Tag Archives: Sudden infant death syndrome

Plagiocephaly

Definition:
The skull isn’t perfectly smooth – it’s covered with lumps, dips and some flatter areas. But sometimes a large area of flattening distorts the skull, making it look parallelogram-shaped. This is known as plagiocephaly.

The most common form is positional plagiocephaly. It occurs when a baby’s head develops a flat spot due to pressure on that area. Babies are vulnerable because their skull is soft and pliable when they’re born.

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Positional plagiocephaly typically develops after birth when babies spend time in a position that puts pressure on one part of the skull. Because babies spend so much time lying on their back, for example, they may develop a flat spot where their head presses against the mattress.

Starting in the early 1990s, parents were told to put their babies to sleep on their back to reduce the risk of SIDS. While this advice has saved thousands of babies’ lives, experts have noticed a fivefold increase in misshapen heads since then.

More rarely, babies develop positional plagiocephaly when movement in the uterus is constricted for some reason – because their mother is carrying more than one baby, for example. It can also happen to breech babies who get wedged under their mother’s ribs.

Another type of plagiocephaly is craniosynostosis, a birth defect in which the joints between the bones of the skull close early. Babies born with craniosynostosis need surgery to allow their brain to grow properly.

Symptoms
Plagiocephaly may become apparent at different ages, depending on the cause. Some babies are born with a flat head (this may be a temporary deformity due to the baby’s passage down the birth canal), while others develop it later as the bones of the skull fuse. The abnormal shape can best be seen if you look down on the baby’s head from above.

Signs of plagiocephaly include:
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•Parallelogram-shaped skull when viewed from above
•Flattening on one side at the back of the head, with a compensatory protrusion or bulge in the forehead on the same side
•Eyes appearing to have unequal positioning
•A bald spot on flattened side (may be asymmetrical)

To learn more you may click to see :Plagiocephaly, Brachycephaly, Brachycephaly with Plagiocephaly and Scaphocephaly

Causes & Risk Factors:
A baby’s skull is very soft and can be forced to grow in different directions fairly easily. When the skull is kept in one particular position for long periods – because the baby is sleeping in a set position (such as on his back) or because muscles attached to the skull go into spasm (known as torticollis) – areas of the skull may be squashed or pulled flat. This is known as positional or deformation plagiocephaly. It generally gets better by itself over time.

Other factors that increase the risk of plagiocephaly include a multiple birth pregnancy (as the babies ‘squash together’ in the womb), prematurity, poor muscle tone and a condition known as oligohydramnios, where there’s insufficient fluid in the womb to cushion the baby.

In the US at least, plagiocephaly has become more common in recent years. Statistics show that while one in 300 healthy infants was affected in 1992, by 1999 one in 60 had the condition.

This increase is thought to be due to the Back to Sleep campaign, designed to reduce the number of sudden infant deaths (cot deaths).

It’s possible to prevent positional plagiocephaly by changing your baby’s resting position frequently. Your baby still needs to be laid on their back to sleep, but try to alternate the position of the head and encourage them to spend time on their tummy while they’re awake and supervised.

Switch between putting them in a sloping chair, car seat or sling, or on a flat surface, so there’s no constant pressure on one area of the skull.Prolonge keeping the baby in the carseat is  very dengerous for the babies.

Plagiocephaly may also be caused by the bones of the skull joining together abnormally early. These bones normally grow together slowly so the skull expands in all directions. But if some fuse too soon (craniosynostosis), that part of the skull can’t grow in the way it should, pulling the head out of shape. This may occur in isolation, or as part of a genetic syndrome such as Apert syndrome or Crouzon syndrome.

Many vaginally delivered babies are born with an oddly shaped head caused by the pressure of passing through the birth canal. This usually corrects itself within about six weeks. But if your baby’s head hasn’t rounded out by age 6 weeks – or if you first notice that your baby has a flat spot on her skull after 6 weeks of age – it’s probably a case of positional plagiocephaly.

Plagiocephaly shows up most often in babies who are reported to be “good sleepers,” babies with unusually large heads, and babies who are born prematurely and have weak muscle tone.

Babies with torticollis can also develop a flat spot on their skull because they often sleep with their head turned to one side. Torticollis occurs when a tight or shortened muscle on one side of the neck causes the chin to tilt to the other side. Premature babies are especially prone to torticollis

Diagnosis:
Most often, your child’s doctor can make the diagnosis of positional plagiocephaly simply by examining your child’s head, without having to order lab tests or X-rays. The doctor will also note whether regular repositioning of your child’s head during sleep successfully reshapes the child’s growing skull over time, whereas craniosynostosis, on the other hand, typically worsens over time.

If there’s still some doubt, X-rays or a CT scan of the head will show your child’s doctor if the skull bones are normally separated or if they fused together too soon. If the bones aren’t fused, the doctor will probably rule out craniosynostosis and confirm that the child has positional plagiocephaly.

It’s important the type and cause of plagiocephaly are determined, as each requires different treatment. X-rays, CT scans and other tests may be needed to confirm diagnosis.

