch or a homograft. Additional reparative or reconstructive surgery may be done on patients as required by their particular cardiac anatomy

Prognosis:-
Untreated, Tetralogy of Fallot rapidly results in progressive right ventricular hypertrophy due to the increased resistance on the right ventricle. This progresses to heart failure (dilated cardiomyopathy) which begins in the right heart and often leads to left heart failure. Actuarial survival for untreated Tetralogy of Fallot is approximately 75% after the first year of life, 60% by four years, 30% by ten years, and 5% by forty years.

Patients who have undergone total surgical repair of Tetralogy of Fallot have improved hemodynamics and often have good to excellent cardiac function after the operation with some to no exercise intolerance (New York Heart Association Class I-II). Surgical success and long-term outcome greatly depends on the particular anatomy of the patient and the surgeon’s skill and experience with this type of repair.

Ninety percent of patients with total repair as infants develop a progressively leaky pulmonary valve as the heart grows to its adult size but the valve does not. Patients also may have damage to the electrical system of the heart from surgical incisions if the middle cardiac nerve is accidentally tapped during surgery. If the nerve is touched, it will cause abnormalities as detected by EKG and/or arrhythmias.

Long-term follow up studies show that patients with total repair of TOF are at risk for sudden cardiac death and for heart failure. Therefore, lifetime follow-up care by an adult congenital cardiologist is recommended to monitor these risks and to recommend treatment, such as interventional procedures or re-operation, if it becomes necessary.

The use of antibiotics is no longer required by cardiologists and varies from case to case.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:–
http://www.bbc.co.uk/health/physical_health/conditions/fallotstetralogy.shtml
http://en.wikipedia.org/wiki/Tetralogy_of_Fallot
http://www.drattawarsandeep.com/tetralogy_of_fallot.php
http://www.mayoclinic.com/health/tetralogy-of-fallot/DS00615/DSECTION

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