With great interest we read the recent case report by Wachowski et al. about bronchiolitis obliterans organising pneumonia associated with
Mycoplasma pneumoniae infection in a 10 year old boy.[1]
We recently
investigated a similar case of community-acquired M. pneumoniae infection
in a non-immunocompromised 12-year-old girl with fatal outcome.
The girl was seen by her general practit...
With great interest we read the recent case report by Wachowski et al. about bronchiolitis obliterans organising pneumonia associated with
Mycoplasma pneumoniae infection in a 10 year old boy.[1]
We recently
investigated a similar case of community-acquired M. pneumoniae infection
in a non-immunocompromised 12-year-old girl with fatal outcome.
The girl was seen by her general practitioner with a sore throat and a
dry, nonproductive cough and fever as high as 40°C (104.0°F). Chest
auscultation revealed mild dry rales. The family physician prescribed
amoxicillin and sent the girl home to bed. Two days later she presented
with dyspnea and acrocyanosis. Auscultation revealed rales and rhonchi.
The general practitioner now prescribed amoxicillin-clavulonate. On day 7
the girl was found collapsed at home and carried to hospital immediately.
On admission, chest auscultation revealed weakened breath sounds but no
rales or rhonchi. The leukocyte count was 29,100 cells/mm3 and C-reactive
proteine was 93 mg/l. Chest radiography was performed showing bilateral
patchy infiltrates in the lungs. Shortly after, dyspnea deteriorated and
despite endotracheal intubation and mechanical ventilation the girl died 1
hour after admission to hospital. IgM antibodies (57 U/ml) against
Mycoplasma pneumoniae were detected by serology in a venous blood sample
collected 1 hour after death.
At medico-legal autopsy, the lungs showed a patchy consolidation of all
lobes with confluent whitish-yellowish speckles. Histologically, a dense
lymphoplasmacytic infiltrate was present in the interstitium and within
the alveolar spaces accompanied by intraalveolar hemorrhages and edema.
Small bronchioli showed densely infiltrated and partly destroyed
bronchiolar walls with necrotic epithelium and plugs of granulation tissue
within the bronchiolar lumen according to bronchiolitis obliterans. Death
was attributed to bronchiolitis obliterans organising pneumonia due to
Mycoplasma pneumoniae infection. Autopsy, histology, toxicologic and
labortatory analysis excluded any underlying debilitating illnesses such
as metabolic disorders, pre-existing cardiopulmonary disorders,
immunodeficiency or immunocompromisation induced by external noxae.
Bronchiolitis obliterans associated with Mycoplasma pneumoniae infection
as observed in the present case has been reported in humans in less than
20 autopsies and biopsy specimens.[2] Even though M. pneumoniae is
usually a benign self-limited disease and only 3-10% of infected subjects
show serious clinical symptoms due to bronchopneumonia [3,4] most
significantly demonstrated by our case is the potentially fatal outcome of
Mycoplasma pneumoniae pneumonia in non-immunocompromised children when the
diagnosis is overlooked or delayed.
References
(1) Wachowski O, Demirakça S, Müller KM, et al. Mycoplasma pneumoniae
associated organising pneumonia in a 10 year old boy. Arch Dis Child
2003;88:270-2.
(2) Ebenöther M, Schoenenberger RA, Perruchoud AP, et al. Severe
bronchiolitis in acute Mycoplasma pneumoniae infection. Virchows Arch
2001;439:818-22.
(3) Ferwerda A, Moll HA, de Groot R. Respiratory tract infections by
Mycoplasma pneumoniae in children: a review of diagnostic and therapeutic
measures. Eur J Pediatr 2001;160:483-91.
(4) Clyde WA Jr. Clinical overview of typical Mycoplasma pneumoniae
infections. Clin Infect Dis 1993;17 Suppl 1:S32-36.
We read with great interest the paper by Yilmaz HL and colleagues on
amitraz poisoning and its epidemiology, clinical features, management, and
preventive strategies.[1]
We wish to raise some matters not discussed in
the paper.
First, clinical features are depending on ingested dose. Dose for
intoxication estimated by the authors is 89.2 and 163 mg/kg. But, amitraz
is sold as 12.5% solution and u...
We read with great interest the paper by Yilmaz HL and colleagues on
amitraz poisoning and its epidemiology, clinical features, management, and
preventive strategies.[1]
We wish to raise some matters not discussed in
the paper.
First, clinical features are depending on ingested dose. Dose for
intoxication estimated by the authors is 89.2 and 163 mg/kg. But, amitraz
is sold as 12.5% solution and used for agricultural purposes as diluted
with water. Therefore, clinical features are concerning with ingested
amitraz that toxic amount of drug related to how much it is diluted. It’s
possible that some clinical variables such as onset, duration of action,
biochemical alterations, necessity of mechanical ventilation may depend
upon the dilution proportion.
Second, monoamine oxidase (MAO) inhibition of amitraz is still
controversial. Moser VC and MacPhail RC [2] claimed that while amitraz
inhibit MAO, the dose range over which produces this action is much higher
than which suppress motor activity. Thus, MAO inhibition is probably not
responsible for amitraz induced alterations in motor activity . However,
in 1993, Florio JC and colleagues [3] concluded that the pesticide effects
of amitraz on motor function were the consequences of the inhibitory
effects on MAO activity, most probably through the increased catecholamine
levels within the central nervous system. Yilmaz and colleagues
recommended that inotropic agents (dopamine or noradrenaline) should be
added as a second line therapy, but dopamine might potantiate MAO
inhibiting drugs, therefore, dosage should be as low as possible. If
amitraz has inhibitory effect on MAO activity, we must avoid usage of
dopamine since dopamine also has inhibitory affect on MAO activity. It is
reasonable that dopamine may increase amitraz induced alterations in motor
activity.