Treatment:
The condition will sometimes improve as the baby grows, but in many cases, treatment can significantly improve the shape of a baby’s head. Initially, treatment usually takes the form of reducing the pressure on the affected area through repositioning of the baby onto his or her tummy for extended periods of time throughout the day. Other treatments include repositioning the child’s head throughout the day so that the rounded side of the head is placed dependent against the mattress, repositioning cribs and other areas that infants spend time in so that they will have to look in a different direction to see their parents, or others in the room, repositioning mobiles and other toys for similar reasons, and avoiding extended time sleeping in car-seats (when not in a vehicle), bouncy seats, or other supine seating which is thought to exacerbate the problem. If the child appears to have discomfort or cries when they are repositioned, they may have a problem with the neck.  If this is unsuccessful, treatment using a cranial remoulding orthosis (baby helmet) can help to correct abnormal head shapes. These helmets are used to treat deformational plagiocephaly, brachycephaly, scaphocephaly and other head shape deformities in infants 3-18 months of age. For years, infants have been successfully treated with cranial remolding orthoses. A cranial remolding orthoses (helmet) provides painless total contact over the prominent areas of the skull and leaves voids over the flattened areas to provide a pathway for more symmetrical skull growth. Treatment generally takes 3-4 months, but varies depending on the infant’s age and severity of the cranial asymmetry.

Prognosis:
There are some beginning studies that indicate that babies with plagiocephaly tend to have learning difficulties later on in school, however these studies are still early, and do not yet represent a scientific consensus. Other more complete studies suggest that there is no evidence to suggest that plagiocephaly is harmful to brain development, vision, or hearing

Prevention:

To successfully prevent Plagiocephaly, prenatal education on skull deformation   is crucial.
Being aware of preventative measures can help reduce the chance your child will develop positional plagiocephaly. Different repositioning techniques and adequate Tummy Time are keys to prevention and also help your baby meet developmental milestones.

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/plagiocephaly2.shtml
http://en.wikipedia.org/wiki/Plagiocephaly
http://www.babycenter.com/0_plagiocephaly-flat-head-syndrome_1187981.bc
http://www.cranialtech.com/index.php?option=com_content&view=article&id=73&Itemid=76

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http://www.monroeoandp.com/diagnosis_of_plagiocephaly.html

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Long QT Syndrome

Definition:
The long QT syndrome (LQTS) is a rare inborn heart condition in which delayed repolarization of the heart following a heartbeat increases the risk of episodes of torsade de pointes (TDP, a form of irregular heartbeat that originates from the ventricles). These episodes may lead to palpitations, fainting and sudden death due to ventricular fibrillation. Episodes may be provoked by various stimuli, depending on the subtype of the condition.
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You can be born with a genetic mutation that puts you at risk of long QT syndrome. In addition, certain medications and medical conditions may cause long QT syndrome.

The condition is so named because of the appearances of the electrocardiogram (ECG/EKG), on which there is prolongation of the QT interval.

Long QT syndrome is treatable. You may need to limit your physical activity, avoid medications known to cause prolonged Q-T intervals or take medications to prevent a chaotic heart rhythm. Some people with long QT syndrome need surgery or an implantable device.

Symptoms :
Many people with long QT syndrome don’t have any signs or symptoms. They may be aware of their condition only from results of an electrocardiogram (ECG) performed for an unrelated reason, because they have a family history of long QT syndrome or because of genetic testing results.

For people who do experience signs and symptoms of long QT syndrome, the most common symptoms include:

*Fainting. This is the most common sign of long QT syndrome. In people with long QT syndrome, fainting spells (syncope) are caused by the heart temporarily beating in an erratic way. These fainting spells may happen when you’re excited, angry or scared, or during exercise. Fainting in people with long QT syndrome can occur without warning, such as losing consciousness after being startled by a ringing telephone.

Signs and symptoms that you’re about to faint include lightheadedness, heart palpitations or irregular heartbeat, weakness and blurred vision. However, in long QT syndrome, such warning signs before fainting are unusual.

*Seizures. If the heart continues to beat erratically, the brain becomes increasingly deprived of oxygen. This can then cause generalized seizures.

*Sudden death. Normally, the heart returns to its normal rhythm. If this doesn’t happen spontaneously and paramedics don’t arrive in time to convert the rhythm back to normal with an external defibrillator, sudden death will occur.Signs and symptoms of inherited long QT syndrome may start during the first months of life, or as late as middle age. Most people who experience signs or symptoms from long QT syndrome have their first episode by the time they reach age 40.

Rarely, signs and symptoms of long QT syndrome may occur during sleep or arousal from sleep.

Causes:
Your heart beats about 100,000 times a day to circulate blood throughout your body. To pump blood, your heart’s chambers contract and relax. These actions are controlled by electrical impulses created in the sinus node, a group of cells in the upper right chamber of your heart. These impulses travel through your heart and cause it to beat.

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After each heartbeat, your heart’s electrical system recharges itself in preparation for the next heartbeat. This process is known as repolarization. In long QT syndrome, your heart muscle takes longer than normal to recharge between beats. This electrical disturbance, which often can be seen on an electrocardiogram (ECG), is called a prolonged Q-T interval.

Prolonged Q-T interval
An electrocardiogram (ECG, also called an EKG) measures electrical impulses as they travel through your heart. Patches with wires attached to your skin measure these impulses, which are displayed on a monitor or printed on paper as waves of electrical activity.

An ECG measures electrical impulses as five distinct waves. Doctors label these five waves using the letters P, Q, R, S and T. The waves labeled Q through T show electrical activity in your heart’s lower chambers.

The space between the start of the Q wave and the end of the T wave (Q-T interval) corresponds to the time it takes for your heart to contract and then refill with blood before beginning the next contraction.

By measuring the Q-T interval, doctors can tell whether it occurs in a normal amount of time. If it takes longer than normal, it’s called a prolonged Q-T interval. The upper limit of a normal Q-T interval takes into account age, sex, and regularity and speed of the heart rate.

Long QT syndrome results from abnormalities in the heart’s electrical recharging system. However, the heart’s structure is normal. Abnormalities in your heart’s electrical system may be inherited or acquired due to an underlying medical condition or a medication.

