We read with interest “Job syndrome masquerading as non-accidental
injury” published in January of this year. We note that the diagnosis of
Job (Hyper- IgE) syndrome was made on the basis of dysmorphism, eczema, a
single staphylococcal skin abscess, fractures and a raised serum IgE
level.
We are concerned that the clinical features presented are not typical
of Hyper IgE syndrome (HIES) and th...
We read with interest “Job syndrome masquerading as non-accidental
injury” published in January of this year. We note that the diagnosis of
Job (Hyper- IgE) syndrome was made on the basis of dysmorphism, eczema, a
single staphylococcal skin abscess, fractures and a raised serum IgE
level.
We are concerned that the clinical features presented are not typical
of Hyper IgE syndrome (HIES) and the investigations presented are
incomplete and inadequate to support the conclusions.
A serum IgE level of 1615 KU/l (equivalent to 1615 IU/ml) is not
unusual and would be consistent with uncomplicated atopic eczema (1). In
HIES, IgE levels higher than 2000 IU/ml are seen in 97% of patients and
characteristically range between 10,000-100,000 IU/ml. Eosinophilia is a
consistent laboratory finding in HIES, however these data were not quoted
in this case (2,3).
This patient had a single staphylococcal abscess and no history of
recurrent infection. This makes the diagnosis of a primary
immunodeficiency extremely unlikely.
The occurrence of fractures in this case was attributed to HIES.
Fractures secondary to minimal trauma are a feature of sporadic and
autosomal dominant forms of HIES and occur in 57%-71% of patients (2,3).
The authors state that no molecular testing is available to confirm
the diagnosis. However, in 2007 Minegishi et al (4) and Holland et al (5)
identified dominant negative STAT 3(signal transducer and activator of
transcription 3) gene mutations as the predominant cause of autosomal
dominant and sporadic HIES.
Given that the possibility of non-accidental injury (NAI) was
considered in this case, we would recommend that an eosinophil count and
testing for STAT3 mutations are undertaken, and the case reviewed by a
multidisciplinary team familiar with the diagnosis and management of HIES
before confirming this diagnostic label and excluding NAI as the cause of
fractures.
References:
1. Laske N, Niggemann B. Does the severity of atopic dermatitis
correlate with serum IgE levels? Pediar Allergy Immunol 2004;15:86-88.
2.Grimbacher B, Holland SM, Puck JM. Hyper-IgE syndromes. Immunol Rev
2005;203:244-250.
3.Freeman AF, Holland SM. The Hyper-IgE Syndromes. Immunol Allergy
Clin N Am 2008;28:277-291.
4. Minegishi Y, Saito M, Tsuchiya S, Tsuge I, Takada H, et al.
Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper
-IgE syndrome. Nature 2007;448:1058-1062.
5.Holland SM, Deleo FR, Elloumi HZ, Hsu AP, Gulbu Uzel BA, et el.
STAT3 mutations in the Hyper-IgE syndrome. N Eng J
Med 2007;18:1608-1619.
Reflecting to the letter of Mark P Tighe, et al.[1] we would like to
report our case with rhesus-haemolytic disease treated with D-penicillamine (DPA) and phototherapy without exchange transfusion:
We recently cared for a term infant boy (blood group B, Rh-positive, weighed 3100 gm) who was born at 37. gestation to a 33-year old, blood group B, Rh-negativ mother. During pregnancy the indirect Coom...
Reflecting to the letter of Mark P Tighe, et al.[1] we would like to
report our case with rhesus-haemolytic disease treated with D-penicillamine (DPA) and phototherapy without exchange transfusion:
We recently cared for a term infant boy (blood group B, Rh-positive, weighed 3100 gm) who was born at 37. gestation to a 33-year old, blood group B, Rh-negativ mother. During pregnancy the indirect Coombs tests showed: 1 : 16 and 1:32 titres, respectively. The baby was born as an 11.offspring of his mother and appeared jaundice at 10 hours of life and had moderate anaemia. The direct Coombs test was strongly positive (++++) in the cord blood. At 12 hours of age, the bilirubin level was 207 micromol/liter; the haemoglobin value was 119 g/liter. Phototherapy and orally administered D-penicillamine (300 mg/kg per day divided in four doses for 5 days) were started. The clinical characteristics of the infant with Rh-haemolytic disease are shown in Table 1.
