Inaccurate classification of the cause and manner of infant deaths
impedes prevention efforts by limiting researchers’ ability to accurately
identify risk factors for SIDS and other sudden, unexpected deaths in
infancy (SUDI). Sheehan and colleagues[1] present evidence of inaccurate
reporting of SIDS in Ireland and underscore the necessity for standardized
SUDI criteria and definitions, as well as a mu...
Inaccurate classification of the cause and manner of infant deaths
impedes prevention efforts by limiting researchers’ ability to accurately
identify risk factors for SIDS and other sudden, unexpected deaths in
infancy (SUDI). Sheehan and colleagues[1] present evidence of inaccurate
reporting of SIDS in Ireland and underscore the necessity for standardized
SUDI criteria and definitions, as well as a multidisciplinary approach to
improve the diagnostic reliability of SUDI cases. Two recent US studies
also provide evidence that cause-of-death reporting for SUDI may be
unreliable by demonstrating that the decline in the SIDS rate since 1999
is offset by increasing mortality rates for cause unknown/unspecified and
accidental suffocation and strangulation in bed.[2,3]
We agree with Sheehan and colleague’s approach for improving the
accuracy of SUDI reporting.[1] In addition, we believe it is imperative
that a thorough death scene investigation be conducted before a death can
be classified as SIDS. Studies have presented evidence to support the
contention that SIDS and other SUDI are more accurately diagnosed when
information from a death scene investigation is used to make the
diagnosis.[4,5] A thorough infant death scene investigation should at a
minimum include interviewing witnesses, examining the death scene, staging
a doll reenactment, reviewing medical history, and carefully assessing the
infant’s exposures prior to death.
To improve the accuracy and consistency with which SUDI are
classified, the Centers for Disease Control and Prevention (CDC) is
leading a US effort to develop standards for the conduct of infant death
scene investigations. We are developing training curricula and materials
to instruct those investigating and certifying infant deaths on how to
gather information at the scene and use the data to interpret autopsy
findings. This training will help ensure that accurate and consistent
diagnoses of SIDS and SUDI are made.
References
1 Sheehan KM, McGarvey C, Devaney DM, et al. How reliable are SIDS
rates? Arch Dis Child 2005;90:1082-3.
2 Malloy MH, MacDorman M. Changes in the classification of sudden
unexpected infant deaths: United States, 1992-2001. Pediatrics
2005;115:1247-53.
3 Shapiro-Mendoza CK, Tomashek KM, Anderson RN, et al. Recent
National Trends in Sudden, Unexpected Infant Deaths: More Evidence
Supporting a Change in Classification or Reporting. American Journal of
Epidemiology (in press).
4 Bass M, Kravath RE, Glass L. Death-scene investigation in sudden
infant death. N Engl J Med 1986;315:100-5.
5 Byard RW, Carmichael E, Beal S. How useful is postmortem
examination in sudden infant death syndrome? Pediatr Pathol 1994;14:817-
22.
We agree to a large extent with the views and practices expressed by Professor Hassall and colleagues at The British Columbia Children’s Hospital which were highlighted and published recently in Archives of Disease in Childhood.[1]
At the Royal Liverpool Children’s Hospital (Alder Hey) we have developed a multi-disciplinary medical - surgical gastro-oesophageal reflux (GOR) assessment clinic where ove...
We agree to a large extent with the views and practices expressed by Professor Hassall and colleagues at The British Columbia Children’s Hospital which were highlighted and published recently in Archives of Disease in Childhood.[1]
At the Royal Liverpool Children’s Hospital (Alder Hey) we have developed a multi-disciplinary medical - surgical gastro-oesophageal reflux (GOR) assessment clinic where over the last five years we have consequently noted a similar dramatic reduction in fundoplication as definitive treatment for gastro-oesophageal reflux disease. An audit of our current practice reveals a 50% reduction in Nissen fundoplication and a recent trend towards adopting the oesophago-gastric dissociation procedure in those most vulnerable and challenging children with severe neuro-disability.[2]
Annually almost 60 new children with complicated gastro-oesophageal reflux are reviewed in the multi-disciplinary clinic - the majority with co-existent complex neurological disorders. It is noteworthy that the fundoplication to gastrostomy procedures as interventional treatments for GOR have shifted from 1:2 in 1997 to 1:5 in 2005 (Table 1), indicating the utility of co-ordinated care pathways developed by a multidisciplinary team in evaluating gastro-oesophageal reflux disorders. We would conclude that careful attention to the specific feeding needs of the severely neurologically disabled child cannot be over emphasised. The authors declare no competing interests.