Inherited long QT syndrome
At least 12 genes associated with long QT syndrome have been discovered so far, and hundreds of mutations within these genes have been identified. Mutations in three of these genes account for about 70 to 75 percent of long QT syndrome, and cause the forms referred to as LQT1, LQT2 and LQT3.

Doctors have described two forms of inherited long QT syndrome:

*Romano-Ward syndrome. This more common form occurs in people who inherit only a single genetic variant from one of their parents.

*Jervell and Lange-Nielsen syndrome. Signs and symptoms of this rare form usually occur earlier and are more severe than in Romano-Ward syndrome. It’s seen in children who are born deaf and have long QT syndrome because they inherited genetic variants from each parent.

Additionally, scientists have been investigating a possible link between SIDS and long QT syndrome and have discovered that about 10 percent of babies with SIDS had a genetic defect or mutation for long QT syndrome.

Acquired long QT syndrome
More than 50 medications, many of them common, can lengthen the Q-T interval in otherwise healthy people and cause a form of acquired long QT syndrome known as drug-induced long QT syndrome.

Medications that can lengthen the Q-T interval and upset heart rhythm include certain antibiotics, antidepressants, antihistamines, diuretics, heart medications, cholesterol-lowering drugs, diabetes medications, as well as some antifungal and antipsychotic drugs.

People who develop drug-induced long QT syndrome may also have some subtle genetic defects in their hearts, making them more susceptible to disruptions in heart rhythm from taking drugs that can cause prolonged Q-T intervals.

Risk Factors:
People at risk of long QT syndrome include:

*Children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Family members of children, teenagers and young adults with unexplained fainting, unexplained near drownings or other accidents, unexplained seizures, or a history of cardiac arrest

*Blood relatives of people with known long QT syndrome

*People taking medications known to cause prolonged Q-T intervals

Long QT syndrome often goes undiagnosed or is misdiagnosed as a seizure disorder, such as epilepsy. However, researchers believe that long QT syndrome may be responsible for some otherwise unexplained deaths in children and young adults. For example, an unexplained drowning of a young person may be the first clue to inherited long QT syndrome in a family.

People with low potassium, magnesium or calcium blood levels — such as those with the eating disorder anorexia nervosa — may be susceptible to prolonged Q-T intervals. Potassium, magnesium and calcium are all important minerals for the health of your heart’s electrical system.

Diagnosis:
The diagnosis of LQTS is not easy since 2.5% of the healthy population have prolonged QT interval, and 10–15% of LQTS patients have a normal QT interval. A commonly used criterion to diagnose LQTS is the LQTS “diagnostic score”. The score is calculated by assigning different points to various criteria (listed below). With four or more points, the probability is high for LQTS; with one point or less, the probability is low. A score of two or three points indicates intermediate probability.

*QTc (Defined as QT interval / square root of RR interval)
#>= 480 msec – 3 points
#460-470 msec – 2 points
#450 msec and male gender – 1 point

*Torsades de pointes ventricular tachycardia – 2 points

*T wave alternans – 1 point

*Notched T wave in at least 3 leads – 1 point

*Low heart rate for age (children) – 0.5 points

*Syncope (one cannot receive points both for syncope and torsades de pointes)
#With stress – 2 points
#Without stress – 1 point

*Congenital deafness – 0.5 points

*Family history (the same family member cannot be counted for LQTS and sudden death)
#Other family members with definite LQTS – 1 point
#Sudden death in immediate family (members before the age 30) – 0.5 points
Treatment options:
Those diagnosed with long QT syndrome are usually advised to avoid drugs that would prolong the QT interval further or lower the threshold for TDP.  In addition to this, there are two intervention options for individuals with LQTS: arrhythmia prevention and arrhythmia termination.

Arrhythmia prevention:
Arrhythmia suppression involves the use of medications or surgical procedures that attack the underlying cause of the arrhythmias associated with LQTS. Since the cause of arrhythmias in LQTS is after depolarizations, and these after depolarizations are increased in states of adrenergic stimulation, steps can be taken to blunt adrenergic stimulation in these individuals. These include:

*Administration of beta receptor blocking agents which decreases the risk of stress induced arrhythmias. Beta blockers are the first choice in treating Long QT syndrome.
In 2004 it has been shown that genotype and QT interval duration are independent predictors of recurrence of life-threatening events during beta-blockers therapy. Specifically the presence of QTc >500ms and LQT2 and LQT3 genotype are associated with the highest incidence of recurrence. In these patients primary prevention with ICD (Implantable cardioverter-defibrillator) implantation can be considered.

*Potassium supplementation. If the potassium content in the blood rises, the action potential shortens and due to this reason it is believed that increasing potassium concentration could minimize the occurrence of arrhythmias. It should work best in LQT2 since the HERG channel is especially sensitive to potassium concentration, but the use is experimental and not evidence based.

*Mexiletine. A sodium channel blocker. In LQT3 the problem is that the sodium channel does not close properly. Mexiletine closes these channels and is believed to be usable when other therapies fail. It should be especially effective in LQT3 but there is no evidence based documentation.

*Amputation of the cervical sympathetic chain (left stellectomy). This may be used as an add-on therapy to beta blockers but modern therapy mostly favors ICD implantation if beta blocker therapy fails.

Arrhythmia termination:
Arrhythmia termination involves stopping a life-threatening arrhythmia once it has already occurred. One effective form of arrhythmia termination in individuals with LQTS is placement of an implantable cardioverter-defibrillator (ICD). Alternatively, external defibrillation can be used to restore sinus rhythm. ICDs are commonly used in patients with syncopes despite beta blocker therapy, and in patients who have experienced a cardiac arrest.

