Moms With Tough Childhoods More Likely to Have Smaller Babies: Study

THURSDAY, March 31 (HealthDay News) -- Women who suffered abuse in childhood are at increased risk of having low birth weight babies, a new study indicates.

It also found that poverty during childhood and substance use during adolescence and pregnancy boosts the chances of having low birth weight babies, who are at increased risk for death before their first birthday and chronic health problems.

About 8 percent of babies born in the United States each year have a low birth weight -- less than 5 pounds, 8 ounces (2,500 grams).

Researchers at the University of Washington in Seattle examined data from 136 mothers who had been part of a study since childhood. They found that women who suffered emotional, physical or sexual abuse or poverty in childhood were more likely to smoke, drink or use drugs during pregnancy, which increases the risk of having a low birth weight baby.

"Our findings suggest that a mother's economic position in childhood and her experience of maltreatment during childhood have implications for her children born years later," study author Amelia Gavin, an assistant professor in the School of Social Work, said in a university news release.

"What is important about this study is that it was the mother's experience of poverty and maltreatment in childhood, not her poverty or depression or obesity in adulthood, that contributed to her infant's low birth weight," she added.

Doctors should ask prospective mothers about any childhood maltreatment and offer help to those at risk for substance abuse during pregnancy, Gavin suggested.

The study was published online recently in the Journal of Adolescent Health.

More information

The March of Dimes has more about low birth weight.

-- Robert Preidt

View the original article here

MY PEDIATRIC CASE

By Dr.Sally Zeinatie















This case was followed by me during internship in the pediatric ward.His CVS went unnoticed till discharge date,while filling the discharge summary I noticed CVS was unexamined,to find later the congenital anomalies he had.Suspecion of T.B was put forward by me to my seniors but unfortunately Mantoux mislead everyone.Still I felt T.B is there somewhere in a hidden form,and suggested CT chest.I noticed the kyphosis which lead me to suggest CT Spine,which then lead to the suggestion of MRI Spine.With the help of these investigations my diagnosis was confirmed.It is a very interesting case,therefore liked sharing it with you.


9 YRS OLD
PAKISTANI
Admitted on 07/05/06

Known case of DOWN’S SYNDROME

Mild to moderate grade fever,
Associated with sweating
At night time ONLY
Accompanied with weight loss
For one month

Negative history:
No Hx of URTI,
No change of bowel habits,
No urinary symptoms,
No Joint pain,
No skin rash,
NO HX OF RECENT TRAVEL TO PAKISTAN

Past Medical:
K/C of DOWN’S SYNDROME
Past Surgical:
Not significant
Medications:
Not on any medications
Family Hx:
No one in the family has down’s syndrome,T.B, or malignancies
Birth Hx:
Normal vaginal delivery,
Preterm at 7 months,
Developmental Hx:
Speech delay,
Cannot say anything.
Diet Hx:
Normal solid diet
Immunization up to date

O/E:
Pale
Not in respiratory distress
Well hydrated
Afebrile
Multiple post cervical lymphadenopathy
BP:120/85
Pulse:77/min

Chest:decreased air entry on right side,right mid zone.
CVS:S1+S2+early diastolic murmur with fixed splitting of S2
CNS:intact,alert,no meningeal signs
Abdomen:soft,non tender,hepatomegaly 2cm below costal margin.
ENT:normal

D/D:
TUBERCULOSIS
MALIGNANCY
BRUCELLA
EBV
AUTOIMMUNE

INVESTIGATIONS:
CBC:
Hb 10.7
WBC 16
Platelets 550
Neutrophils 65
Glucose 4.9
CRP 161
ESR 72
U/E Normal
LFT Normal
Mantoux test negative
Brucella negative
EBV IGM negative
ANA negative
Mycoplasma negative
Urine culture :No growth
Blood film Normal

On 09/05/06 ECHO was done
Small PDA with left to right shunt
Possible ASD secundum
Bicuspid Aortic valve with raphae
Mild mitral valve prolapse
Good LV function

Was discharged on 09/05/06
With the impression of
Pneumonia
Was given KLACID 150mg BD