References
1. Hassall E. Outcomes of fundoplication: causes for concern, newer options. Arch Dis Child; 90:1047-1052.
2. Goyal A, Khalil B, Choo K, Mohammed K, Jones M. Esophagogastric dissociation in the neurologically impaired: an alternative to fundoplication? J Pediatr Surg. 2005 Jun;40(6):915-8; discussion 918-9.
Ellis et al [1] ought to be commended for spearheading and reporting
on their experience with the provision of HIV post-exposure prophylaxis
(PEP) to children sexually abused (CSA) at the Queen Elizabeth Central
Hospital (QECH) in Malawi. I wish to comment on a number of issues raised
in the article. Firstly the authors indicated that in the protocols they
follow children presenting with previous abus...
Ellis et al [1] ought to be commended for spearheading and reporting
on their experience with the provision of HIV post-exposure prophylaxis
(PEP) to children sexually abused (CSA) at the Queen Elizabeth Central
Hospital (QECH) in Malawi. I wish to comment on a number of issues raised
in the article. Firstly the authors indicated that in the protocols they
follow children presenting with previous abuse within the preceding 6
months are not eligible for PEP ‘because of the possibility of the child
having already acquired HIV infection and being in the "window period"
prior to sero-conversion’. I agree with the authors in that such a
situation is one possibility, but not all possibilities. There is also the
possibility that the child who had been previously sexually abused may not
have acquired HIV infection in the previous assaults. Now, what if it is
the index assault that will be responsible for infection? It is not
possible to know, until after the fact. It may therefore be prudent to err
on the side of caution by nonetheless providing prophylaxis to the child
who is HIV sero-negative now regardless of whether they may or may not be
in the window period. This ought to be explained to the parents/guardians
as in the event that follow-up HIV tests shows HIV sero-conversion, it
ought to be considered that one possibility may be that the child was in
the "window period".
It is important that Ellis et al identifies the shortage of experienced
medical personnel to deal with CSA in their setting. I find the suggestion
to "make our service to abused children consultant led" may have
implications in ensuring timely provision of PEP to eligible children. In
Malawi, just like many other African countries, most of the clinical care
is provided by nurses and non-specialist medical doctors [2]. Allowing non
-consultants to care for CSA potentially endangers the quality of service
to be provided, but may permit transfer of skills to the majority of
clinicians who most often cares for children and must be able to
clinically recognize and manage CSA cases when they occur. Perhaps,
currently the service as QECH is yet to mature, consultants could still
lead while slowly trying to bring on board the common health cadres. The
poor management of sexual assault cases in the pre-PEP era in Malawi has
been described before [3].
Finally, I agree with the authors that in a high HIV prevalence setting,
as in most of southern Africa, there is need to seriously consider HIV
post-exposure prophylaxis in cases of confirmed CSA, even without evidence
of genital trauma. As the practice of medicine generally is to be cautious
especially when we do not know the possible harms to treatments (like in
this case where PEP is just being introduced in a developing country), the
authors are justified in how they have trodden so far. However, in a
situation where there is a real possibility of getting HIV infection, some
of us think that there are very few clinical situations that can outweigh
HIV infection in a risk-benefit analysis. Unfortunately we may not have
evidence to objectively demonstrate that.
References
1. Ellis JC, Ahmad S, Molyneux ME. Introduction of HIV post-exposure
prophylaxis for sexually abused children in Malawi. Arch Dis Child.
