I read with interest Sivaramakrishnan et al's structured approach to a child with toe walking [1]. Various levels of contexts such as parenting, maternal education, poverty and social networks interact with each other and with genetic expression to create long-lasting consequences for development [2,3]. Sometimes, single or isolated negative environmental factors may make a major contribution to developmental problems with most n...
I read with interest Sivaramakrishnan et al's structured approach to a child with toe walking [1]. Various levels of contexts such as parenting, maternal education, poverty and social networks interact with each other and with genetic expression to create long-lasting consequences for development [2,3]. Sometimes, single or isolated negative environmental factors may make a major contribution to developmental problems with most negative influence occurring in infancy. Here, we discussed two infants without any underlying medical condition who walk on their toes.
Case 1: A 18-month-old girl comes with delay the attainment of standing and independent walking. Her perinatal and family history was unremarkable. Her antropometric measurements were all appropriate for his age. Her Denver II was normal at 9 months of age, however, gross motor development was abnormal at 18 months. While the infant was kept standing with holding her arms, she jumped continuously or she did toe walking and she couldn't stand alone. Further history revealed that she had sat on "doorway jumper" as a baby-sitter, 2-3 hours a day for 6 months. Then, parents were urged not to use jumper and put their infant on carpet to crawl and creep. The infant begin to walk alone within three months.
Case 2: A 21-month-old boy, presented to our center with toe walking. Her delivery and neonatal-infant course were uneventful. There was no positive family history. He achieved gait at 13 months and walked independently at 16 months. On physical examination weight, height and head circumference were all appropriate for his age. Physical examination revealed intermittent toe walking. His Denver II Test was normal. Specific history revealed that he used a baby walker between 9 and 15 months of age and the infant begin to walk predominantly on the forefoot at 16 months of age. Parents was reassured that it was likely to resolve spontaneously. We advised parents to play "heel down, squate, pick a ball up, stand up". Toe walking was corrected at 23 months of age.
The American Association of Pe?diatrics advice against the use of baby walker due to the high number of accidents and the possible delay of gait acquisition related to its use [4]. This is the first report about jumper and delay the attainment of standing. If clinician didn't ask these environmental risk factors, unnecessary analysis, misdiagnosis and inappropriate treatment could be done. We would thus like to emphasize that a child with toe walking should also be assessed for baby walker or jumper.
Competing interests: None.
References
1. Sivaramakrishnan S, Seal A. Fifteen-minute consultation: A child with toe walking. Arch Dis Child Educ Pract Ed. 2015 Apr 8. pii: edpract-2014-307852.
2. Lagstrom H, Rautava P, Kaljonen A, et al. Cohort profile: Steps to the healthy development and well-being of children (the STEPS Study). Int J Epidemiol 2013;42:1273-84.
3. Yalcin SS, Yurdakok K, Tezel B, et al. Family and infant characteristics in relation to age at walking in Turkey. Turk J Pediatr 2012;54:260-8.
4. American Academy of Pediatrics; Committee on Injury and Poison Prevention. Injuries associated with infant walkers. Pediatrics 2001;108:790-2.
This was succinct and helpful article. However as a paediatric
emergency doctor I would query the phrase "There is still a risk of
meningococcal disease even when blood tests are normal; therefore, admit
all children for 4-6 hours with hourly observations". It may seem
pedantic, but this is not what NICE says. The pathway states "Assess
clinical progress (vital signs) and carry out observations at least hourly
over t...
This was succinct and helpful article. However as a paediatric
emergency doctor I would query the phrase "There is still a risk of
meningococcal disease even when blood tests are normal; therefore, admit
all children for 4-6 hours with hourly observations". It may seem
pedantic, but this is not what NICE says. The pathway states "Assess
clinical progress (vital signs) and carry out observations at least hourly
over the next 4-6 hours." the next step in the full guideline(1) is "If
doubt remains, treat with antibiotics and admit to hospital". Even a
short hospital admission is several times more expensive than an ED
attendance and these children should not automatically be admitted as the
great majority can safely be observed then discharged.
1) National Institute for Health and Care Excellence. Bacterial
meningitis and meningococcal septicaemia: management of bacterial
meningitis and meningococcal septicaemia in children and young people
younger than 16?years in primary and secondary care. CG 102. London:
National Institute for Health and Care Excellence, 2010
We agree that baby walkers and door suspenders can be associated with
transient toe walking and delayed walking, which usually would correct
spontaneously relatively quickly once the children stop using the device.