Was seen in clinic on 16/05/06
Repeated CBC:
Hb 10.4
WBC 12.4
ESR 58
CRP 125
Mantoux test Negative

Was seen in clinic on 27/05/06
C/O: Running low grade fever on&off
CBC:
Hb 11.1
WBC 18.8
ESR 42
CRP 129

Was admitted:
to repeat
CBC,ESR,CRP,U/E,LFT,
Blood culture,brucella,
ECHO to R/O endocarditis,
Mantoux test
Readmitted on 27/05/06

D/D:
TB
Malignancy
Endocarditis

3 Blood culture taken at spike of fever at 10pm
Showed NO growth

CBC:
Hb 10.6
WBC 21.2
PCV 501
Glucose 4.4
U/E Normal
CRP 161
ESR 55
Urine culture:NO growth

ECHO done on 28/05/06
No vegetations seen in LV,mitral valve,or aortic valves
Normal pulmonary valves
No pericardial effusion
Normal LV function
Normal aortic arch
Conclusion: NO evidence of endocarditis

Repeat
Mantoux test
CT chest
To consider
Bone marrow examination & culture

CXR
Showed pulmonary infiltration with cavity formation.



CT Chest
Multiple bilateral confluent opacities are seen extending in both the upper lobes &right lobe,
Showing air bronchogram as well as reticulonodular infiltrates.
No hilar or mediastinal lymphadenopathies,
No pleural masses or collections are seen.




D8+D9 vertebral body partial collapse.




CT SPINE



Kyphus deformity at D8+D9 with destruction of opposing articular surface




Opposing subarticular osteosclerosis



Soft tissue,
pravertebral collection
with marginal calcification
is seen abutting D8+D9 vertebrae



Conclusion
D8+D9 vertebrae collapse
Discal destruction
With paravertebral collection
Multiple bilateral pulmonary opacities
Suggestive of long standing infectious spondolytis
Probably of Tuberculous etiology with Pulmonary T.B




MRI of DORSO-LUMBAR SPINE
Spondylodistal erosive process is seen involving D8 & D9 & intervening disc space.
D9 vertebra showed anterior wedging.
Vertebral body, its posterior neural arches are seen to be involved.
D8 & D9 disc space is almost obliterated.



Pre & paraspinal multinoculated cystic component is seen.
Anterior epidural intraspinal component is also noted mildly impressing on the cord at this level.
Another enhancing component is seen posterior epidurally opposite D7 down to D9 levels not causing any cord compression.



Conclusion
Spondylo-discal inflammatory erosive process of D8 & D9 & its intervening disc with pre & para & intraspinal cystic component.



The picture is most likely representing POTT’S disease

DIAGNOSIS:
PULMONARY TUBERCULOSIS
WITH POTT’S DISEASE

ON 07/06/06 MANTOUX TEST REPEATED WAS POSITIVE upto 20mm

STARTED & DISCHARGED ON:
STREPTOMYCIN 500mg OD
ISONIAZIDE 200mg OD
RIFAMPICIN 300mg OD
PYRAZINAMIDE 500mg OD
MULTIVITAMIN 5ml OD

POTT’S DISEASE

Pott's disease is a presentation of extrapulmonary tuberculosis that affects the spine, a kind of tuberculous arthritis of the intervertebral joints.
More precisely it is called tuberculous spondyloarthropathy and the original name was formed after Percivall Pott (1714-1788), a London surgeon.
It is most commonly localized in the thoracic portion of the spine. The fictional (hunch back of notre dame) had a gibbous deformity
humpback
that is thought to have been caused by tuberculosis

SIGNS & SYMPTOMS
back pain
fever
night sweating
anorexia
weight loss
Spinal mass, sometimes associated with numbness, tingling or muscle weakness
of the legs

DIAGNOSIS
blood tests - elevated blood sedimentation rate
tuberculin skin test
radiographs of the spine
bone scan
CT of the spine
bone biopsy

LATE COMPLICATIONS
Vertebral collapse resulting in kyphosis
Spinal cord compression
sinus formation
paraplegia
(so called Pott's paraplegia)

MANAGEMENT

non-operative - antituberculous drugs
analgesics
immobilization of the spine region
Surgery may be necessary, especially to drain spinal abscesses or to stabilize the spine

PREVENTION
Controlling the spread of tuberculosis infection can prevent tuberculous spondylitis and arthritis.
Patients who have a positive PPD test (but not active tuberculosis) may decrease their risk by properly taking medicines to prevent tuberculosis.
To effectively treat tuberculosis, it is crucial that patients take their medications exactly as prescribed.

