UMBILICAL CORD and IVH

Umbilical Cord Milking Helpful in Extremely Preterm

Aug 16, 2013

By David Douglas

NEW YORK (Reuters Health) Aug 16 - Milking the umbilical cord of preterm neonates had some beneficial effects in a recent trial.

Dr. Melissa Marsh of Beth Israel Deaconess Medical Center, Boston and colleagues studied women who were expected to deliver after only 24 to 28 completed weeks of gestation. The researchers randomly assigned the women to cord milking before clamping, or immediate cord clamping.

In all, 36 in the milking group and 39 in the immediate clamping group completed the study. The risk of the primary outcome - need for transfusion - was lower in the milking group, but the difference did not reach significance (risk ratio, 0.86).

Babies in the milking group did have significantly higher hematocrits and were significantly less likely to develop an intraventricular hemorrhage.

"Given that intraventricular hemorrhage is an important contributor to mortality and serious long-term neurodevelopmental disability, if this finding is replicated in other studies, active milking of the umbilical cord could substantially improve neonatal outcomes," the authors wrote in a paper online in the Journal of Perinatology.

There were no significant differences in between-group median Apgar scores at up to 10 minutes, or in rates of other diagnoses or complications of prematurity, including neonatal death.

Summing up, Dr. March noted in an email to Reuters Health, "Our study showed that milking may lessen the need for blood transfusion and reduce brain hemorrhage in these babies. Further study is warranted to validate our findings but preliminary data is certainly encouraging."

In the meantime, the researchers conclude, "routinely implementing this simple practice could potentially have a dramatic benefit on outcomes for preterm infants."

"Milking the umbilical cord when delivering preterm infants, rather than immediately clamping the cord, is an easy intervention that seems to improve outcomes in this extremely susceptible population," Dr. Marsh said.

SOURCE: http://bit.ly/19yffI1

G6PD DEFICIENCY

G6PD deficiency is an inherited condition in which the body doesn't have enough of the enzyme glucose-6-phosphate dehydrogenase, or G6PD, which helps red blood cells (RBCs) function normally. This deficiency can cause hemolytic anemia, usually after exposure to certain medications, foods, or even infections.Most people with G6PD deficiency don't have any symptoms, while others develop symptoms of anemia only after RBCs have been destroyed, a condition called hemolysis. In these cases, the symptoms disappear once the cause, or trigger, is removed. In rare cases, G6PD deficiency leads to chronic anemia.With the right precautions, a child with G6PD deficiency can lead a healthy and active life.

About G6PD Deficiency

G6PD is one of many enzymes that help the body process carbohydrates and turn them into energy. G6PD also protects red blood cells from potentially harmful byproducts that can accumulate when a person takes certain medications or when the body is fighting an infection.In people with G6PD deficiency, either the RBCs do not make enough G6PD or what is produced cannot properly function. Without enough G6PD to protect them, RBCs can be damaged or destroyed. Hemolytic anemia occurs when the bone marrow (the soft, spongy part of the bone that produces new blood cells) cannot compensate for this destruction by increasing its production of RBCs.

Causes of G6PD Deficiency

G6PD deficiency is passed along in genes from one or both parents to a child. The gene responsible for this deficiency is on the X chromosome.G6PD deficiency is most common in African-American males. Many African-American females are carriers of G6PD deficiency, meaning they can pass the gene for the deficiency to their children but do not have symptoms; only a few are actually affected by G6PD deficiency.People of Mediterranean heritage, including Italians, Greeks, Arabs, and Sephardic Jews, also are commonly affected. The severity of G6PD deficiency varies among these groups — it tends to be milder in African-Americans and more severe in people of Mediterranean descent.Why does G6PD deficiency occur more often in certain groups of people? It is known that Africa and the Mediterranean basin are high-risk areas for the infectious diseasemalaria. Researchers have found evidence that the parasite that causes this disease does not survive well in G6PD-deficient cells. So they believe that the deficiency may have developed as a protection against malaria.