His physical growth and developmental processes at 18 months of age revealed no abnormalities of neurodevelopmental maturation, as based on an evaluation of motor developmental milestones, and date obtained by the classic neurologic
examination, and cerebral neuromotor maturational markers. Although this combined therapy of hyperbilirubinaemia has been performed successfully in our case concerning the avoidance of an exchange transfusion in the infant with haemolytic disease, care must be taken not to overlook developing anaemia which may require transfusion. Table 1 showes that the baby's lowest haemoglobin level was 67 g/liter on day 9 and 130 g/liter on day 12, clarifiying the existence of a serious haemolytic process and the efficacy of a single red blood cell transfusion.
According to our calculation the cost of DPA treatment would be about 15 - USD (5 days treatment for a newborn with 3 kg of body weight needs 5x900 mg DPA, i.e. 300 mg/kg daily, in divided doses. That is 4500 mg DPA total). 18 capsules of 250 mg orally administered D-penicillamine costs about 15.3 - USD in the USA. The performance of an exchange transfusion with 600 ml donor blood, however, costs approximately 150 - USD, not to speak about the risk of the exchange itself: 3 death per 1000 procedures and the risk of AIDS and hepatitis from transfusion. Furthermore, without proper treatment about 25% of infants suffering from serious hyperbilirubinaemia are expected to be at risk of neurodevelopmental disorders at 1 year of age in developing countries [2].
Finally, we would like to emphasize that the combined alternative treatment of rhesus haemolytic disease described herein is a safe, inexpensive and effectice therapy even for the extremely jaundiced African infants.
(1) Mark P Tighe, Alyson O'Donnell, Mary Morgan Bloodless treatment
of infants with rhesus-haemolytic disease Electronic letter (29 November
2004)
(2) Wolf MJ, Wolf B, Bijleveld C et al. The predictive value of
developmental testing of extremely jaundiced African infants.
Developmental Medicine& Child Neurology 1998; 40:405-410.
Poor postnatal growth, especially of the head, was associated with
increased levels of motor impairment at 7 years of age in children born
with a gestational age of less then 32 weeks. The difference between head
growth (circumference at 7 years and after birth) was related to outcome
at 7 years. The study of Foulders-Hughes et al. described the developmental
outcome, measured with the same tests...
Poor postnatal growth, especially of the head, was associated with
increased levels of motor impairment at 7 years of age in children born
with a gestational age of less then 32 weeks. The difference between head
growth (circumference at 7 years and after birth) was related to outcome
at 7 years. The study of Foulders-Hughes et al. described the developmental
outcome, measured with the same tests and in the same 280 children, as in
the study of Cooke, concluding that the lowest birthweight and most
pretermn individuals tended to score the lowest. Though many factors has
been related to outcome in preterm born children, the two different
conclusions in the same study group is remarkable and confusing.
Recently, Brandt et al. described the relation between early postnatal energy intake
(first 10 days) and the developmental/intelligence quotients in preterm
born children at 6 years of age. In the study of Coocke head circumference
in only 78% of the studied children in the first 7 days after birth could
be analysed. We suggest that energy intake in the first week after birth
also could be responsible for the difference in developmental outcome.
Moreover, Cooke described the severity of illness in the preterm born
children, discussing that the majority of infants did not had major
medical disease. However, more then 50% of the investigated children had
some degree of retinopathy of prematurity and 50% were mechanical
ventilated. In our opinion, these figures are present in children with
major problems during the neonatal period, such as frequently seen in
preterm infants born with these gestational ages (23 - 32 weeks). The
neonatal problems could have been translated to a medical scoring index,
such as the Neonatal Medical Index of Korner et al. This index has been
proved to predict neuromotor outcome in children born as high-risk preterm
infants (Samsom et al.). Though both authors (Cooke and Foulder-Hughes)
discussed the methodological limitations of their study, the conclusion
they made should be taken with cautious.