Published online 20 Sep 2005; doi: 10.1136/adc.2005.080432
2. Dovlo D. Using mid-level cadres as substitutes for internationally
mobile health professionals in Africa: a desk review. Hum Resour Health
2004; 2: 7
3. Muula A. The management of sexual assault cases at LCH. Malawi Med J
2001; 13: 34
We read this recent paper with interest as it deals with a clinically
important question in the area of growth and lung function in different
ethnic groups. The authors hypothesise that there may be intrinsic ethnic
differences in lung function between British-born Asian and non-Asian
females. That this difference exists was first reported in 1986 (1), when
the differences in FEV1 and FVC were reporte...
We read this recent paper with interest as it deals with a clinically
important question in the area of growth and lung function in different
ethnic groups. The authors hypothesise that there may be intrinsic ethnic
differences in lung function between British-born Asian and non-Asian
females. That this difference exists was first reported in 1986 (1), when
the differences in FEV1 and FVC were reported to be of the order of 13%.
Our own data (2,3) confirmed these ethnic differences. Ethnic differences
in lung function have been well recognised in adults (4-7) and children (8
-13) and in some reports have been attributed to differences in chest
dimensions. Our own work (3) showed that this was not the case when Asian
and white children were compared in Leicester.
It is noteworthy that Callaghan et al found no differences in the z-
scores for height or weight, and no difference between BMI between the
ethnic groups. In our study we were looking at healthy volunteers of
primary school age. We did find significant differences between Asians and
white children with respect to z-scores for weight and BMI, though not for
height. The relationship between BMI and age is not linear and we
recommend a cautious approach to direct comparisons of BMI in patient
groups of different ethnic origins.
References
1. Patrick JM, Patel A. Ethnic differences in the growth of lung
function in children: a cross- sectional study in inner-city Nottingham.
Ann Hum Biol 1986;13:307-315.
2. Whittaker AL, Sutton A and Beardsmore CS. Do variations in chest
wall dimensions explain ethnicity-related differences in lung function?
Thorax 2002; vol.57 suppl III: 41.
3. Whittaker AL, Sutton AJ and Beardsmore CS. Do chest wall
dimensions explain ethnicity-related differences in lung function in
children? Arch Dis Child 90:F423-F428 (2005)
4. Schoenberg JB, Beck GJ, Bouhuys A. Growth and decay of pulmonary
function in healthy blacks and whites. Respir Physiol 1978;33:367-393.
5. Rossiter CE, Weill H. Ethnic differences in lung function:
evidence for proportional differences. Int JEpidemiol 1974;3:55-61.
6. Jacobs DR Jr, Nelson ET, Dontas AS, et al. Are race and sex
differences in lung function explained by frame size? The CARDIA Study. Am
Rev Respir Dis 1992;146:644-649.
7. Korotzer B, Ong S, Hansen JE. Ethnic differences in pulmonary
function in healthy nonsmoking Asian- Americans and European-Americans. Am
J Respir Crit Care Med 2000;161:1101-1108.
8. Binder RE, Mitchell CA, Schoenberg JB, et al. Lung function among
black and white children. Am Rev Respir Dis 1976;114:955-959.
9. Boggs PB, Stephens AL, Walker RF, et al. Racially specific
reference standards for commonly performed spirometric measurements for
black and white children, ages 9-18 years. Ann Allergy 1981;47:273-277.
10. Asher MI, Douglas C, Stewart AW, et al. Lung volumes in
Polynesian children. Am Rev Respir Dis 1987;136:1360-1365.
11. Coultas DB, Howard CA, Skipper BJ, et al. Spirometric prediction
equations for Hispanic children and adults in New Mexico. Am Rev Respir
Dis. 1988;138:1386-1392.
12. Strope GL, Helms RW. A longitudinal study of spirometry in young
black and young white children. Am Rev Respir Dis 1984;130:1100-1107.
13. Schwartz J, Katz SA, Fegley RW, et al. Sex and race differences
in the development of lung function. Am Rev Respir Dis 1988;138:1415-1421.
A role for computerised tomography(CT) which is just as challenging
as the identification of mediastinal lymphadenopathy when patients with
suspected pulmonary tuberculosis(PTB) present either with normal chest
radiographs(1) or with non-specific pulmonary infiltrates(2) may be the
role of establishing the diagnosis of miliary tuberculosis(MTB) when chest
radiography only shows a non-specific interstitia...