G6PD Deficiency Symptom Triggers

Kids with G6PD deficiency typically do not show any symptoms of the disorder until their red blood cells are exposed to certain triggers, which can be:illness, such as bacterial and viral infectionscertain painkillers and fever-reducing drugscertain antibiotics (especially those that have "sulf" in their names)certain antimalarial drugs (especially those that have "quine" in their names)Some kids with G6PD deficiency can tolerate the medications in small amounts; others cannot take them at all. Check with your doctor for more specific instructions, as well as a complete list of medications that could pose a problem for a child with G6PD deficiency.Other substances can be harmful to kids with this condition when consumed — or even touched — such as fava beans and naphthalene (a chemical found in mothballs and moth crystals). Mothballs can be particularly harmful if a child accidentally swallows one, so ANY contact should be avoided.

Symptoms of G6PD Deficiency

A child with G6PD deficiency who is exposed to a medication or infection that triggers the destruction of RBCs may have no symptoms at all. In more serious cases, a child may exhibit symptoms of hemolytic anemia (also known as a hemolytic crisis), including:paleness (in darker-skinned kids, paleness is sometimes best seen in the mouth, especially on the lips or tongue)extreme tirednessrapid heartbeatrapid breathing or shortness of breathjaundice, or yellowing of the skin and eyes, particularly in newbornsan enlarged spleendark, tea-colored urineOnce the trigger is removed or resolved, the symptoms of G6PD deficiency usually disappear fairly quickly, typically within a few weeks.If symptoms are mild, no medical treatment is usually needed. As the body naturally makes new red blood cells, the anemia will improve. If symptoms are more severe, a child may need to be hospitalized for supportive medical care.

Diagnosis and Treatment

In most cases, cases of G6PD deficiency go undiagnosed until a child develops symptoms. If doctors suspect G6PD deficiency, blood tests usually are done to confirm the diagnosis and to rule out other possible causes of the anemia.If you feel that your child may be at risk because of either a family history or your ethnic background, talk to your doctor about performing a screening with blood tests to check for G6PD deficiency.Treating the symptoms associated with G6PD deficiency is usually as simple as removing the trigger — that is, treating the illness or infection or stopping the use of a certain drug. However, a child with severe anemia may require treatment in the hospital to receive oxygen, fluids, and, if needed, a transfusion of healthy blood cells. In rare cases, the deficiency can lead to other more serious health problems.

Caring for Your Child

The best way to care for a child with G6PD deficiency is to limit exposure to the triggers of its symptoms. With the proper precautions, G6PD deficiency should not keep your child from living a healthy, active life.

RESEARCH INTESTINAL FLORA

New Study shows Caesarean section weakens baby's intestinal flora....

• APA
• Aug 15, 2013

Birth by Caesarian section weakens the gut microbiota, leading to increased risk of developing allergies, according to a study by universities in Sweden and Scotland.

The researchers from, among others, the KTH Royal Institute of Technology and Science in Stockholm and the University of Glasgow, followed gut microbiota development in 24 children up to the age of two, nine delivered through Caesarean and 15 delivered naturally, through vaginal birth.

Those that were delivered by Caesarean section had a less diverse gut microbiota during their first two years of life than those born vaginally. The low diversity was particularly clear among bacteroidetes, which are chiefly associated with protection against allergies. Thus, these children may run greater risk of developing allergies, but diabetes and irritable bowel syndrome are also more common among them.

Everything indicates that right up until the moment of birth the child's gut is completely sterile. With natural birth the child is exposed to bacteria in the mother's birth canal, a good start to the formation of the child's own gut microbiota.

Besides a greater diversity in their intestinal flora, children delivered vaginally in the Linköping study also had higher blood plasma levels of substances linked to Th1 cells, a kind of "chief cells" in the immune system, which can inhibit allergic immune responses.