References
1. Foulder-Hughes L, Coocke RWI. Motor, cognitive and behavioural
disorders in children born very preterm. Dev Med Child Neurol 2003; 45: 97
-103.
2. Brandt I, Sticker EJ, Lentze MJ. Catch-up growth and head circumference
of very low birth weight, small for gestational ager preterm infants and
mental development to adulthood. J Pediatr 2003; 142: 463-8.
3. Korner AF, Stevenson DK, Forest T, et al. Preterm medical complications
differentially affect neuroneurobehavioral functions: results from a new
medical index. Infant Behav Dev 1993;17:37-43.
4. Samsom JF, de Groot L, Bezemer PD, et al. Muscle power development
during the first year of life predicts neuromotor behaviour at 7 years in
preterm born high-risk infants. Early Hum Dev 2002;68:103-118.
Dear Experts,
What behaviour,symptoms, tests etc absolutely concluded that the children
were suffering from Asperger's and not the effects of emotional abuse?
If the children had Asperger's, would you expect their blood to have less
stress hormones than a similar child that was emotionally abused?
If the children were treated for Asperger's but actually were emotionally
abused, would you expect their behaviour/symptoms to...
Dear Experts,
What behaviour,symptoms, tests etc absolutely concluded that the children
were suffering from Asperger's and not the effects of emotional abuse?
If the children had Asperger's, would you expect their blood to have less
stress hormones than a similar child that was emotionally abused?
If the children were treated for Asperger's but actually were emotionally
abused, would you expect their behaviour/symptoms to become more
challenging and difficult?
Yours sincerely,
Tricia McGill
We read the recent letter on buccal midazolam by Hindley and Jameson
(1) with much interest. The main reason some recommend a buccal midazolam
test dose is concern about the risk of an adverse reaction, particularly
respiratory depression or apnoea, especially should it occur outside
hospital. However, there is evidence that buccal midazolam is more
effective than rectal diazepam and is not associated...
We read the recent letter on buccal midazolam by Hindley and Jameson
(1) with much interest. The main reason some recommend a buccal midazolam
test dose is concern about the risk of an adverse reaction, particularly
respiratory depression or apnoea, especially should it occur outside
hospital. However, there is evidence that buccal midazolam is more
effective than rectal diazepam and is not associated with an increased
incidence of respiratory depression (2).
We recently undertook a survey of epilepsy nurse specialists. Thirty
questionnaires were sent to paediatric neurology and epilepsy nurse
specialists looking after children with epilepsies from all regions of the
Great Britain. Twenty-four responses were received (80% response rate).
All preferred the buccal to the rectal route and reported an increased use
and acceptance of buccal midazolam in recent years. Four of the 24 (16% of
responders) reported that their patients were routinely given a test dose
in hospital for “safety reasons”, to demonstrate the procedure, to
reassure parents, or because of local guidance. Conversely 20/24 (84%) of
responders’ patients were not routinely admitted to hospital for a test
dose. However, 14/20 (70%), whose patients were not admitted for a test
dose, did recommend that the parent or carers call paramedics if their
child was having a prolonged seizure and that they should wait for the
paramedics to be present before administering the first ever dose of
buccal midazolam. Twenty of the 24 (83%) responders’ patients used
“Epistatus”, a proprietary oral solution (10 mg/ml), 2/24 responders
patients used midazolam “intravenous” solution (5 mg/ml), and 2/24
responders patients used either preparation. There was no consistent
practice with respect to the lower age limit for its use, the recommended
dose (0.2 - 0.5 mg/Kg to 2.5 mgs for 6-12 month old, 5mgs for a 1-5 yr
old, 7.5 mgs for a 5-10 yr and 10 mgs for a 10-16 yr old) or the frequency
of repeated doses.