MEDITERRANAEN SEA FEVER

By Dr.Sally Zeinatie




SYNONYMS:

periodic disease,
recurrent polyserositis,
familial Mediterranean fever

DEFINITION:

Familial Mediterranean fever (FMF) is an inherited disorder of the inflammatory response characterized by recurring attacks of fever, accompanied by intense pain in the abdomen, chest, or joints. Attacks usually last 12-72 hours, and can occasionally involve a skin rash.

Kidney disease is a serious concern if the disorder is not treated. FMF is most prevalent in people of Armenian, Sephardic-Jewish, Arabic, and Turkish ancestry.

PATHOPHYSIOLOGY:

Nonsense or missense mutations in the MEFV (Mediterranean fever) gene appear to cause the disease. This gene produces a protein called pyrin (derived from the association with predominant fever) or marenostrin (derived from the phrase "our sea," because of the Mediterranean heritage of most patients).

Mutations occur in exons 2, 3, 5 and 10.
The function of pyrin has not been completely elucidated, but it appears to be a suppressor of the activation of caspase 1, the enzyme that stimulates production of interleukin 1β, a cytokine central to the process of inflammation.

It is not conclusively known what exactly sets off the attacks, and why overproduction of IL-1 would lead to particular symptoms in particular organs (e.g. joints or the peritoneal cavity).

GENETICS:

The MEFV gene is located on the short arm of chromosome 16 (16p13). The disease inherits in an autosomal recessive fashion. Therefore, two asymptomatic carrier parents have a 25% chance of a child with the disorder. FMF patients who marry a carrier or another FMF patient have a 50% and 100% chance, respectively, in having a child with FMF.

CLINICAL SYMPTOMS:

Fever:
An FMF attack is nearly always accompanied by a fever, but it may not be noticed in every case. Fevers are typically 100-104°F (38-40°C). Some people experience chills prior to the onset of fever.

Abdominal pain:
Nearly all people with FMF experience abdominal pain at one point or another, and for most it is the most common complaint. The pain can range from mild to severe, and can be diffuse or localized. It can mimic appendicitis, and many people with undiagnosed FMF have had appendectomies or exploratory surgery of the abdomen done, only to have the fever and abdominal pain return.

Chest pain:
Pleuritis, also called pleurisy, occurs in up to half of the affected individuals in certain ethnic groups. The pain is usually on one side of the chest. Pericarditis would also be felt as chest pain.

Joint pain:
About 50% of people with FMF experience joint pain during attacks. The pain is usually confined to one joint at a time, and often involves the hip, knee, or ankle. For some people, however, the recurrent joint pain becomes chronic arthritis.

Myalgia:
Up to 20% of individuals report muscle pain. These episodes typically last less than two days, and tend to occur in the evening or after physical exertion. Rare cases of muscle pain and fever lasting up to one month have been reported

Skin rash:
A rash, described as erysipelas-like erythema, accompanies attacks in a minority of people, and most often occurs on the front of the lower leg or top of the foot. The rash appears as a red, warm, swollen area about 4-6 in (10-15 cm) in diameter.

Amyloidosis:
FMF is associated with high levels in the blood of a protein called serum amyloid A (SAA). Over time, excess SAA tends to be deposited in tissues and organs throughout the body.