The use of such devices should be strongly discouraged as part of normal
parenting practice. Enquiry regarding inappropriate use of either of these
devices in a toddler who has tip toe gait on independent or sup...
We agree that baby walkers and door suspenders can be associated with
transient toe walking and delayed walking, which usually would correct
spontaneously relatively quickly once the children stop using the device.
The use of such devices should be strongly discouraged as part of normal
parenting practice. Enquiry regarding inappropriate use of either of these
devices in a toddler who has tip toe gait on independent or supported
walking can be helpful in evaluation.
Thank you for outlining so clearly the current basis for "deferred
consent" studies and suggesting good practice in dealing with the issues
it raises.
Unfortunately I believe that the current practice is the worst of possible
worlds: not only do we submit vulnerable subjects to interventions without
the expression of their/their parents' autonomy (ie consent), but also we
risk losing any data obtained because we retrospect...
Thank you for outlining so clearly the current basis for "deferred
consent" studies and suggesting good practice in dealing with the issues
it raises.
Unfortunately I believe that the current practice is the worst of possible
worlds: not only do we submit vulnerable subjects to interventions without
the expression of their/their parents' autonomy (ie consent), but also we
risk losing any data obtained because we retrospectively seek permission
to use their data. In other words we would have put the subject at
risk/burden with no gain.
Current rules of governance for research, based ultimately on the
declaration of Helsinki, are designed to protect the subject/society from
harm, understanding that ends do not justify means. There is no
possibility that the RECs and REC members of which I have experience would
approve a study where undue harm could result.
I believe that if an REC has approved such a study, this is an endorsement
of its relative safety and utility, and should automatically permit
inclusion of the data gathered. Retrospectively inform the
subject/parents, but do not seek permission for inclusion. If they go as
far as requesting withdrawal of the data, then that could be honored.
I enjoyed reading the first edition of the "Education and Practice
Edition" a lot. However, after having read the article "Use your eyes" I
was not convinced that Oliver's clinical presentation truely was caused by
Borrelia burgdorferi infection, and I would like to challenge the authors
for the following reasons:
1. Erythema migrans usually is a mild disease that hardly ever leads
to...
I enjoyed reading the first edition of the "Education and Practice
Edition" a lot. However, after having read the article "Use your eyes" I
was not convinced that Oliver's clinical presentation truely was caused by
Borrelia burgdorferi infection, and I would like to challenge the authors
for the following reasons:
1. Erythema migrans usually is a mild disease that hardly ever leads
to hospitalisation. Painful lesions and lymphadenopathy are also unusual
features. Furthermore, although I am not aware of formal studies, markers
of inflammation in blood specimens in my experience are only mildly
elevated, if at all. Oliver's values of CRP (227 mg/l), ESR (98 mm) and
white blood count (19,4 x 102. In the majority of patients, serological markers are negative on
intial presentation but seroconversion may occur later during the disease.
Furthermore, IgM and IgG antibody values may remain positive for many
years after primary infection.[1] Also, asymptomatic infection will lead
to development of serum antibodies.[2] Therefore, the presence of IgM and
IgG (and a positive western blot) in Oliver's blood does not proof acute
infection with B. burgdorferi. A diagnosis of "erythema migrans" is
usually made on clinical grounds and, as stated above, clinical symptoms
do not suggest early localized Lyme disease.
3. Duration of antibiotic treatment for 28 days, as done in this
patient, is recommended for Lyme arthritis, but not for early localized
disease, where arthralgia (but not arthritis) may be present.
Although results of blood culture were not reported (presumably
negative), the inital diagnosis of "cellulitis" appears much more likely
to me than erythema migrans and the patient's clinical improvement on
prolonged antibiotic treatment (despite the delayed initial response) is
consistent with this.
References
1) Kalish RA, McHugh G, Granquist J, Shea B, Ruthazer R, Steere AC.
Persistence of immunoglobulin M or immunoglobulin G antibody responses to
Borrelia burgdorferi 10-20 years after active Lyme disease. Clin Infect
Dis. 2001;33:780-5.
2) Heininger U, Zimmermann T, Schoerner C, Brade V, Stehr K. Tick
bite and Lyme borreliosis. An epidemiologic study in the Erlangen area.
Monatsschr Kinderheilkd. 1993;141:874-7.
We read with great interest the article by O’Hare et al [1]. We
commend the general educational messages of the authors but feel compelled
to highlight some important errors and omissions.