We agree with the authors that the use of routine, in hospital,
buccal midazolam test doses is not supported by current evidence.
However, more evidence about the risks and safety of both rectal diazepam
and buccal midazolam use outside hospital is urgently needed.
At present therefore it seems sensible to recommend an individualised
approach, in discussion with the epilepsy nurse specialist, the family and
carers. Furthermore, there are good reasons to recommend basic life
support training to all citizens, particularly the parents and carers of
children with epilepsies, and especially to those whose children are
prescribed rectal diazepam or buccal midazolam for use outside hospital.
References:
1. Hindley D, Jameson H. Buccal midazolam: is a test dose in hospital
needed? Archives of Disease in Childhood 2006; 91:544-545.
2. McIntyre J, Robertson S, Norris E, Appleton R, Whitehouse WP, Phillips
B, Martland T, Berry K, Collier J, Smith S, Choonara I. Safety and
efficacy of buccal midazolam versus rectal diazepam for emergency
treatment of seizures in children: a randomised controlled trial. Lancet.
2005 Jul 16-22; 366(9481): 205-10.
Dr N Hussain
Specialist Registrar in Paediatric Neurology
Ms E Regan
Children’s Nurse Specialist in Neurology
Dr J Gosalakkal
Consultant Paediatric Neurologist
Leicester Royal Infirmary
Leicester UK
Dr W P Whitehouse
Clinical Senior Lecturer in Paediatric Neurology School of Human
Development University of Nottingham Nottingham UK
Richards and colleagues1 suggest abandoning the term “shaken baby
syndrome” (SBS), because “it is the responsibility of the authorities, not
of the doctors, to investigate how the injuries occurred” and
Chandrakantha and collegues2 share and reinforce this opinion by affirming
that “to separate the therapeutic and clinical investigative aspect of the
condition” would be advantageous for the safety of both...
Richards and colleagues1 suggest abandoning the term “shaken baby
syndrome” (SBS), because “it is the responsibility of the authorities, not
of the doctors, to investigate how the injuries occurred” and
Chandrakantha and collegues2 share and reinforce this opinion by affirming
that “to separate the therapeutic and clinical investigative aspect of the
condition” would be advantageous for the safety of both children and
doctors.
I agree with Le Fanu3: SBS is not a “term”, but a diagnosis, classified in
The International Classification of Diseases. Physicians have the task to
make diagnosis. SBS is a syndrome, manifesting with different signs and
symptoms, coming from the clinical and familiar hystory, the presentation
of the case, the imaging results. Only on a clinical level and setting, it
is possible to put together all elements and come to a definite diagnosis
explaining them all together. How would be the therapeutic pathway of a
child with the separate diagnoses of “cardiac malformation” and “mental
retardation”, instead of “Down syndrome”? Surely, non specific and wrong.
For a specific and efficacious prise en charge of the patient the first
step is making a correct diagnosis.
That is true, the clinical and juridical levels must be separate, even if
collateral. In fact, judges focus on guilt and doctors on suffering, both
of the child and the parents. Moreover, only putting the attention of the
parents on the health of the child it is possible to stimulate the
resources of the parents, when present, in order to activate them for the
child. It is the first step of the structural diagnosis of residual
resources of the family, useful to start a collaborative relationship,
when possible.
The reasons behind the supposed failing of the child protection system2
and of the contrasting decisions of the courts on the cases of SBS1, could
be found in the difficult integration among the different institutions
involved in the cases (health system, social care, judicial system). They
need further research about the determinants, but also about the
organizing models to solve them.
References:
1) Richards PG, Bertocci GE, Bonshek RE, et al. Shaken Baby syndrome.
Arch Dis Child 2006; 91: 205-6.
2) Chandrakantha LE, Sunderland R, Williams A. Child abuse: diagnosis,
reporting, and investigation. Arch Dis Child 2007; 91: 715.