DIAGNOSIS:

Symptoms involving one or more of the following broad groups should lead to suspicion of FMF: Unexplained recurrent fevers, polyserositis, skin rash, and/or joint pain; abnormal blood studies; and renal or other disease associated with amyloidosis

LAB STUDIES:

Results of routine blood tests performed during the acute attacks are nonspecific. Levels of acute phase reactants (ie, C-reactive protein, amyloid A protein, fibrinogen) are elevated, as is the erythrocyte sedimentation rate. The white blood cell count is usually elevated during an attack. The elevated levels rapidly return to the reference range as the attack abates.
Proteinuria should raise a concern about possible amyloidosis. For unknown reasons, hematuria occurs in 5% of patients.


Synovial fluid is inflammatory, with cell counts as high as 100,000/mL.
From the successful cloning of the MEFV gene, researchers have developed a rapid test for the most common mutations. Compared with gene sequencing, the test has a sensitivity and specificity of 100%. However, not every patient with FMF based on clinical criteria has a mutation as determined by testing for specific mutations. One explanation for this is that, although at least 30 identified mutations exist, 5 of them account for 99% of FMF cases, so testing for all 30 mutations, particularly in defined populations, is not cost-effective.

TREATMENT:

Attacks are self-limiting, and require analgesia and non-steroidal anti-inflammatory drugs (such as diclofenac.

Since the 1970s, colchicine, a drug otherwise mainly used in gout has been shown to decrease attack frequency in FMF patients. The exact way in which colchicine suppresses attacks is unclear. While this agent is not without side-effects abdominal painmuscle pains it may markedly improve quality of life in patients. The dosage is typically 1-2 mg a day.

Development of amyloidosis is delayed with colchicine treatment.


Interferon is being studied as a therapeutic modality.

PROGNOSIS:

For those individuals who are diagnosed early enough and take colchicine consistently, the prognosis is excellent.

Patients who are compliant with daily colchicine can probably expect to have a normal lifespan if colchicine is started before proteinuria develops.
Even with amyloidosis, the use of colchicine, dialysis, and renal transplantation should extend a patient's life beyond age 50 years.

COMPLICATIONS:

AA-amyloidosis with renal failure is a complication and may develop without overt crises. AA (amyloid protein) is produced in very large quantities during attacks and at a low rate between them, and accumulates mainly in the kidney, as well as the heart, spleen gastrointestinal tract and the thyroid.

There appears to be an increase in the risk for developing particular vasculitis-related diseases (e.g. Henoch-Schoenlein purpura spondylarthropathy, prolonged arthritis of certain joints and protracted myalgia.

Complications of Prematurity

By Dr.Sally Zeinatie


RESPIRATORY DISTRESS SYNDROME (RDS)
BRONCHOPULMONARY DYSPLASIA
PNEUMOTHORAX
PNEUMOMEDIASTINUM
INTERSTITIAL EMPHYSEMA
PULMONARY HYPOPLASIA
PULMONARY HEMORRHAGE
APNEA

CARDIOVASCULAR:
PATENT DUCTUS
ARTERIOSUS(PDA)

CONGENITAL MALFORMATIONS

BRADYCARDIA WITH APNEA


HYPOTENSION


HYPERTENSION

REFRACTORY CAUSES OF BRONCHIAL ASTHMA

By Dr.Sally Zeinatie



UPPER RESPIRATORY TRACT CONDITIONS
ALLEGIC RHINITIS
CHRONIC RHINITIS
SINUSITIS:nasal discharge unilateral or bilateral,cough,fever


ADENOIDAL OR TONSILLAR HYPERTROPHY
NASAL FOREIGN BODY:unilateral nasal discharge,obstruction.

MIDDLE RESPIRATORY TRACT CONDITIONS:

LARYNGOTRACHEOBRONCHOMALACIAmost common congenital laryngeal anomaly,most frequent cause of stridor in infants and children.stridor is inspiratory,low pitched,excarbated by any exertion.symptoms appear 1st 2 weeks upto 6 months.


LARYNGOTRACHEOBRONCHITIS:

fever,barking cough

LARYNGEAL WEB:
are glottic or subglottic,cry is high pitched,treatmane is by incision or dialation.