"Sometimes Caesarean sections are necessary. But it is important that both expectant mothers and doctors are aware that such a delivery may affect the child's health," said Maria Jenmalm from Linköping University, one of the authors of the article.

NICUniversity

NICUniversity has a wealth of information for NICU nurses.... And one of our own MDs is a guest lecturer, there, as well. Highly recommend this site for up to date NICU news!

SACRAL DIMPLE RULE

UMBILICAL CORD COMMON PROBLEMS

 The umbilical cord usually has 2 arteries, 1 vein, the allantois, the omphalomesenteric duct remnant and Wharton’s jelly. It is spiraled (usually to the left), and is approximately 55 centimeters in a term infant. It usually detaches around 1 week of life and is entirely healed by about 2 weeks of life.

The arteries and vein still have some patentcy until ~1 month of life when they become the lateral umbilical ligaments and liamentum teres.

There are several common umbilical cord problems:

• Congenital omphalocoele – a herniated peritoneal sac at the base of the umbilicus. It is often associated with Tristomy 13, 18, cardiac anomalies and Beckwith-Wiedemann syndrome (which also has macrosomia and hypoglycemia). Immediate treatment includes covering the omphalocoele with saline gauze or other wet protectant and a surgical consultation. A glucose and chromosomal analysis are also indicated.
• Delayed separation of the cord – persistence of the cord more than 4-6 weeks may indicate a congenital leukocyte adherence defect (an autosomal recessive disorder of neutrophil adherence). Delayed separation is also associated with a higher risk of infection includingStaphlococcus, Escherichia coli, Aspergillus and Candida. Treatment of infections and an evaluation for leukocyte adherence defect are indicated.
• Granuloma – persistence of granulation tissue after 2 weeks. This is associated with bacterial invasion of the tissue, inadequate epithelialization and formation of granular, erythematous, seropurulent tissue. Treatment with silver nitrate cauterization and frequent alcohol applications is recommended.
• Hemorrhage – usually due to inadequate ligation, but also due to sepsis, coagulation defects, or hemorrhagic disease of the newborn. Treatment depends on the cause.
• Hernia – caused by incomplete closure or laxity of the umbilical ring. This is more common in dark-skinned individuals. Most resolve by 6 -12 months of age. They can spontaneously close by up to 6 years of age, but the older the child or the greater the hernia size, the less likely spontaneous closure will occur. Treatment includes observation and surgery if strangulation occurs which is rare. Surgery may also be indicated if the hernia is enlarging or the child is more than 5-6 years old.
• Omphalitis – usually this is due to Staphlococcus aureas and Escherichia coli. The localized infection can quickly spread to the peritoneum and blood stream. Treatment includes antibiotics and possibly surgical drainage of abscesses.
• Persistent omphalomesenteric duct – a lesion associated with an intestinal fistula and Meckel’s diverticulum. A Meckel’s scan or fistulogram may be indicated for diagnosis
• Persistent urachus – a lesion resulting from inappropriate closure of the allantoic duct that is associated with bladder communication. Urinary fluid drainage is seen. A bladder and/or renal ultrasound often demonstrates the lesion.
• Polyp – partial or complete present of omphalomesenteric duct or urachus. This presents as a pedunculated firm, red mass often with a mucoid secretion. This requires surgical excision.
• Tumors – these are rare and most are benign. The differential diagnosis includes urachal cyst, omphalomesenterid duct cyst, angioma, dermoid cyst or myxosarcoma.

Learning Point

About 1% of all infants have a single umbilical artery and of those, ~15% have one or more congenital anomalies. These often involve the gastrointestinal, genitourinary, pulmonary, cardiovascular or nervous systems.

Occult renal abnormalities are common in children with single umbilical arteries and a significant proportion have Grade II or higher vesicoureteral reflux. Therefore, a renal ultrasound is a recommended screening procedure. A voiding cystourethrogram is sometimes also ordered. If other anomalies are found on careful physical examination, a chromosomal analysis might be considered.