3) Le Fanu J. Shaken baby syndrome. Arch Dis Child 2007; 91: 715.
The authors of this paper on Hindu Birth Customs have highlighted
most practices which are part of hindu culture.
However some more practices which are benficial for mothers and neonates
are being mentioned here.
Place of delivery: first delivery mostly occured at girl,s parents
house,where she is sent from inlaws house about 2-3 months before
term, where she is treated as special person, ge...
The authors of this paper on Hindu Birth Customs have highlighted
most practices which are part of hindu culture.
However some more practices which are benficial for mothers and neonates
are being mentioned here.
Place of delivery: first delivery mostly occured at girl,s parents
house,where she is sent from inlaws house about 2-3 months before
term, where she is treated as special person, gets good affordable diet, rest
with no tension of any sort. This also has the benfit of abstinence ,which
helps in reduction of amniotic infection and preterm labour,as in a study
at government hospital in delhi, had noted 10-15%incidence of preterm
labour following cohabitation within last 24hours and higher incidence of
congenital pneumonia if cohabitatin was frequent within a week preceeding
delivery.
After delivery mother infant dyads are together for more period as she
is not involved in household cores as when in her own house,where as
daughter inlaw she is supposed to carry out her duries as soon after
delivery as possible.
Girl's parents in north india, give to their nursing daughters a gift of
sweetdish called panjiri which has high fat and protein content and act as
nutiernt supplement for mother for about 2 months. This practice promotes
breast milk secretion.it was noted by me that mothers who consumed more
than 5 kg of ffats in addition to family dier had 300gm more weight at 3
months than those who had <_3kg fat.="fat." p="p"/> However,due to distance and cost involved many young
couples in urban are do not avail of above good practices,
We read with interest Smith and Anderson’s audit on education and
training in the paediatric senior house officer (SHO) grade as assessed
from Royal College visits.[1] One aspect that was found to be of great
concern was the lack of adequate protected education in many departments.
We suggest that the concept of adequate protected teaching is unattainable
and outmoded in the modern NHS.
We read with interest Smith and Anderson’s audit on education and
training in the paediatric senior house officer (SHO) grade as assessed
from Royal College visits.[1] One aspect that was found to be of great
concern was the lack of adequate protected education in many departments.
We suggest that the concept of adequate protected teaching is unattainable
and outmoded in the modern NHS.
In the audit it was found that “only” 60% of hospitals fulfilled the
RCPCH standard of three bleep-free hours of protected education for SHOs
each week with > 75% attendance. The authors noted that most
departments had developed appropriate structured educational programmes
but that there were difficulties in achieving the required level of
attendance and in ensuring that attendance was protected. In their
discussion, the authors state that the reason for this was mostly because
SHOs were undertaking educationally inappropriate duties instead of being
educated. The authors suggest that this situation is compounded by the
New Deal and the introduction of shift working for junior doctors. We
would maintain that the introduction of shift working has been far more
deleterious to attendance at protected teaching than the misuse of SHOs.
In our department there are ten SHOs working on two separate shift
systems, one for General Paediatrics and one for Neonatology. The impact
of shift working and the limitation of junior doctor’s hours is such that
between three and five of the ten SHOs are in the hospital on any given
day during normal working hours. The others are either on night duty,
nights off or leave. In these circumstances, it is clear that we will
never achieve 75% attendance at our meetings, even though most are bleep-
free. We imagine the same is true in many other hospitals. Furthermore,
the situation can only get worse with the continuing implementation of the
European Working Time Directive.
The difficulties in delivering formal education to junior doctors
have been recognised in many branches of medicine other than Paediatrics,
and it is acknowledged that training methods will have to change. Many
involved in medical education advocate a change to apprentice learning
where much teaching is opportunistic and learner-centred. The
postgraduate Deans in the United Kingdom have recently produced a
document, Liberating Learning, in which it is explained that any contact
between consultants and juniors can be transformed into a genuine training
experience.[2] This is the approach that we have taken, and handovers,
ward rounds, and clinics are now integral parts of the department’s
educational programme. We are also not too concerned if someone has to
answer a bleep during one of these sessions. Surely a brief interruption
cannot negate the educational value of the event.