A role for computerised tomography(CT) which is just as challenging
as the identification of mediastinal lymphadenopathy when patients with
suspected pulmonary tuberculosis(PTB) present either with normal chest
radiographs(1) or with non-specific pulmonary infiltrates(2) may be the
role of establishing the diagnosis of miliary tuberculosis(MTB) when chest
radiography only shows a non-specific interstitial pattern(3), the latter
having the potential to be erroneously attributed to pneumocystis carinii
in those co-infected with the Human Immunodeficiency Virus, or the role of
establishing the diagnosis of MTB when chest radiography has failed to
detect any parenchymal abnormality. In the former instance the resulting
diagnostic confusion is one which is capable of being resolved by recourse
to CT(4). Of even more crucial importance is the ability of CT to
demonstrate MTB even when near-contemporaneous chest radiography shows no
abnormality, imaging interval, in one instance being of the order of 3-7
days(5), or when a truly contemporaneous chest radiograph shows only
mediastinal lymphadenopathy, parenchymal miliary nodules having totally
escaped detection by chest radiography even on two months follow-up(6).
Given the significantly higher prevalence of CT-diagnosed miliary
tuberculosis(p < 0.01) among HIV-seropositive than among HIV-
seronegative subjects with PTB(7), and the recognition that,
notwithstanding the diagnostic limitations of chest radiography(where the
sensitivity for detection of MTB is, at most 69%)(8), the use of the
latter modality nevertheless yields a significantly higher prevalence of
MTB(p < 0.001) among HIV infected patients with tuberculosis than among
counterparts in whom tuberculosis is not associated with HIV infection(9),
the clear message from the HIV/AIDS era is that all doctors dealing with
suspected PTB should have a heightened awareness of miliary tuberculosis,
and guidelines for the "work up" of these patients should highlight the
role of CT and the importance of the timeliness of its involvement in the
diagnostic process, so as to avoid a repeat of the scenario antedating
either the CT or the HIV/AIDS era where fourteen out of 224 children with
miliary tuberculosis died without the correct radiographic diagnosis having been made
because miliary tubercles had escaped detection by chest radiography(10).
References
(1) Delacourt C., de Blic J., Scheinmann P.,et al
Computed tomography with normal chest radiograph in tuberculous infection
Archives if Disease in Childhood 1993:69:430-2
(2) Swingler GH., du Toit G., Andronilou S., van der Merwe L., Zar HJ
Diagnostic accuracy of chest radiography in tetecting mediastinal
lymphadenopathy in suspected pulmonary tuberculosis
Aechives of Disease in Childhood 2005:90:1153-6
(3) Sharma SK., Mohan A., Pande JN., et al
Clinical profile, laboratory charcteristics and outcome in miliary
tuberculosis
Quarterly Journal of Medicine 1995:88:29-37
(4) Optican RJ., Ost A., Ravin CE
High-resolution computed tomography in the diagnosis of miliary
tuberculosis
Chest 1992:102:941-3
(5) Amos A., Denning D., Katz D., Smith H
Computed tomography of chest in diagnosis of miliary tuberculosis
Lancet 1987:i: 1269-70
(6) Oh Y-W., Kim YH., Lee NJ., et al
High-resolution CT appearance of miliary tuberculosis
Journal of Computer Assisted Tomography 1994:18:862-66
(7) Leung AN., Brauner MW., Gamsu G., et al
Pulmonary tuberculosis; Comparison of CT findings in HIV-seropositive and
HIV-seronegative patients
Radiology 1996:198:687-91
(8) Kwong JS., Carignan S., Kang E-Y., et al
Miliary tuberculosis: Diagnostic accuracy of chest radiography
Chest 1996:110:339-42
(9) Shafer RW., Kim DS., Weiss JP., Quale JM
Extrapulmonary tuberculosis in patients with Human Immunodeficiency Virus
infection
Medicine(Baltimore) 1991:70:384-96
(10) Illingworth RS and Lorber J
Tubercles of the choroid
Archives of Disease in Childhood 1956:31:467-9
I found the best evidence review very interesting.
I just wanted to comment that there seems to be a very strong suggention
that all babies with single umbilical artery should have a renal USG and
an MCUG and the author has provided a strong arguement for the same.
but having worked in 7 hospitals all over the country, I am amazed at the
variability of practices.