EXTERNAL MASS

COMPRESSING ON AIRWAY :

FOREIGN BODY ASPIRATION.
CHRONIC BRONCHITIS FROM ENVIRONMENTAL TOBACCO SMOKE EXPOSURE.


VOCAL CORD PARALYSIS:3rd most common congenital laryngeal anomaly producing stridor.paralysis occurs as a result of surgical correction of congnital cardiac anomaly or tracheoesophageal fistula.


TRACHEOESOPHAGEAL FISTULA:frothing from the mouth after feeding.

TOXIC INHALATION.

LOWER RESPIRATORY TRACT CONDITIONS:

BRONCHOPULMONARY DYSPLASIA:due to prematurity.tachpnea,wheeze or coarse crackles,in severe conditions mechanical ventilation is required.


VIRAL BRONCHIOLITIS:

RSV,parainfluenza,
adenovirus.wheezy cough,dyspnea,irritability,fever

GASTROESOPHAGEAL REFLUX

CAUSES OF BRONCHIECTASIS:

1-CYSTIC FIBROSIS:autosomal recessive,mutations in long arm of chromosome 7respiratory symptoms are presenting features.bronchiectasis and obstructive pulmonary disaese are primary causes of morbidity and mortality.
2-IMMUNE DEFICIENCY
3-ALLERGIC BRONCHOPULMONARY MYCOSES
4-CHRONIC ASPIRATION
5-IMMOTILE CILIA SYNDROME
Primary ciliary dyskinesia:situs inversus,chronic sinusitis,otitis,airway disease.-KARTAGENER’S SYNDROME


BRONCHOLITIS OBLITERANS:

fever,cough,cyanosis,respiratory distress,sputum production,wheezing.
INTERSTITIAL LUNG DISEASE:
causes disruption of alveolar gas exchange.cough,tachpnea,dyspnea,
wheezing.


PULMONARY EOSINOPHILIA,BRONCHIAL ASTHMA,VASCULITIS-CHURG STRUASS DISAESE

TUBERCULOSIS

PNEUMONIA
PULMONARY EDEMA

CONGENITAL HYPOTHYRODISM

By Dr.Sally Zeinatie



At birth, clinical recognition of hypothyroidism is difficult and most infants appear normal.

The full-blown picture develops progressively over weeks and months.
Early suspicion in a neonate
Prolongation of physiological icterus
Feeding difficulties, chocking during feeds
Respiratory difficulties-apnea
Cry little,sleep much

Early symptoms:

Weakness,Fatigue,pale color
Cold intolerance
Constipation,Weight gain
Joint & muscle pain,brittle nails & hair


Late symptoms:

Slow speech
Dry flaky skin
Puffy face,hands & feet
Broad flat nose
Widely set eyes
Decreased taste & smell
Thinning of eyebrows
Hoarseness

Impaired mental development
Retarded bone age

Additional symptoms:

Muscle spasm
Muscle atrophy
Uncoordinated movements
Joint stiffness
Hair loss
Drowsiness
Appetite loss

Neurological manifestations:

Infantile hypotonia,psychomotor delay
Lack of cry “good baby”,
somnolence
Sluggish/
disinterested

Respiratory manifestations:

Apnea
Choking spells with feeds
Nasal obstruction
Noisy respirations
Respiratory distress syndrome

Cardiovascular manifestations:

Cardiomegaly
Murmers
Slow heart rate
Electrocardiographic findings:

Sinus bradycardia(usual)
Sinus tachcardia(rare)
QT prolongation
Decreased amplitude of p wave
Ventricular tachycardia
Atrioventricular & interventricularblock
Incomplete or complete right bundle branch block
Atrial fibrillation



Gastrointestinal manifestations:

Delayed dentation
Feeding difficulties
High birth weight
Large abdomen
Macroglossia
Poor appetite
Prolonged jaundice
Umbilical hernia

Endocrinal manifestations:

goiter

Hematological manifestations:

Anemia
Iron deficiency
Or
Pernicious anemia
With vitB12 deficiency
Renal manifestations
Decreased glomerular filtration rate
Impaired ability to excrete water load
Musculoskeletal manifestations
Increased head size
Broad, short fingers
Pseudohypertrophy of calf muscles
Short limbs ,Short thick neck
Cutaneous manifestations
Carotenemia
Coarse, brittle, scanty hair
Cold & mottled skin
Dry, scaly skin
Edema of genitals & extremeties
Low hair line

CROUP

By Dr.Sally Zeinatie


DEFINITION:

The term croup does not refer to a single illness, but rather a group of conditions involving inflammation of the upper airway that leads to a cough that sounds like a bark, particularly when a child is crying.