SUBGALEAL OR APONEUNEUROIC HEMATOMA

Bleeding into the soft tissues of the head is a common problem associated with birth and usually does not require intervention. These include:

• A caput succedaneum is localized serosanguineous edema of the scalp that occurs between the skin and aponeurosis of the scalp. These swellings can cross suture lines and are usually due to pressure from the pelvis, uterus or vagina.
• A subgaleal or aponeuneuroic hematoma occurs between the aponeurosis of the scalp and the periosteum of the bone. The galea aponeurotica occurs from the occiput to the eyebrows and laterally to the temporalis fascia. It therefore can cross suture lines and is a large potential space where hemorrhage can occur.
  Subgaleal hematomas usually occur due to shearing of emissary veins between the intracranial venous sinus and the scalp.

• A cephalohematoma is due to bleeding beneath the periosteum of the bone, i.e. between the periosteum and cortical bone. Therefore these swellings occur only over bone and do not cross suture lines. They occur in 2.5% of births.

Subgaleal hematomas are the least common and can occur along with caputs and cephalohematomas and therefore it is important to be aware of this diagnosis.

Caputs have localized skin edema. Subgaleal hematomas may be ballotable and have a fluid wave. As noted previously, a cephalohematoma does not cross suture lines, whereas the other two may.

Learning Point

Subgaleal hematomas are more common after assisted deliveries such as forceps and vacuum.

Moderate to severe subgaleal hematomas occur in 30/10,000 live births.

Of those cases, progressive anemia leading to hypovolemic shock and death occurs in 12-25% of cases.

Blood loss can be life threatening and even modest bleeding can cause exaggerated hyperbilirubinemia necessitating phototherapy and even exchange transfusion.

It is estimated that ~260 ml of blood increases the head circumference by 1 cm.

Intracranial hemorrhages are also more frequently associated with subgaleal hematomas (~50% in one study) and therefore seizures are also a possible complication.

Secondary infection of the hematoma is also an very uncommon complication.

Treatment includes treating the underlying hemorrhage with blood volume replacement, and treatment of congenital or acquired coagulopathies if present. Careful monitoring of the clinical condition and vital signs is necessary. Physical compression of the head may be helpful.

POSSIBLE GENETIC SWITCH FOR AMBLYOPIA - "LAZY EYE"

APA Aug. 7, 2013

There is only a limited so-called "critical period" in patients with amblyopia, during which "lazy eye" and other serious visual problems can be corrected until they become permanent. But US researchers have now discovered a gene that may change that. In experiments with animals where the gene was not present, there was no critical period. Therefore, they concluded in "Neuron", a treatment of amblyopia may be possible at any age.

"The generally accepted view has been that as the inhibitory neurons develop, synaptic plasticity declines, which was thought to occur at about five weeks of age in rodents," roughly equivalent to five years of age in humans," said Elizabeth M. Quinlan from the University of Maryland, who led the project with Alfredo Kirkwood from Johns Hopkins University. But in earlier experiments, Quinlan and Kirkwood found no correlation between the development of these inhibitory neurons and the loss of plasticity.

The team therefore looked "one synapse upstream from these inhibitory neurons," studying the control of that synapse by a protein called NARP (Neuronal Activity-Regulated Pentraxin). Working with mice lacking the NARP gene as well as a control group, the researchers covered one eye in each animal to simulate conditions that produce amblyopia.

The mice in the control group developed amblyopia, but the mice that lacked NARP did not. Without NARP, the mice simply had no critical period in which the brain circuitry was weakened in response to the impaired blocking vision in one eye. Except for the lack of this plasticity, their vision was normal. "It's remarkable how specific the deficit is," Quinlan said. "We can completely turn off the critical period for plasticity by knocking out this protein." The discovery raises hope that a treatment could allow correction of amblyopia late in life.