I have worked in hospitals which follow the...
I found the best evidence review very interesting.
I just wanted to comment that there seems to be a very strong suggention
that all babies with single umbilical artery should have a renal USG and
an MCUG and the author has provided a strong arguement for the same.
but having worked in 7 hospitals all over the country, I am amazed at the
variability of practices.
I have worked in hospitals which follow the suggested management plan to
the letter and there are other hospitals where SUA is considered a benign
condition and no further action is advised.
considering that reflux nephropathy is an important cause of morbidity,
should there not be a national consensus onthe management of babies with
single umbilical artery?
Walter and Olivares question whether the anaemia present in the
enrolled children was due to iron deficiency or due to the acute infection
that precipitated their admission to hospital. They state that anaemia
and all other measures of iron normalize without therapy. Both their
reference to their earlier work and other published literature do not
support this statement.
Walter and Olivares question whether the anaemia present in the
enrolled children was due to iron deficiency or due to the acute infection
that precipitated their admission to hospital. They state that anaemia
and all other measures of iron normalize without therapy. Both their
reference to their earlier work and other published literature do not
support this statement.
Their referenced study of 93 infants showed that while haemoglobin
and iron saturation decreased and ferritin increased following measles
immunisation, mean cell volume did not change significantly.[1] Similarly
no decrease in mean cell volume was seen in a study of anaemia associated
with Haemophilus influenzae meningitis nor in a study that determined the
influence of mild prior infection on haemoglobin and other measures of
iron deficiency.[2,3] Therefore, although both iron deficiency and acute
infection cause anaemia and low iron saturation, only iron deficiency
results in changes in red cell size.
In our manuscript we reported the data collected on infants with iron
deficiency anaemia who were randomised to treatment with iron medicine,
iron fortified milk or iron fortified milk formula. We showed that these
infants had iron deficiency anaemia on admission and that the proportion
with iron deficiency anaemia decreased significantly with each
intervention. The enrolment definition of iron deficiency included a
measure of red cell size (red cell distribution width) hence we believe
these children had anaemia secondary to iron deficiency rather than
infection. The significant increase in mean cell volume in the iron-
follow-on and iron-milk groups also demonstrates that iron status improved
in infants receiving these interventions.
We also collected data on 70 infants hospitalised with acute
illnesses who were not treated for iron deficiency but who did have a
follow up blood test performed three months later. This group included
infants with iron deficiency anaemia whose caregivers did not want them
randomised but did want a follow-up measure of iron status, infants with
anaemia but not iron deficiency, and infants with haemoglobin (110 to 119
g/L) and red cell distribution width (13.6 to 14.5%) measurements that
were in the lower range of normal.
On admission, in comparison to the infants with iron deficiency
anaemia, these infants had higher mean haemoglobin concentrations (112 vs.
102 g/L, p<0.001), mean cell volumes (76 vs. 71 fL, p<0.001) and
median iron saturations (10 vs. 5%, p<0.001), lower median red cell
distribution width (15 vs. 16%, p=0.001) and median c-reactive protein
concentrations (6 vs. 18 mg/L, p=0.003), and median serum ferritin
concentrations that did not differ (36 vs. 42 ug/L, p=0.49). In
contrast to the infants treated for iron deficiency anaemia the mean cell
volume at follow-up was not significantly different from that at enrolment
(Table). Thus abnormal values for parameters that measure red cell size
can be used to differentiate iron deficiency anaemia from anaemia
secondary to acute infection and to demonstrate response to iron therapy.
Table. Enrolment and follow up measures of iron status in 70 infants 9 to 23 months of age hospitalised with acute illness who did not receive treatment for iron deficiency.