It is a respiratory disease which afflicts infants and young children, typically aged between 3 months and 3 years.

CAUSES:

Most croup is caused by viruses, but similar symptoms may occasionally be caused by bacteria or an allergic reaction.


The viruses most commonly involved are parainfluenza virus (accounting for most cases), adenovirus, respiratory syncytial virus, influenza, and measles.

Signs and symptoms:

Croup is characterized by a harsh 'barking' cough, inspiratory stridor (a high-pitched sound heard on inhalation), nausea/vomiting, and fever. Hoarseness is usually present. More severe cases will have respiratory distress.


The 'barking' cough (often described as a "seal like bark") of croup is diagnostic. Stridor will be provoked or worsened by agitation or crying. If stridor is also heard when the child is calm, critical narrowing of the airway may be imminent.


In diagnosing croup, it is important for the physician to consider and exclude other causes of shortness of breath and stridorsuch as foreign body aspiration and epiglottitis.


On a frontal X-ray of the C-spine, the steeple sign suggests the diagnosis of croup.


Treatment:

The treatment of croup depends on the severity of symptoms.
Mild croup with no stridor or stridor only on agitation, and just a cough may simply be observed, or a dose of inhaled, oral, or injected steroids may be given.


When steroids are given, dexamethasone is often used, due to its prolonged physiologic effects.

Moderate to severe croup may require nebulized adrenaline in addition to steroids. Oxygen may be needed if hypoxia develops. Children with moderate or severe croup are typically hospitalized for observation, usually for less than a day.

Intubation is rarely needed (less than 1% of hospitalized patients).

Prognosis:

Viral croup is a self-limited disease, but can very rarely result in death from complete airway obstruction.

Symptoms may last up to 7 days, but typically peak around the second day of illness. Rarely, croup can be complicated by an acute bacterial tracheitis which is more dangerous.

Complications:

Respiratory distress
Respiratory arrest
Epiglottitis
Bacterial tracheitis
Atelectasis
Dehydration

Prevention:

Frequent hand washing and avoiding contact with people who have respiratory infections are the best ways to reduce the chance of spreading the viruses that cause croup.

Immunization Overview

By Dr.Sally Zeinatie
Immunization Overview
Most humans live their lives ignoring the certainty of their own mortality. Perhaps this fact explains why the adage “an ounce of prevention is worth a pound of cure.”
Immunization Overview
Immunization represents one of the most cost effective means of prevention of infectious disease.
Immunization Overview
A vaccine is a suspension of attenuated live or killed microorganism or antigenic portions presented to a potential host to induce immunity and prevent disease.
Immunization Overview

Types of vaccines:
Immunization Overview
Inactivated or killed
Live attenuated vaccine
Toxoids
Cellular fractions
Combinations
Polyvalent vaccines
Adjuvant vaccine
Immunoglobulin
Immunization Overview
Three types of preparations used in passive immunization:
Immunization Overview
Standard human immune serum globulin
Immunization Overview
Special immune serum globulins with a known content of antibody for specific agents
Immunization Overview
Animal sera or antitoxins
Immunization Overview
Constituents of vaccines:
Immunization Overview
Preservatives, stabilizer,& antibiotics
Immunization Overview
Adjuvant
Immunization Overview
Suspending fluid
Immunization Overview
Main vaccine used:
Immunization Overview
MMR
DPT
OPV+IPV
BCG
HiB
HBV
Pneumoccocus vaccine
Influenza vaccine
Immunization Overview
Contraindications:
Immunization Overview
TUBERCULOSIS
Breast feeding
Pregnancy
Intracranial pressure
HIV
Contact dermatitis
eczema
deficient immunity
History of Hepatitis
Immunization Overview
COMPLICATIONS:
Immunization Overview
ACUTE ENCEPHALITIS
Immunization Overview
HYPERSENSITIVITY
Immunization Overview
VACCINE ASSOSIATED PARALYTIC POLIO
Immunization Overview
GUILLIAN BARR SYNDROME
Immunization Overview
PRECAUTION:
Immunization Overview
COLD CHAIN:
Immunization Overview
Is a system of storage and transport of vaccines at low temperatures from the site of manufacture to the actual vaccination site.
Immunization Overview