In the table of
differential diagnosis of monoarticular arthritis, it is also important to
consider the diagnoses of trauma/non-accidental injury, the exclusion of
which would be the prime indication for...
We read with great interest the article by O’Hare et al [1]. We
commend the general educational messages of the authors but feel compelled
to highlight some important errors and omissions.
In the table of
differential diagnosis of monoarticular arthritis, it is also important to
consider the diagnoses of trauma/non-accidental injury, the exclusion of
which would be the prime indication for radiography. In addition,
haemophilia should be considered as well as sarcoidosis, crystal
arthritis, avascular necrosis, foreign body, pigmented villonodular
synovitis and neuroblastoma.
Table 2 considers the differential
diagnosis of arthritis and rash. Monoarthritis in a child would be
considered under the heading of oligoarticular juvenile idiopathic
arthritis (JIA) [2]. Oligoarticular JIA is not characterised by a ‘salmon
pink’ rash, lymphadenopathy or hepatosplenomegaly which are features of
systemic onset JIA [2]. Reactive arthritis is also an important
differential but neither hepatosplenomegaly or a compatible rash are
typical features. Arthralgia is a common feature of the viral
hepatitides. Hepatitis B is associated with polyarteritis nodosa and
hepatitis C with cryoglobulinaemia. However, monoarthritis is not a feature
of hepatitis B. Instead a flitting, self-limiting polyarthritis is more
typical in up to 20% of patients infected with the virus [3].
References
(1). O’ Hare BAM, Kader A, Powell CVE. Use your ears.Arch Dis Child
Educ Pract Ed 2004;89:ep9-ep14.
(2). Petty RE, Southwood TR, Manners P et al. International League of
Associations for Rheumatology classification of idiopathic arthritis:
second revision, Edmonton, 2001. J Rheumatol 2004;31(2):390-2
(3). Inman RD. Rheumatic manifestations of hepatitis B virus infection.
Semin Arthritis Rheum 1982;11:406-20
We read with interest the article by O’Hare et al [1] and would like
to congratulate the authors on their interesting case, but would like to
make the following points:
Assessment of the musculoskeletal system is poorly performed not
only by adult medical trainees [2,3] , but also by paediatric trainees: a
recent survey showed that only 1.6% of general paediatric admissions...
We read with interest the article by O’Hare et al [1] and would like
to congratulate the authors on their interesting case, but would like to
make the following points:
Assessment of the musculoskeletal system is poorly performed not
only by adult medical trainees [2,3] , but also by paediatric trainees: a
recent survey showed that only 1.6% of general paediatric admissions had
any form of joint examination documented [4]. Thus musculoskeletal
examination skills may be poor in trainees and physicians with no
specialist knowledge. Consequently we are not reassured that the remainder
of the musculoskeletal examination by the admitting team was normal.
The joint was never aspirated. The only way to make (or exclude)
a diagnosis of septic arthritis is culture of synovial fluid.
If staphylococcal septic arthritis is suspected, then current
recommendations suggest the use of two antibiotics active against this
organism [5]. Clindamycin would be an appropriate choice to add to
flucloxacillin, but oral fusidic acid is an alternative [6].
The “salmon pink rash” in juvenile arthritis is not seen in
pauciarticular JIA but is a feature of systemic onset JIA.
In this case the Lyme IgG and IgM were both positive, thus
supporting the diagnosis. We have in our own practice, however,
encountered cases where a clinical diagnosis of Lyme arthritis was made
despite initial negative assays for both IgG and IgM. Subsequent serology
became positive. Beware the false negative!
References
(1). O’Hare BAM, Kader A, Powell CVE. Use Your Ears. Arch Dis Child
Educ Pract Ed 2004; 89:ep9-ep14
(2). Marshall RW, Hull RG. For crying out loud: musculoskeletal
assessment of inpatients referred to rheumatology. In press (Rheumatology
2004)
(3). Lillicrap MS, Byrne E, Speed CA. Musculoskeletal assessment of
general medical in-patients—joints still crying out for attention.
Rheumatology 2003;42:951–4.
(4). Myers A, McDonagh JE, Gupta K et al. More ‘cries from the joints’:
assessment of the musculoskeletal system is poorly documented in routine
paediatric clerking. Rheumatology 2004 43: 1045-1049
(5). The management of septic arthritis. Drugs and Therapeutics
Bulletin 41(9) Sept 2003: 65-68
(6). Atkins B, Gottlieb T. Fusidic acid in bone and joint infections.
Int J Antimicrob Agents. 1999 Aug;12 Suppl 2:S79-93.