It is hoped that with better knowledge of the genetics underlying the long QT syndrome, more precise treatments will become available.
Prognosis:
The risk for untreated LQTS patients having events (syncopes or cardiac arrest) can be predicted from their genotype (LQT1-8), gender and corrected QT interval.

*High risk (>50%)
QTc>500 msec LQT1 & LQT2 & LQT3 (males)

*Intermediate risk (30-50%)
QTc>500 msec LQT3 (females)

QTc<500 msec LQT2 (females) & LQT3

*Low risk (<30%)
QTc<500 msec LQT1 & LQT2 (males)

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/longqt1.shtml
http://www.mayoclinic.com/health/long-qt-syndrome/DS00434
http://en.wikipedia.org/wiki/Long_QT_syndrome
http://paramedicine101.blogspot.com/2009/09/long-qt-syndrome-part-iii.html
http://www.itriagehealth.com/disease/long-qt-syndrome-(qt-prolongation)

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SIDS (Sudden Infant Death Syndrome)

Definition:
Sudden infant death syndrome (SIDS) or crib death is a syndrome marked by the sudden death of an infant that is unexpected by history and remains unexplained after a thorough forensic autopsy and a detailed death scene investigation. The term cot death is often used in the United Kingdom, Ireland, Australia, India, South Africa and New Zealand.In USA the term SIDS  is widely spread and  many times  under educated parents  are very much panicky over SIDS and do overdoes  which  may causes harm to babies.

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Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.The cause of death never identified is the actual SIDS  which is very rare in case of healthy babies.

 

SIDS is a diagnosis of exclusion. It should only be applied to an infant whose death is sudden and unexpected and remains unexplained after the performance of an adequate postmortem investigation including:

1.an autopsy;
2.investigation of the scene and circumstances of the death;
3.exploration of the medical history of the infant and family.

Australia and New Zealand are shifting to the term Sudden Unexplained Death in Infancy (SUDI) for professional, scientific and coronial clarity.

The term SUDI is now often used instead of  SIDS   because some coroners prefer to use the term ‘undetermined’ for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.

Causes:
SIDS is most likely to occur between 2 and 4 months of age, and 90% occur by 6 months of age. It occurs more often in winter months, with the peak in January. There is also a greater rate of SIDS among Native and African Americans.

The following have been linked to an increased risk of SIDS (as they call it):

*Babies who sleep on their stomachs (habitually)
*Babies who are around cigarette smoke while in the womb or after being born
*Babies who sleep in the same bed as their parents and the parents are tired to take proper care during sleep.
*Babies who have soft bedding in the crib
*Multiple birth babies (being a twin, triplet, etc.)
*Premature babies
*Babies who have a brother or sister who had SIDS
*Mothers who smoke or use illegal drugs
*Teen mothers
*Short time period between pregnancies
*Late or no prenatal care
*Situations of  extreme poverty

*Parents & baby sleep with animals inside the room (you may click to see how much carbon dioxide dogs exhale )

The dog’s respiratory system serves two purposes. First, it is the exchange mechanism by which the body’s carbon dioxide is replaced with oxygen. It is also a unique cooling system. Since dogs do not have sweat glands (except on their feet), they cannot perspire to lower their body’s temperature like humans do. To cool their body they must breathe harder (pant). By breathing faster, warm air is exchanged from the body for the cooler outside air. Additionally, moisture within the respiratory system evaporates, further cooling these surfaces. Therefore, the lungs function both to exchange carbon dioxide for oxygen and to cool the body.So,dogs need more oxygen than man.

*Death due to long driving without taking care of baby much
*Stuffy room (oxygen level falls during night)
*Not bothering about baby’s consisting crying

SIDS affects boys more often than girls. While studies show that babies with the above risk factors are more likely to be affected, the impact or importance of each factor is not well-defined or understood.

In most cases if no specific cause can be found to explain the death, it’s defined as SIDS. Research has suggested that a number of different factors may be linked to SIDS. It’s believed that these factors don’t actually cause SIDS, but may make a baby more at risk. These factors include:

*allergies
*bacterial and viral infections
*unknown genetic conditions
*problems in the area of the brain that controls breathing
*irregular heartbeat
*accidental suffocation
*overheating

Symptoms:
There are no symptoms. Babies who die of SIDS  do not appear to suffer or struggle.

Risk  Factors:-
The cause of SIDS
is unknown. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome’s biological cause or potential causes. The frequency of SIDS appears to be a strong function of the infant’s sex, age and ethnicity, and the education and socio-economic-status of the infant’s parents.

According to a study published on November 1, 2006 in the Journal of the American Medical Association, babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata), which helps control functions like breathing, blood pressure and arousal, and abnormalities in serotonin signaling. According to the National Institutes of Health, which funded the study, this finding is the strongest evidence to date that structural differences in a specific part of the brain may contribute to the risk of SIDS.

In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be a risk factor in some cases of SIDS. Both bacteria were present at greater than usual concentrations in infants who died from SIDS. SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.

Listed below are several risk factors associated with increased probability of the syndrome based on information available prior to this recent study.