Hemangioma Overview

By Health Tips & Technics

A blood vessel Tumor with active cell dividing activity is called a Hemangioma. They are often found on the head or the neck region. Most children have only one and only in rare cases children have a few of them. The hemangioma is more common among girls than boys.

Hemangiomas are tuffs of Blood Vessels which are mostly superficial on the skin. It can be termed as a birthmark. These appear on the skin at birth or may appear within one month of birth. They appear as faint red marks first and then grow rapidly in size. The exact reason due to which these occur is still unknown. They occur mostly in premature infants.

With the advancement in medical sciences, the hemangiomas can be treated using laser treatments, surgical excision etc., In many cases treatment is not required as some areas start greying, in many cases there would be a rapid regression. Rarely it needs corrective surgery. Its difficult without medical advice to predict if the hemangioma is a complicated one or not. It is essential to seek medical advice. Treatments depends on the size and location where it is present. Small non intervening ones do not need surgical correction.

Its essential to acertain through ultrasound that there are not internal hemagioma present either on the liver or the abdomen. There are two types of hemangioma the one that is superficial is the "Strawberry hemangioma" which are usually bright red and soft. Those that are deeper in the skin are called cavernous hemangioma, these often appear bluish. Hemangiomas are not contagious in nature.

http://www.healthtips.in/hemangioma.asp

Consumer Group: Zhu Zhu Pet Toys Are Unsafe

By Daniel J. DeNoon WebMD Health News

Reviewed By Louise Chang, MD

GoodGuide Says Toys Are Contaminated With Antimony; Manufacturer Denies Any Health Hazards.

Zhu Zhu Pets, one of the hottest-selling toys this holiday season, are contaminated with unsafe levels of antimony, says GoodGuide, a new consumer group.

That's just not so, says Cepia LLC, the company that makes Mr. Squiggles and other Zhu Zhu Pets. To prove it, Cepia released premarketing test results from a highly respected independent lab.

Contrary to the GoodGuide tests, the report from Bureau Veritas labs shows that none of the Zhu Zhu Pets caries unsafe levels of antimony or any other contaminant.

In a news release, GoodGuide said the "higher-than-allowed presence" of antimony on the toys "can lead to lung and heart problems, and impacts on fertility."

Because of the GoodGuide complaint, the Consumer Product Safety Commission (CPSC) says it will investigate the toy. CPSC spokesman Scott Wolfson tells WebMD that the CPSC takes the GoodGuide allegation seriously, but that the investigation does not mean the toy should be considered unsafe.

"CPSC is looking into the Zhu Zhu pet toy and we will complete our review swiftly," the CPSC says in an official statement.

Meanwhile, Cepia is vigorously defending the safety of Zhu Zhu Pets. No recall is planned.

"Mr. Squiggles is absolutely safe and has passed the most rigorous testing in the toy industry to consumer heath and safety," Cepia says in a news release.

GoodGuide, started in September 2008, is a consumer group led by Dara J. O'Rourke, PhD, assistant professor of environmental science at the University of California, Berkeley. The group issues ratings of toys and other products based on product ingredients, screening for contaminants, and manufacturers' social policies.

GoodGuide tests for contaminants using a handheld device called an X-ray fluorescence gun. The test can detect antimony but cannot accurately measure toxic levels of the metal. That requires a different test, called a solubility test.