In India, we come across many cases of status epilepticus in
toddler age group. These children usually do not have a fever associated and
have an history of improper breast feeding and weaning.
The children may have clinical evidence of rickets, which had been
neglected. The common cause of these children getting rickets is
dietary, namely lack of vit D and inadequate sun exposure. The chil...
In India, we come across many cases of status epilepticus in
toddler age group. These children usually do not have a fever associated and
have an history of improper breast feeding and weaning.
The children may have clinical evidence of rickets, which had been
neglected. The common cause of these children getting rickets is
dietary, namely lack of vit D and inadequate sun exposure. The children
invariably present with status epilepticus due to associated
hypocalcemia and they do not respond promptly to sedation and muscle
relaxants. We need to collect blood for Calcium analysis and give
empirical IV Calcium gluconate which settles seizures in a minute.
I find that the metabolic cause of status epilepticus always gets
neglected in developing countries and invariably the child lands up being
loaded with 2-3 anticonvulsants and at times on ventilator.
With the high incidence of nutritional hypocalcemia, hypomagnesemia
in developing countries, I recommend that all status epilepticus (at least
in malnourished children)should get IV Calcium gluconate as a secondline
therapy, if not replacing IV diazepam, but definitely before loading with
other anticonvulsants.
In presenting various therapeutic approaches for the
management of Cystic Fibrosis (CF), Smyth RL primarily considers evidence
obtained from The Cochrane Library as either systematic reviews of
randomised controlled trials (RCTs) or RCTs .[1] The antibiotic treatment
of Pseudomonas aeruginosa (PA) when first isolated, is still an open
question. When discussing this aspect, Smyth RL considers only the...
In presenting various therapeutic approaches for the
management of Cystic Fibrosis (CF), Smyth RL primarily considers evidence
obtained from The Cochrane Library as either systematic reviews of
randomised controlled trials (RCTs) or RCTs .[1] The antibiotic treatment
of Pseudomonas aeruginosa (PA) when first isolated, is still an open
question. When discussing this aspect, Smyth RL considers only the RCT by
Valerius et al.[2]
In our critical review of published clinical studies evaluating the
early antibiotic treatment in asyntomatic PA-colonised CF patients [3], we
identified 3 relevant RCTs (2 vs placebo).[2,4,5] Our study also included
8 cohort studies, 2 of which with historical controls. Overall, 309
patients (range 7-91) were recruited. There was a high variability between
the individual studies for age, outcomes measures, duration of follow-up
and treatment (3 studies- 2 RCTs, 1 cohort used only aerosol tobramycin,
1 colistin, 4 aerosol colistin plus ciprofloxacin, 1 used intravenous
treatment and 2 miscellaneous therapy).
An overall critical evaluation
indicated that early antibiotic treatment can reduce the rate of positive
cultures and of anti-PA antibody titres. Long-term benefit is expected but
not yet proven. Moreover, we recently conducted an observational study
which found that nearly all CF centres in Italy treat asyntomatic PA-colonised patients in order to prevent or postpone chronic pulmonary
infection (unpublished data). However, the adopted prescribing practice
varies largely even within the same centre, highlighting the existing lack
of formal consensus on this subject.
Several therapeutic options (aerosol therapy alone or oral therapy
associated with aerosol inhalation) are available for the early treatment
of PA colonisation but no direct comparison has so far been made.
Prospective multi-centre randomised studies with relevant outcomes
measures [6] are needed to investigate which of the different proposed
antibiotic schemes has the best benefit/risk ratio and the best patient
compliance.
Department of Paediatrics Institute of Child Health Burlo Garofolo
University of Trieste
Via dell'Istria 65/1 34100 Trieste Italy
Competing interests: None declared
References
1. Smyth RL. Diagnosis and management of cystic fibrosis. Arch Dis
Child Ed Pract 2005;90:ep1-ep6.
2. Valerius N, Koch C, Hoiby N. Prevention of chronic Pseudomonas
aeruginosa colonisation in cystic fibrosis by early treatment. Lancet
1991;338:725–6.
3. Marchetti F, Giglio L, Candusso M, Faraguna D, Assael BM. Early
antibiotic treatment of pseudomonas aeruginosa colonisation in cystic
fibrosis: a critical review of the literature Eur J Clin Pharmacol
2004;60:67-74.
4. Wiesemann HG, Steinkamp G, Ratjen F et al Placebo-controlled,
double-blind, randomized study of aerosolized tobramycin for early
treatment of Pseudomonas aeruginosa colonization in cystic fibrosis.