Prenatal risks:

*maternal nicotine use (tobacco or nicotine patch)
*inadequate prenatal care
*inadequate prenatal nutrition
*use of heroin, cocaine and other drugs
*subsequent births less than one year apart
*alcohol use
*infant being overweight
*mother being overweight
*Teen pregnancy (if the baby has a teen mother, it has a greater risk)
*infant’s sex (60% of SIDS cases occur in males)

Post-natal risks:

*mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnosis and death). It is often misdiagnosed as a virus, flu, and/or asthma-like conditions.
*low birth weight (in the U.S. from 1995-1998 the rate for 1000-1499 g was 2.89/1000 and for 3500-3999 g it was 0.51/1000)
*exposure to tobacco smoke
*prone sleep position (lying on the stomach, see sleep positioning below)
*not breastfeeding
*elevated or reduced room temperature
*excess bedding, clothing, soft sleep surface and stuffed animals
*co-sleeping with parents or other siblings may increase risk for SIDS, but the mechanism remains unclear
*infant’s age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)
*premature birth (increases risk of SIDS death by about 4 times.  In 1995-1998 the U.S. SIDS rate for 37–39 weeks of gestation was 0.73/1000; The SIDS rate for 28–31 weeks of gestation was 2.39/1000)
*anemia

Hypotheses:-

Mattress bugs
A 2004 study hypothesized that insects (called “bugs”) feeding on baby vomit and dust could be fatal for small children, creating “supertoxins” which spur the baby’s body into overreacting, leading to anaphylactic shock.

Brain disorder
A recently published research article showed evidence that cells in the brainstem fail to develop receptors for serotonin in the womb. This abnormality can continue postpartum until the end of the first year. This would account for there being few to no SIDS deaths after the first year of infancy and the reason the risk is greater for premature infants. Males have fewer serotonin receptors than females, perhaps contributing to the increased incidence of SIDS in the demographic.

In addition, a study done in 2006 showed that a possible cause of SIDS is because parents leave their infants in a position known as the Trendelenburg position.[28] This position can cause the brain stem to fall, and in a result, the brain becomes “crushed”. The proper position for an infant is either Fowler’s position or Sims’.

Air circulation with fan use

According to a study of nearly 500 babies published the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments. Author De-Kun li said that “the baby’s sleeping environment really matters” and that “this seems to suggest that by improving room ventilation we can further reduce risk.”

However, Dr. John Olssen at East Carolina University has pointed out that this study had a number of methodological flaws, such selection and recall bias, low enrollment numbers, and dissimilar study groups. Olssen argues that although fan use is probably not harmful, it should not be recommended as a means to reduce the risk of SIDS.

Vitamin C
In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS, although the claim was controversial even then. Subsequent studies failed to support a preventive role for vitamin C in SIDS. To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.

Toxic gases
In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.

Support for this hypothesis was based on the observation that the risk of cot death rises from one sibling to the next.[citation needed] Richardson claimed that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair[39] references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.

However, a final report of “The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis”, published in May 1998, concluded that “there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants.”[41] The report also states that “in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses” and “babies have also been found to die on wrapped mattresses.”

Contrary to media publicity, the 1998 UK Limerick Report did not disprove the toxic gas theory—as a highly qualified environmental scientist has stated in the New Zealand Medical Journal. In fact, the Limerick Committee’s experiments proved the fungal generation of toxic gases (forms of stibine and arsine) from cot mattress materials.

According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:

In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.[42]

Central respiratory pattern deficiency
There is ongoing research in the pediatric/neonatal community that has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Bötzinger complex.[43]

Cervical spinal injury from birth trauma
During birth, if the infant’s head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury. When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe.

Genetics
There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61. This value of 61% in the U.S. is an average of 57% black male SIDS, 62.2% white male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved, infant “race” is arbitrarily assigned to one category or the other; most often it is chosen by the mother. The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele that occurs with a frequency of ? that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of ? and an unprotected XX female would occur with a frequency of 4?9. The ratio of ? to 4?9 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS.

Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examination of other causes of infant respiratory death, such as suffocation by inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS.

The JAMA 2006 study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys “had significantly fewer serotonin binding sites than girls”, but the authors could not reproduce it in their 2010 paper. However, such neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life. Furthermore, this cannot explain the identical male fraction of 0.61 in other respiratory mortality causes such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for all ages 1 to 14 years in the U.S. from 1979 to 2005.

Child abuse
Several instances of infanticide have been uncovered where the diagnosis was originally SIDS. This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides. In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:

The misdiagnosis of infanticide as SIDS “happens all over,” Ms. Talan, a medical reporter at Newsday, said. “A lot of doctors and police don’t know how to handle it. They don’t take it as seriously as they should.” As a result of the book’s revelations, people are starting to scrutinize possible cases of this “perfect crime,” which involves no physical evidence and no witnesses.

A former pediatrician, Roy Meadow, from the UK believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent displaying Munchausen syndrome by proxy (a condition which he was first to describe, in 1977). During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of murder, to varying degrees on the basis of Meadow’s opinion. In 2003 a number of high-profile acquittals brought Meadow’s theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned. Meadow was struck off in 2005.

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.

Nitrogen dioxide
A 2005 study by researchers at the University of California, San Diego found that “SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life.” While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.Animal sleeping in the same room where  parents  sleep with baby   is not administered.

Vaccination
According to the U.S. Centers for Disease Control and Prevention, several studies have failed to provide sufficient evidence of a causal link between vaccinations and SIDS. They state:

From 2 to 4 months old, babies begin their primary course of vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.

Inner ear damage
Records of hearing tests (oto-acoustic emissions, OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. To be specific the OAE signal to noise ratio was reduced in the right ear in the SIDS babies (Rubens DD et al. Early Human Development 84, 225-9 (2008)). It should be noted this was a small study (n=31 cases and 31 controls), had serious limitations (several significant factors were not controlled), and has been criticised from various perspectives. The authors’ suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the “line of fire” for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.