In summary, we would urge paediatricians to learn the lessons of
Liberating Learning and introduce a more flexible apprentice-based
training programme. We would also urge the RCPCH to consider abandoning
its requirement for three hours of protected teaching with > 75%
attendance. In many places it simply cannot be done.
References
(1) Smith CP, Anderson JM. Education and training in the paediatric senior
house officer grade: analysis of RCPCH hospital/child health visits
reports, 1997-2001. Arch Dis Child 2003;88: 450-453.
(2) Conference of Postgraduate Medical Deans (CoPMeD). Liberating
Learning. London: CoPMeD; 2002. Available from: <ahref="http://www.copmed.org.uk/publications/liberatinglearning">http://www.copmed.org.uk/publications/liberatinglearning
It is my hypothesis that most prematurity results from reduced
availability of maternal dehydroepiandrosterone (DHEA). The mother is the
source of DHEA for herself and her developing fetus. I suggest the major
cause of reduced maternal DHEA is increased maternal testosterone. Later
in life, the testosterone of puberty, may again, adversely affect the
child. This mechanism may explain the findings of...
It is my hypothesis that most prematurity results from reduced
availability of maternal dehydroepiandrosterone (DHEA). The mother is the
source of DHEA for herself and her developing fetus. I suggest the major
cause of reduced maternal DHEA is increased maternal testosterone. Later
in life, the testosterone of puberty, may again, adversely affect the
child. This mechanism may explain the findings of O'Brien, et al. (see
"prematurity" at www.anthropogeny.com/research.html)
DHEA is the "active" form, derived from the large background source,
dehydroepiandrosterone sulfate (DHEAS). Testosterone inhibits steroid
sulfatase [1] which converts
DHEAS to DHEA. It is my hypothesis that all growth and development is
optimized by DHEA, especially the brain. Therefore, reduced DHEA
decreases growth and development. Blacks exhibit disproportionate levels
of prematurity than whites with or without prenatal care [2] and black mothers produce more
testosterone than white mothers.[3] It has been determined that high DHEAS is most commonly associated
with "small for gestational age" infants with a much smaller association
with low DHEAS.[4] I suggest individuals
exist whose reserve DHEAS is low so a "normal" conversion to DHEA would be
low. However, high DHEAS is, by far, connected with reduced fetal growth
and I suggest this is the result of increased maternal testosterone.
Neonates produce their own DHEA. Therefore, neonates should exhibit
varying degrees of "recovery growth" from the negative effects of maternal
testosterone. This should continue until near puberty when adolescent
testosterone production begins. In children, abnormally high levels of
testosterone have been associated with learning disabilities [5] and children exhibiting early puberty frequently
exhibit problems with learning. I suggest this results from a decrease in
available DHEA from DHEAS because of the testosterone.
O'Brien, et al. found "an apparent deterioation in
neurodevelopmental outcome category, cognitive function, and [necessary]
extra educational support" in "very preterm survivors at school age
compared with controls. " I suggest these findings result from diminished
neurodevelopment in utero as a result of high DHEAS caused by high
maternal testosterone, or simply low maternal DHEA in some mothers, both
of which are later exacerbated by the effects of increasing testosterone
of puberty. In those children who exhibit early puberty, this situation
would manifest itself earlier and be worsened by high testosterone.
References
(1) Snyder VL, Turner M, Li PK, El-Sharkawy A, Dunphy G, Ely DL. Tissue steroid sulfatase levels, testosterone and blood pressure. J Steroid Biochem Mol Biol. 2000; 73: 251-6
(2) Vintzileos AM, Ananth CV, Smulian JC, Scorza WE, Knuppel RA. The impact of prenatal care in the United States on preterm births in the presence and absence of antenatal high-risk conditions. Am J Obstet Gynecol. 2002 Nov;187(5):1254-7.