Pediatr Pulmonol 1998;25(2):88-92.
5. Gibson RL, Emerson J, McNamara S, et al. Significant
microbiological effect of inhaled tobramycin in young children with cystic
fibrosis. Am J Respir Crit Care Med 2003;167 (6):841-9.
6. Ramsey BW, Boat TF. Outcome measures for clinical trials in cystic
fibrosis. J Pediatr 1994; 124:177-192.
I am a corporate member of UKAMB and consider issue
three of the Guidelines to be an excellent reference.
However, to minimise the risks after feed preparation
the thermal treatment (Pasteurisation)requirements
should not only mirror issue two published by RCPCH
but also include the following amplification of
treatment, based on work by the late Prof J David
Baum.
I am a corporate member of UKAMB and consider issue
three of the Guidelines to be an excellent reference.
However, to minimise the risks after feed preparation
the thermal treatment (Pasteurisation)requirements
should not only mirror issue two published by RCPCH
but also include the following amplification of
treatment, based on work by the late Prof J David
Baum.
The Pasteurisation method is raising the
temperature of the milk to 62.5°C, holding for 30
minutes, immediately cooled rapidly to less than
10 C. within the Pasteurisation Cycle.
Bottles must be submerged during the heating cycle
Bottles should not be submerged during the cooling
cycle (unless foil sealed bottles are used).
Independent verification of satisfactory treatment of
the milk (not the water bath) for the complete cycle
(heating & cooling) must be kept for future
reference.
A free fully evidence based 25 year practice proven
treatment guide can be obtained
from: info@sterifeed.com
This was succinct and helpful article. However as a paediatric emergency doctor I would query the phrase "There is still a risk of meningococcal disease even when blood tests are normal; therefore, admit all children for 4-6 hours with hourly observations". It may seem pedantic, but this is not what NICE says. The pathway states "Assess clinical progress (vital signs) and carry out observations at least hourly over t...
We agree that baby walkers and door suspenders can be associated with transient toe walking and delayed walking, which usually would correct spontaneously relatively quickly once the children stop using the device. The use of such devices should be strongly discouraged as part of normal parenting practice. Enquiry regarding inappropriate use of either of these devices in a toddler who has tip toe gait on independent or sup...
Thank you for outlining so clearly the current basis for "deferred consent" studies and suggesting good practice in dealing with the issues it raises. Unfortunately I believe that the current practice is the worst of possible worlds: not only do we submit vulnerable subjects to interventions without the expression of their/their parents' autonomy (ie consent), but also we risk losing any data obtained because we retrospect...
Dear Editor
I enjoyed reading the first edition of the "Education and Practice Edition" a lot. However, after having read the article "Use your eyes" I was not convinced that Oliver's clinical presentation truely was caused by Borrelia burgdorferi infection, and I would like to challenge the authors for the following reasons:
1. Erythema migrans usually is a mild disease that hardly ever leads to...
Dear Editor,
We read with great interest the article by O’Hare et al [1]. We commend the general educational messages of the authors but feel compelled to highlight some important errors and omissions.
In the table of differential diagnosis of monoarticular arthritis, it is also important to consider the diagnoses of trauma/non-accidental injury, the exclusion of which would be the prime indication for...
Dear Editor,
We read with interest the article by O’Hare et al [1] and would like to congratulate the authors on their interesting case, but would like to make the following points:
Dear Editor,
In India, we come across many cases of status epilepticus in toddler age group. These children usually do not have a fever associated and have an history of improper breast feeding and weaning.
The children may have clinical evidence of rickets, which had been neglected. The common cause of these children getting rickets is dietary, namely lack of vit D and inadequate sun exposure. The chil...
Dear Editor,
In presenting various therapeutic approaches for the management of Cystic Fibrosis (CF), Smyth RL primarily considers evidence obtained from The Cochrane Library as either systematic reviews of randomised controlled trials (RCTs) or RCTs .[1] The antibiotic treatment of Pseudomonas aeruginosa (PA) when first isolated, is still an open question. When discussing this aspect, Smyth RL considers only the...
Dear Editor,
I am a corporate member of UKAMB and consider issue three of the Guidelines to be an excellent reference.
However, to minimise the risks after feed preparation the thermal treatment (Pasteurisation)requirements should not only mirror issue two published by RCPCH but also include the following amplification of treatment, based on work by the late Prof J David Baum.
The Pasteurisati...
Pages