Differential diagnosis
Some conditions that may be undiagnosed and thus could be alternative diagnoses to SIDS include:

*medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency)
*infant botulism.
*long QT syndrome (accounting for less than 2% of cases)
*infections with the bacterium Helicobacter pylori
*shaken baby syndrome and other forms of child abuse.
*overlying

For example an infant with MCAD deficiency could have died by “classical SIDS” if found swaddled and prone with head covered in an overheated room where parents were smoking. Genes of susceptibility to MCAD and Long QT syndrome do not protect an infant from dying of classical SIDS. Therefore presence of a susceptibility gene, such as for MCAD, means the infant may have died either from SIDS or from MCAD deficiency. It is impossible for the pathologist to distinguish between them.

Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases “Back To Bed” and “Back to Sleep”. The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the U.S. and New Zealand. However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the U.S., from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991.

Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their bedding—the brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react “normally” by moving away from the pooled CO2, and thus smother. Another theory is that babies sleep more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants.

Hospital neonatal-intensive-care-unit (NICU) staff commonly place preterm newborns on their stomach, although they advise parents to place their infants on their backs after going home from the hospital.

Breastfeeding
A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had ? the rate of SIDS compared with non-breastfed infants, but that “it became nonsignificant in the multivariate model that included the other environmental factors”. These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective.” However, a more recent study shows that breast feeding reduces the risk of SIDS by approximately 50% at all infant ages.

Secondhand smoke reduction

According to the U.S. Surgeon General’s Report, secondhand smoke is connected to SIDS. Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their body fluids than those who die from other causes. Parents who smoke can significantly reduce their children’s risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free.

The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.

Bedding
Product safety experts advise against using pillows, sleep positioners, bumper pads, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib “naked.”

Blankets should not be placed over an infant’s head. It has been recommended that infants should be covered only up to their chest with their arms exposed. This reduces the chance of the infant shifting the blanket over his or her head.

Sleep sacks
In colder environments where bedding is required to maintain a baby’s body temperature, the use of a “baby sleep bag” or “sleep sack” is becoming more popular. This is a soft bag with holes for the baby’s arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998 has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study “The use of a sleeping-sack should be particularly promoted for infants with a low birth weight.” The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head. The use of swaddling clothes, a traditional form of infant restraint which leaves only the head uncovered, is controversial.

Pacifiers
According to a 2005 meta-analysis, most studies favor pacifier use. According to the American Academy of Pediatrics, pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear. SIDS experts and policy makers haven’t recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated with pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species. A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambient factors, and it reduced the effect of other risk factors. It has been speculated that the raised surface of the pacifier holds the infant’s face away from the mattress, reducing the risk of suffocation. If a postmortem investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS.

Bumper pads
Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government’s health department, issued an advisory[92] recommending against the use of bumper pads, stating:

The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.

Concerns regarding recommendations
Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the U.S. have stated that they believe that the American Academy of Pediatrics’ recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.

According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed. Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis.[96] Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated “I do not think it is a medical problem—it is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense.”[97] A research study on children with plagiocephaly found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.

Because of the delays caused by back sleep some medical professionals have suggested that the “normal” ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider “normal” children who previously were considered developmentally delayed.

Additional studies have reported that the following negative conditions are associated with the back sleep position: increase in sleep apnea, decrease in sleep duration, strabismus, social skills delays, deformational plagiocephaly, and temporomandibular jaw difficulties. In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with gross motor milestone delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills. In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic. In addition, prior to the “Back to Sleep” campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position. Supine sleeping infants cannot self-treat their own torticollis.

Epidemiology
SIDS was reported  responsible for 0.543 deaths per 1,000 live births in the U.S. in 2005. It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age.Actual death due to pure  SIDS  is perhaps one in million today.

SIDS deaths in the U.S. decreased from 4,895 in 1992 to 2,247 in 2004 But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%. According to Dr. John Kattwinkel, chairman of the Center for Disease Control (CDC) Special Task Force on SIDS “A lot of us are concerned that the rate (of SIDS) isn’t decreasing significantly, but that a lot of it is just code shifting”.

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://hcd2.bupa.co.uk/fact_sheets/html/sids.html
http://en.wikipedia.org/wiki/Sudden_infant_death_syndrome
http://www.nlm.nih.gov/medlineplus/ency/article/001566.htm
*Simon C, Everitt H, Kendrick T. Oxford Handbook of General Practice. 2nd ed. Oxford: Oxford University Press, 2007:906

*Sudden unexpected death in infancy: a multi-agency protocol for care and investigation. Royal College of Pathologists and Royal College of Paediatrics and Child Health. 2004. www.rcpch.ac.uk

*Cot death facts & figures. Foundation for the Study of Infant Deaths. 2006. www.fsid.org.uk

*What is cot death? Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 9 July 2008

*FAQ – current topics. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 9 July 2008

*Thach B. Tragic and sudden death: potential and proven mechanisms causing sudden infant death syndrome. EMBO J 2008; 9:114-118. www.nature.com

*Reduce the risk of cot death – an easy guide. Department of Health, 2007. www.dh.gov.uk

*Department of Health. The Pregnancy Book. 2007:119-127. www.dh.gov.uk, accessed 2 January 2009

*Anderson ME, Johnson DC, Batal HA. Sudden infant death syndrome and prenatal maternal smoking: rising attributed risk in the Back to Sleep era. BMC Med 2005; 3:4. www.biomedcentral.com

*Looking after your baby. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*New dummy advice for parents. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Breastfeeding reduces the risk of cot death. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Keep an eye on your baby’s room temperature. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*If you are bereaved. Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*Care of the next infant (CONI). Foundation for the Study of Infant Deaths. www.fsid.org.uk, accessed 11 July 2008

*UNICEF UK statement on dummy use, sudden infant death syndrome and breastfeeding. UNICEF. www.babyfriendly.org.uk, accessed 8 December 2008

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Craniosynostosis

{{Gray's Anatomy plate|The skull at birth, sho...