(3) Troisi R, Potischman N, Roberts J, Siiteri P, Daftary A, Sims C, Hoover RN. Associations of maternal and umbilical cord hormone concentrations with maternal, gestational and neonatal factors (United States). Cancer Causes Control. 2003 May;14(4):347-55.
(4) Francois I, de Zegher F. Adrenarche and fetal growth. Pediatr Res. 1997 Mar;41(3):440-2).
(5) Kirkpatrick SW, Campbell PS, Wharry RE, Robinson SL. Salivary testosterone in children with and without learning disabilities. Physiol Behav. 1993; 53: 583-6
Dear Sir,
We read with interest “Job syndrome masquerading as non-accidental injury” published in January of this year. We note that the diagnosis of Job (Hyper- IgE) syndrome was made on the basis of dysmorphism, eczema, a single staphylococcal skin abscess, fractures and a raised serum IgE level.
We are concerned that the clinical features presented are not typical of Hyper IgE syndrome (HIES) and th...
Dear Editor,
Reflecting to the letter of Mark P Tighe, et al.[1] we would like to report our case with rhesus-haemolytic disease treated with D-penicillamine (DPA) and phototherapy without exchange transfusion:
We recently cared for a term infant boy (blood group B, Rh-positive, weighed 3100 gm) who was born at 37. gestation to a 33-year old, blood group B, Rh-negativ mother. During pregnancy the indirect Coom...
Dear Editor
Poor postnatal growth, especially of the head, was associated with increased levels of motor impairment at 7 years of age in children born with a gestational age of less then 32 weeks. The difference between head growth (circumference at 7 years and after birth) was related to outcome at 7 years. The study of Foulders-Hughes et al. described the developmental outcome, measured with the same tests...
Dear Experts, What behaviour,symptoms, tests etc absolutely concluded that the children were suffering from Asperger's and not the effects of emotional abuse? If the children had Asperger's, would you expect their blood to have less stress hormones than a similar child that was emotionally abused? If the children were treated for Asperger's but actually were emotionally abused, would you expect their behaviour/symptoms to...
Dear Editor,
We read the recent letter on buccal midazolam by Hindley and Jameson (1) with much interest. The main reason some recommend a buccal midazolam test dose is concern about the risk of an adverse reaction, particularly respiratory depression or apnoea, especially should it occur outside hospital. However, there is evidence that buccal midazolam is more effective than rectal diazepam and is not associated...
Dear Editor,
Richards and colleagues1 suggest abandoning the term “shaken baby syndrome” (SBS), because “it is the responsibility of the authorities, not of the doctors, to investigate how the injuries occurred” and Chandrakantha and collegues2 share and reinforce this opinion by affirming that “to separate the therapeutic and clinical investigative aspect of the condition” would be advantageous for the safety of both...
Dear Editor,
The authors of this paper on Hindu Birth Customs have highlighted most practices which are part of hindu culture. However some more practices which are benficial for mothers and neonates are being mentioned here.
Place of delivery: first delivery mostly occured at girl,s parents house,where she is sent from inlaws house about 2-3 months before term, where she is treated as special person, ge...
Dear Editor
We read with interest Smith and Anderson’s audit on education and training in the paediatric senior house officer (SHO) grade as assessed from Royal College visits.[1] One aspect that was found to be of great concern was the lack of adequate protected education in many departments. We suggest that the concept of adequate protected teaching is unattainable and outmoded in the modern NHS.
In...
Dear Editor
It is my hypothesis that most prematurity results from reduced availability of maternal dehydroepiandrosterone (DHEA). The mother is the source of DHEA for herself and her developing fetus. I suggest the major cause of reduced maternal DHEA is increased maternal testosterone. Later in life, the testosterone of puberty, may again, adversely affect the child. This mechanism may explain the findings of...
ANOTHER ERROR NOTED. AS REFERENCE TO THE ARTICLE IT SHOULD BE PENICILLIN 500 MGM BID NOT QD.
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