"We did not test these toys using the new government standard for toy companies to determine the 'soluble' level of contaminants in a toy," O'Rourke admits in a blog entry posted today on the GoodGuide web site.

Antimony is a silvery white metal element, usually mixed with other metals for use in batteries, solder, sheet and pipe metal, ammunition, and pewter. Antimony can harm health in concentrations greater than 60 parts per million.

SOURCES: News release, GoodGuide.

GoodGuide web site.

News release, Cepia LLC.

Cepia LLC web site.

News release, Consumer Product Safety Commission.

Scott Wolfson, director, office of information and public affairs, Consumer Product Safety Commission.

©2009 WebMD, LLC. All Rights Reserved.

Not All Parents Put Babies to Sleep on Back

By Kelli Miller Stacy WebMD Health News

Reviewed By Louise Chang, MD

Study Shows Advice on SIDS Prevention Isn't Being Heeded.

Despite warnings that it is safest to place a baby to sleep on his or her back, the number of caregivers doing so has not increased in recent years, according to a new report.

The National Institute of Child Health and Human Development's "Back to Sleep" campaign began in 1994 after compelling evidence showed that babies who slept on their backs had a much lower risk for sudden infant death syndrome (SIDS). In the U.S., SIDS is the No. 1 cause of death in children under age 1.

Since the campaign began, the number of babies being put to sleep on their backs jumped from 25% to 70%. But the number of caregivers heeding the advice has not changed since 2001, say Yale School of Medicine researchers.

The researchers looked at how 15,000 caregivers positioned their babies to sleep since the campaign launch, using information from the National Infant Sleep Position Study, an annual telephone survey of about 1,000 households with infants. The survey asks nighttime caregivers of babies 7 months old and younger: "Do you have a position you usually place your baby in?"

The study also revealed a racial disparity in sleeping positions. "We ... found that African Americans still lag behind caregivers of other races by about 20 percent in following this practice," Eve Colson, MD, associate professor of pediatrics at Yale School of Medicine, says in a news release.

Choosing Sleep Positions
Colson and her team recently identified three key factors associated with a caregiver's choice of an infant's sleeping position:

•Whether the caregiver was told by a doctor to place the baby to sleep on the back
•Concerns for the baby's comfort
•Fear of the infant choking while sleeping
While a third of the caregivers surveyed said their doctor did recommend putting their babies to sleep on the back, others said they either were given other advice or did not receive a recommendation at all.

More than a third of those surveyed said they didn't think the baby would be comfortable sleeping on his or her back. Those who did not bring up this concern were four times more likely to follow the Back to Sleep guidelines.

Ten percent of caregivers said they thought their infant might choke while sleeping on his or her back. However, those who did not report this concern were much more likely to put their babies in the back position.

"For the vast majority of infants, concerns about choking while back sleeping are unfounded," Marian Willinger, PhD, special assistant for SIDS research at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), emphasizes in a news release. "Placing infants on their backs for sleep remains the single most effective means we know to reduce the risk of sudden infant death syndrome."

Willinger notes that in certain health conditions, a doctor may recommended against back sleeping, but only after carefully weighing the risks and benefits to the infant.

Babies Who Sleep on Their Backs
The study revealed that babies were more likely to be put to sleep on their backs if:

•They were the first-born child
•They were not premature
•Their mothers did not live in the Southern U.S.
•Their mothers had a higher education level
•Their mothers were not African-American
The researchers urge all health care providers to make sure caregivers are told that it's safest to place infants to sleep exclusively on their backs, and that concerns about choking and discomfort are discussed. Doing so, they say, will help reduce the overall SIDS death rate.

"We can't equivocate, or the message gets lost," says Colson. "And we need to serve as role models, placing infants to sleep on their backs, beginning the minute infants are born in our hospital nurseries and pediatric units."

The findings appear in the December issue of the Archives of Pediatrics and Adolescent Medicine.

SOURCES: News release, National Institute of Child Health and Human Development.

News release, American Medical Association.

News release, Yale University.

Colson, E. Archives of Pediatrics and Adolescent Medicine. Dec. 1, 2009: vol 163: pp 1122-1128.

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