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Deffinition:
Craniosynostosis is a defect in which one or more of the flexible and fibrous joints (cranial sutures) between the skull bones closes too soon; it occurs before birth or within a few months after birth.  It is a condition in which one or more of the fibrous sutures in an infant skull prematurely fuses. This results in restricted skull and brain growth. Because the brain cannot expand in the direction of the fused suture, it is forced to grow in the direction of the open sutures, often resulting in an abnormal head shape and facial features. Some cases of craniosynostosis may result in increased pressure on the brain and developmental delays.  It can be the result of an inherited syndrome or sporadic. In sporadic cases, the cause is unknown.Craniosynostosis can occur alone or as part of a syndrome of craniofacial defects.
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Craniosynostosis is a very rare occurrence. The sagittal form of the disorder, in which the sagittal suture closes prematurely, is the most common form of craniosynostosis, occurring in three to five of every 1,000 babies, typically males. The frequencies of the various types of craniosynostosis are 50–60% sagittal, 20–30% coronal, 4–10% metopic, and 2–4% lambdoid.It is estimated that craniosynostosis affects 1 in 2,000 live births.

Description:
The skull of a newborn is composed of five bones that are held together by the fibrous sutures positioned at the front, top, sides, and back of the skull. By remaining open, the sutures allow the skull to normally expand in all directions as the brain is growing.

The premature closing of one or more of these cranial sutures stops the normal capacity of the skull to expand in early childhood. As not all of the cranial sutures will close, the skull expands in the areas that are still flexible. This results in an abnormally shaped skull or face. The forehead may be very pronounced and inclined forward. Viewed from above, the skull may be more rectangular in shape rather than oval.

Other forms of craniosynostosis include coronal craniosynostosis (affecting the coronal suture that crosses the top of the skull from temple to temple), metopic craniosynostosis (affecting the metopic suture of the forehead), sagittal craniosynostosis (affecting the sagittal suture that unites the two parietal bones), and lambdoidal craniosynostosis (affecting the lambdoid suture between the occipital and parietal bones of the skull).

Causes:
The cause of craniosynostosis is unknown.However, there’s a hereditary component to craniosynostosis when it occurs with certain genetic syndromes such as Apert’s syndrome and Crouzon syndrome.It is usually caused by a genetic mutation. Mutations in several genes (designated TWIST, FGFR-1, FGFR-2, and FGFR-3) have been linked with craniosynostosis. In particular, the protein encoded for by TWIST is critical in the initiation and maintenance of the cranial suture process. As of 2004, the favored hypothesis is that the protein that normally functions to ensure that the formation of the cranial sutures occurs at the right time in development somehow goes awry and causes premature fusion of the bones of the brain.

Symptoms:
Infant’s skull has seven bones. Normally, these bones don’t fuse until around age 2, giving your baby’s brain time to grow. Joints called cranial sutures, made of strong, fibrous tissue, hold these bones together. In the front of your baby’s skull, the sutures intersect in the large soft spot (fontanel) on the top of your baby’s head. Normally, the sutures remain flexible until the bones fuse.
Joints called cranial sutures, made of strong, fibrous tissue, hold the bones of your baby’s skull together until the bones fuse, normally around age 2. Until then, the sutures intersect at the fontanels, the soft spots on your baby’s head. The largest of the four fontanels is at the front of the skull (anterior); the next largest is at the back (posterior). Each side of the skull has a tiny fontanel.
Craniosynostosis signs in general
Signs of craniosynostosis include:

#A misshapen skull, with the shape depending on which of the cranial sutures are affected
#Abnormal feeling “soft spot” (fontanel) on your baby’s skull
#Early disappearance of the fontanel
#Slow or no growth of head as your baby grows
#Development of a raised, hard ridge along affected sutures
#Increased pressure within the skull (intracranial pressure)
The signs of craniosynostosis may not be noticeable at birth, but they will become apparent during the first few months of your baby’s life.

Main categories and characteristics :-
There are two categories of craniosynostosis:

1.Primary craniosynostosis. If your baby has primary craniosynostosis, usually one, but sometimes more, of the cranial sutures become rigid, fusing the connecting bones and inhibiting the brain’s ability to grow normally.
2.Secondary craniosynostosis. With secondary craniosynostosis, which occurs more frequently than the primary type, your infant’s brain stops growing, usually due to an underlying hereditary syndrome, allowing the sutures to fuse prematurely. Secondary craniosynostosis is often associated with facial deformities and developmental delays.

Common types and characteristics :-
The most common types of craniosynostosis are:

#Sagittal synostosis (scaphocephaly). Premature fusion of the suture at the top of the head (sagittal suture) forces the head to grow long and narrow, rather than wide. Scaphocephaly is the most common type of craniosynostosis, and it is more common in boys.
#Coronal synostosis (anterior plagiocephaly). Premature fusion of one of the sutures that run from each ear to the sagittal suture on top of the head may force your baby’s forehead to flatten on the affected side. It also may raise the eye socket and cause a deviated nose and slanted skull. This second most common type of craniosynostosis is more common in girls. Untreated, it may lead to vision loss on the affected side (amblyopia).
#Bicoronal synostosis (brachycephaly).
When both of the coronal sutures fuse prematurely, your baby may have a flat, elevated forehead and brow.