Variable
Enrolment
Median (5, 95th centile)
Follow
up
Median (5, 95th centile)
Mean
difference
(95% CI)*
Haemoglobin
(g/L)
113
(97, 125)
119
(106, 133)
7
(5, 10)
Ferritin
(?g/L)
36
(5, 207)†
17
(4, 60)‡
102
(-226, 41)
Iron
saturation (%)
10.5
(3.0, 24.0)
15.0
(3.0, 30.0)§
-5.2 (2.8, 7.6)
Red
cell distribution width (%)
15.0
(14.0, 17.7)
15.0
(13.8, 17.0)||
-0.3
(-0.6, 0.01)
Mean
cell volume (fL)
76
(66, 83)
76
(65, 84)
-0.7
(-1.6, 0.3)
C-reactive
protein mg/L
6
(2, 141)¶
2
(2, 54)**
-18
(-32, -5)
* Except for haemoglobin are geometric means and confidence intervals
† n = 68
‡ n = 67
§ n = 69
|| n = 68
¶ n = 61
** n = 64
It is important to remember that infants with prior infections show a
greater haemoglobin response to iron therapy than infants with no
preceding history of recent illness. This has been demonstrated in a
placebo controlled trial.[3] Thus acute infections, which are common in
infancy, may cause iron deficiency. Therefore infants hospitalised with
acute infection are likely to be a group at increased risk of iron
deficiency anaemia. It is important to try to identify these infants and
provide additional iron to enable normalisation of iron status as their
iron absorption improves with resolution of the acute infection.
Clare R. Wall, Paediatric Nutritionist, Massey University
Cameron C. Grant, Paediatrician, University of Auckland
References:
1. Olivares M, Walter T, Osorio M, Chadud P, Schlesinger L. Anaemia of a
mild viral infection: the measles vaccine as a model. Pediatrics
1989;84:851-5.
2. O'Brien RT, Santos JI, Glasgow L, Landaw SA. Pathophysiologic basis for
anaemia associated with Haemophilus influenzae meningitis: preliminary
observations. Journal Pediatr 1981;98:928-31.
3. Reeves JD, Yip R, Kiley VA, Dallman PR. Iron deficiency in infants: the
influence of mild antecedent infection. J Pediatr 1984;105:874-9.
The authors' "take away message", namely, that the diagnosis of
Klippel-Trenaunay Syndrome (KTS) has prognostic implications extending well
into adulthood[1] has, as its corollary, the recognition that the
implications of underdiagnosis are equally important, especially given the
ease with which underdiagnosis can occur if due cognisance is not taken of
the fact that, of the three diagnostic parameters,...
The authors' "take away message", namely, that the diagnosis of
Klippel-Trenaunay Syndrome (KTS) has prognostic implications extending well
into adulthood[1] has, as its corollary, the recognition that the
implications of underdiagnosis are equally important, especially given the
ease with which underdiagnosis can occur if due cognisance is not taken of
the fact that, of the three diagnostic parameters, namely, venous
varicosities, limb hypertrophy, and cutaneous haemangioma (i.e. cutaeneous
naevus), only two need to be present at any one time, and that cutaneous
naevus may be absent in 4% to 68% of cases.[2,3]
Although, by definition, KTS is present at birth, being even recognisable
at 19 weeks gestation,[4] it may be compatible with normal life
expectancy, one patient being alive at the age of 75 notwithstanding co-existence of visceral manifestations compatible with renovascular
hypertansion.[5] Accordingly, the fact that clinical management of this
disorder "does not necessarily become easier as the patient grows
older"[1] is compounded by the fact that some patients can expect to
survive with their disability for the entire duration of the normal life
expectancy.
Yours sincerely
OMP Jolobe (Retired Geriatrician)
References
(1) Pawel BR., Spencer K., Dormans J
Klippel-Trenaunay Syndrome
Archives of Disease in Childhood 2005;90:1127-8.
(2) Serville M
Klippel-Trenaunay Syndrome: 768 operated cases
Annals of Surgery 1985:201:365-73.
(3) Baskervilee PA., Ackroyd JS., Lea Thoma M., Browse NL
The Klippel-Trenaunay Syndrome: clinical, radiological, and haemodynamic
features and management
British Journal of Surgery 1985:72:232-6.
(4) Jorgenson RJ., Darby B., Patterson R., Trimmer KJ
Prenatal diagnosis of the Klippel-Trenaunay-Weber Syndrome
Prenatal Diagnosis 1994:14:989-92.
(5) Jolobe, OMP
Klippel-Trenaunay Syndrome
Postgraduate Medical Journal 1996:72:347-8.