Rare types and characteristics :-
Two less common types of synostosis are:


#Metopic synostosis (trigonocephaly).
The metopic suture runs from the baby’s nose to the sagittal suture. Premature fusion gives the scalp a triangular appearance.
#Lambdoid synostosis (posterior plagiocephaly)
. This rare form of craniosynostosis involves the lambdoid suture, which runs across the skull near the back of the head. It may cause flattening of the head on the affected side.

Misshapen head may not mean craniosynostosis
:-
A misshapen head doesn’t always indicate craniosynostosis. For example, if the back of your baby’s head appears flattened, it could be the result of your baby’s sleeping on his or her back.

The “Back to Sleep” campaign, co-sponsored by the National Institute of Child Health & Human Development, encourages parents to put healthy babies to sleep on their backs to reduce the risk of sudden infant death syndrome (SIDS). The campaign has resulted in more cases of misshapen heads. In this case, the flattening is a result of positional molding, not craniosynostosis.

Risk Factors:
Babies with craniosynostosis, particularly those with an underlying syndrome, may develop increased intracranial pressure. Their skulls don’t expand enough to make room for their growing brain.

If untreated, increased intracranial pressure can cause these conditions:

#Blindness
#Seizures
#Brain damage
#Death, in very rare instances
In addition, facial deformities that affect the middle of your child’s face may cause:

#Upper airway obstructions, compromising your baby’s ability to breathe
#Permanent head deformity

Diagnosis:
Your doctor will feel your baby’s head for abnormalities such as suture ridges, perform a physical exam and look for facial deformities. In addition, your doctor may order other tests, including:

#Imaging studies. X-rays or a computerized tomography (CT) scan of your baby’s skull will show whether any sutures have fused. Fused sutures are identifiable by their absence, because they’re invisible once fused, and by the ridging of the suture line.

#Genetic testing. If your doctor suspects your baby’s misshapen skull is caused by an underlying hereditary syndrome, genetic testing may help identify the syndrome. Genetic tests usually require a blood sample.
Depending on what type of abnormality your doctor is looking for, your baby may be required to give a hair, skin or other tissue sample, such as cells from the inside of the cheek. The sample is then sent to a lab for analysis.

Treatments:-

Surgery is the common treatment for craniosynostosis:
But for Mild cases of craniosynostosis — those that involve only one suture and no underlying syndrome — may require no treatment. Skull abnormalities may become less obvious as your infant grows and develops hair.

Surgery
:-
For other infants, surgery, usually during infancy, is the primary treatment for craniosynostosis. However, the type and timing of surgery depend on the type of synostosis and whether there’s an underlying syndrome.

The purpose of surgery is to relieve pressure on the brain, create room for the brain to grow normally and improve your child’s appearance. A team that includes a specialist in surgery of the head and face (craniofacial surgeon) and a specialist in brain surgery (neurosurgeon) often performs the surgery.

#Traditional surgery. The surgeon makes an incision in your infant’s scalp and cranial bones, then reshapes the affected portion of the skull. Sometimes plates and screws, often made of material that is absorbed over time, are used to hold the bones in place. Surgery, which is performed during general anesthesia, may take up to seven hours.

After surgery, your infant remains in the hospital for at least three days. Some temporary facial swelling is common after surgery. Complications are rare. Some children may require a second surgery later because the synostosis recurs. Also, children with facial deformities often require future surgeries to reshape their faces.

#Endoscopic surgery
. This less invasive form of surgery isn’t an option for everyone. But in certain cases, the surgeon may use a lighted tube (endoscope) inserted through one or two small scalp incisions over the affected suture. The surgeon then opens the suture to enable your baby’s brain to grow normally. Endoscopic surgery usually takes about an hour, causes less swelling and blood loss, and shortens the hospital stay, often to one day after surgery.

If your baby has an underlying syndrome, your doctor may recommend regular follow-up visits after surgery to monitor head growth and check for increased intracranial pressure.

Recovery and rehabilitation:-
Regardless of the type of surgery performed to correct the defects associated with craniosynostosis, the child will be restricted from vigorous activity or rough play while healing. The protective helmet is required for children after endoscopic strip craniectomy, while permanent plates inserted during other corrective surgeries eliminate the need for the helmet. Children who have had surgery to repair craniosynostosis will continue to need periodic examination by the surgeon until approximately age 18, when the skull has grown to its adult size and shape.

Prognosis:-
The outlook for a complete recovery for a child with craniosynostosis depends on whether just one suture is involved or whether multiple sutures have closed. Also, the presence of other abnormalities can lessen the confidence of a satisfactory outcome. Without surgical intervention, craniosynostosis can lead to increased brain pressure, delayed mental development, mental retardation, seizures, or blindness. After surgery is accomplished, the prognosis is excellent.

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/Craniosynostosis
http://www.mayoclinic.com/health/craniosynostosis/
http://www.answers.com/topic/craniosynostosis

Shunning the Family Bed. Who Benefits Most?

According to Dr. Jay Gordon, babies sleeping on a safe surface with sober, nonsmoking parents respond to their parents, and the parents respond to them. The chance of SIDS occurring in this situation are close to zero. Babies in a crib or in a room away from their parents, on the other hand, will breastfeed less and are at greater risk of infections, including life-threatening ones.

The medical profession, as it often does, is approaching the entire idea of the family bed backward. A baby in the same bed with his or her parents is surrounded by the best possible surveillance and safety system. It must be the responsibility of the manufacturers and proponents of cribs and separated sleep to prove that such disruption is safe, not the other way around.

Newborn babies breathe in irregular rhythms and even stop breathing for a few seconds at a time. To put it simply, they are not designed to sleep alone.

Source: Peaceful Parenting October 15, 2009

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