The positive effects of routine weighing of neonates were examined in
relation to breastfeeding (McKie, Young, Macdonald, 20 October 2005,
doi: 10.1136/adc.2005.074484). This study found that regular weighing of
infants up to 6 weeks did not threaten rates of breastfeeding, despite
some suggestions to the contrary. The authors suggest that the effect may
be from the reassurance and encouragement provid...
The positive effects of routine weighing of neonates were examined in
relation to breastfeeding (McKie, Young, Macdonald, 20 October 2005,
doi: 10.1136/adc.2005.074484). This study found that regular weighing of
infants up to 6 weeks did not threaten rates of breastfeeding, despite
some suggestions to the contrary. The authors suggest that the effect may
be from the reassurance and encouragement provided by the visiting nurses.
Indeed, it is unlikely that the mechanics of weighing the infant would
have any effect at all.
I would like to introduce a note of caution. Some years ago, with
colleagues in Brisbane, Australia, I undertook a study of the amount of
error which can occur when weighing babies. We found that normal
physiological processes can alter the weight of an infant by ±80 g a day.
The calculation of weight gain requires two measurements, and each is
liable to error, so that the error of the difference is greater than the
error for each measurement. The change in weights (between the two
measurements) may be up to 100 g (SD 50g) more or less than the amount
calculated from the two weighings.[1] We
concluded that under 9 months of age, only weighings a fortnight apart
would detect any real weight gain, under that any change was probably not
real.[2] Attaching any significance to the routine weighing of babies
outside the psychological support the child health nurse offers to the
mother could be deleterious.
References
1. Alsop-Shields L, Alexander HG, Dugdale AE. The accuracy of weighing
infants. Med J Aust 1994;161:489-90.
2 Alsop-Shields L, Alexander H. A study if errors that can occur when
weighing infants. J Adv Nurs 1997;25:587-94.
We write to add to the discussion raised in the Short Report, "How
reliable are SIDS rates?"[1] and the accompanying response by
Fleming and Blair[2], by highlighting recent data from Western
Australia (WA).[3] Linked, total population birth and death data
for birth cohorts from 1980-2001 indicated a significant increase in
the later years in the number of infant deaths where the cause of
death, as gi...
We write to add to the discussion raised in the Short Report, "How
reliable are SIDS rates?"[1] and the accompanying response by
Fleming and Blair[2], by highlighting recent data from Western
Australia (WA).[3] Linked, total population birth and death data
for birth cohorts from 1980-2001 indicated a significant increase in
the later years in the number of infant deaths where the cause of
death, as given by the Coroner, was "unascertainable".[3] During
this time, the apparent SIDS rates continued to decrease in a similar
pattern to the data for England and Wales quoted by Fleming and Blair.[2]
When we analysed the WA data separately for the infants of Aboriginal
and non-Aboriginal mothers, the SIDS rates for both populations for
1998-2001 had decreased to approximately half those for 1995-1997 (Table 1).
Table 1 Number and rate (per 1,000 live births) for Aboriginal and
non-Aboriginal infants for SIDS and "unascertainable" deaths.
Birth Year
Aboriginal
Non-Aboriginal
TOTAL
Classification
N
Rate
N
Rate
N
Rate
1995-1997
SIDS
21
4.7
47
0.9
68
0.9
"unascertainable"
4
0.9
2
0.02
6
0.1
1998-2001
SIDS
16
2.5
36
0.4
52
0.5
"unascertainable"
14
2.2
22
0.2
36
0.4
The rate for all "unascertainable" deaths increased four-fold, again
in similar fashion to the rate for England and Wales. These data
show that the problem of diagnostic transfer must be considered in
any analysis of sudden and unexplained infant death. In addition, a
classification system that allows for the role of possible or
probable contributory factors in cases of SIDS, such as that
described by Fleming and Blair[2], would prove useful.
The WA data indicated not only diagnostic transfer but also
differential classification, as the proportion of Aboriginal infant
deaths classified as "unascertainable" in 1998-2001 was significantly
greater than for non-Aboriginal infants.[3] Furthermore, when the
unascertainable deaths were added to those attributed to SIDS, the
decrease in SIDS rates for Aboriginal infants was no longer significant.[3]
These data emphasise that SIDS must be considered in the context of
total, sudden unexplained infant death and that comparisons within
nations as well as between nations[1] are not straightforward.
We declare that we have no competing interests.
Dr Jane Freemantle
Dr Anne Read
Dr Adrian Charles
Professor Nicholas de Klerk
Daniel McAullay
Professor Fiona Stanley AC
References:
Sheehan KM., McGarvey C., Devaney DM, et al. How reliable are
SIDS rates? Arch Dis Child 2005; 90: 1082-3.
Fleming PJ., Blair, PS. How reliable are SIDS rates? The
importance of a standardised, multiprofessional approach to
'diagnosis'. Arch Dis Child 2005; 90: 993-994.
Freemantle CJ., Read AW., DeKlerk NH., et al. Interpretation of
recent SIDS rates in Western Australia. J Paediatr. Child Health
2005; 41(12): pp 669-670.
Dear Editor
Inaccurate classification of the cause and manner of infant deaths impedes prevention efforts by limiting researchers’ ability to accurately identify risk factors for SIDS and other sudden, unexpected deaths in infancy (SUDI). Sheehan and colleagues[1] present evidence of inaccurate reporting of SIDS in Ireland and underscore the necessity for standardized SUDI criteria and definitions, as well as a mu...
Dear Editor
We agree to a large extent with the views and practices expressed by Professor Hassall and colleagues at The British Columbia Children’s Hospital which were highlighted and published recently in Archives of Disease in Childhood.[1]
At the Royal Liverpool Children’s Hospital (Alder Hey) we have developed a multi-disciplinary medical - surgical gastro-oesophageal reflux (GOR) assessment clinic where ove...
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Ellis et al [1] ought to be commended for spearheading and reporting on their experience with the provision of HIV post-exposure prophylaxis (PEP) to children sexually abused (CSA) at the Queen Elizabeth Central Hospital (QECH) in Malawi. I wish to comment on a number of issues raised in the article. Firstly the authors indicated that in the protocols they follow children presenting with previous abus...
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We read this recent paper with interest as it deals with a clinically important question in the area of growth and lung function in different ethnic groups. The authors hypothesise that there may be intrinsic ethnic differences in lung function between British-born Asian and non-Asian females. That this difference exists was first reported in 1986 (1), when the differences in FEV1 and FVC were reporte...
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A role for computerised tomography(CT) which is just as challenging as the identification of mediastinal lymphadenopathy when patients with suspected pulmonary tuberculosis(PTB) present either with normal chest radiographs(1) or with non-specific pulmonary infiltrates(2) may be the role of establishing the diagnosis of miliary tuberculosis(MTB) when chest radiography only shows a non-specific interstitia...
Dear Editor
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Dear Editor,
Walter and Olivares question whether the anaemia present in the enrolled children was due to iron deficiency or due to the acute infection that precipitated their admission to hospital. They state that anaemia and all other measures of iron normalize without therapy. Both their reference to their earlier work and other published literature do not support this statement.
Their referenced study...
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The authors' "take away message", namely, that the diagnosis of Klippel-Trenaunay Syndrome (KTS) has prognostic implications extending well into adulthood[1] has, as its corollary, the recognition that the implications of underdiagnosis are equally important, especially given the ease with which underdiagnosis can occur if due cognisance is not taken of the fact that, of the three diagnostic parameters,...
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The positive effects of routine weighing of neonates were examined in relation to breastfeeding (McKie, Young, Macdonald, 20 October 2005, doi: 10.1136/adc.2005.074484). This study found that regular weighing of infants up to 6 weeks did not threaten rates of breastfeeding, despite some suggestions to the contrary. The authors suggest that the effect may be from the reassurance and encouragement provid...
Dear Editor,
We write to add to the discussion raised in the Short Report, "How reliable are SIDS rates?"[1] and the accompanying response by Fleming and Blair[2], by highlighting recent data from Western Australia (WA).[3] Linked, total population birth and death data for birth cohorts from 1980-2001 indicated a significant increase in the later years in the number of infant deaths where the cause of death, as gi...
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