We studied amitraz poisoning in 16 children,[4] found similar
results concluded by Yilmaz and colleagues. All children had taken orally,
CNS depression appeared in all within 30±25 min, and all children
recovered within 10±3.2 hours. We added atropine to treatment in three
children and they improved immediately. However, we are in agreement with
Yilmaz et al. that asymptomatic bradycardia or miosis does not require use
of atropine in amitraz poisoning.
In conclusion, although amitraz poisoning seems to be hardly undying, it
should be dangerous intoxication is depend on the concentration of amitraz
solution. A concentrated amitraz solution is the most important risk
factor for severe clinical findings and associated with difficulties in
management and poor prognosis. In addition, it should not be forgotten
that dopamine may be responsible for augmentation of amitraz induced motor
activity.
References
(1) Yilmaz HL, Yildizdas DR. Amitraz poisoning, an emerging problem:
epidemiology, clinical features, management, and preventive strategies.
Arch Dis Child 2003;88:130-134.
(2) Moser VC, MacPhail RC. Investigations of amitraz neurotoxicity in rats.
III. Effects on motor activity and inhibition of monoamine oxidase. Fundam
Appl Toxicol 1989;12:12-22.
(3) Florio JC, Sakate M, Palermo-Neto J. Effects of amitraz on motor
function. Pharmacol Toxicol 1993;73:109-14.
(4) Bosnak M, Soker M, Dikici M et al. Amitraz Intoxication in Children. New J Med 1997;14:155-7.
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
Wraige et al describe three children suffering from idiopathic
intracranial hypertension (IIH) in the absence of papilloedema [1]. MRI
findings in two cases along with an initial symptomatic improvement
following lumbar puncture support the diagnosis. In the third case MRI
scan was normal and the child's headaches did not respond to lumbar
puncture or Acetazolamide. In all three cases CSF...
Wraige et al describe three children suffering from idiopathic
intracranial hypertension (IIH) in the absence of papilloedema [1]. MRI
findings in two cases along with an initial symptomatic improvement
following lumbar puncture support the diagnosis. In the third case MRI
scan was normal and the child's headaches did not respond to lumbar
puncture or Acetazolamide. In all three cases CSF pressure was measured
under general anaesthetic with control of position and of carbon dioxide
concentration presumably by end-tidal CO2 monitoring. The anaesthetic
technique is not reported.
The message that children with IIH may not have papilloedema is a
valuable one. However, we would like to add a note of caution regarding
the measurement of CSF pressure under general anaesthesia. We have found
unexpectedly raised CSF pressure when performing lumbar punctures under
sevoflurane anaesthesia, administered to facilitate MRI scanning, in
children with a variety of neurological disorders.
All inhalational anaesthetic agents have a cerebral vasodilating
action and will increase cerebral blood volume and hence intracranial
pressure (ICP). In addition the spontaneously breathing child will
sustain an appreciable rise in ICP from the respiratory depressant action
of these drugs and consequent hypercarbia. This increase can be prevented by controlled ventilation. Volatile agents may also reduce cerebral perfusion pressure by their hypotensive effect which is due to a combination
of systemic vasodilation and direct myocardial depression; in higher
doses cerebral autoregulation may be abolished altogether [2,3].
Obstruction to venous return also increases ICP. The flexed position
of the anaesthetised child during lumbar puncture may be more marked than
when performed without anaesthesia. Coughing and straining at induction of
anaesthesia and obstruction to respiration from bronchospasm or the
introduction of positive end expiratory pressure (PEEP) will all cause a
rise in ICP which may remain a factor at the time of lumbar puncture.
Finally, end-tidal CO2 is always lower than arterial CO2 and it is not
always possible or desirable to check a blood gas prior to lumbar
puncture.
It seems likely that the use of general anaesthesia to facilitate
lumbar puncture will increase as deep sedation on paediatric wards becomes
less acceptable and increasingly de-skilled paediatricians perform fewer
lumbar punctures. We are concerned that children having lumbar puncture
under general anaesthesia could be erroneously diagnosed as having
intracranial hypertension. Until a standard anaesthetic technique is
developed which can be shown to have a minimal effect on intracranial
pressure, we believe that measurements of CSF opening pressure under
general anaesthesia should be interpreted with caution. If doubt exists,
and certainly if surgical treatment is contemplated, insertion of an
intracerebral transducer allows definitive measurement of ICP over a
period of hours or days.
References
(1) Wraige E, Chandler C, Pohl KRE. Idiopathic intracranial
hypertension: is papilloedema inevitable? Arch Dis Child 2002;87:223-224.
(2) Moss E. Volatile anaesthetic agents in Neurosurgery. Br J
Anaesthesia 1989; 63(1): 46-48.
(3) Talke P, Caldwell JE, Richardson CA. Sevoflurane increases lumbar
cerebrospinal fluid pressure in normocapnic patients undergoing trans-
sphenoidal hypophysectomy. Anesthesiology 1999; 91(1): 127-130.
We have read the interesting paper by F Jewkes and B Phillips about
resuscitation training of paediatricians [1]. In our opinion, the authors
have made a description focused on the development of teaching in
paediatric resuscitation in United Kingdom, with some but incomplete
reference to the correspondent activities in other countries. In this
sense, we would like to contribute with a summary of the...
We have read the interesting paper by F Jewkes and B Phillips about
resuscitation training of paediatricians [1]. In our opinion, the authors
have made a description focused on the development of teaching in
paediatric resuscitation in United Kingdom, with some but incomplete
reference to the correspondent activities in other countries. In this
sense, we would like to contribute with a summary of the paediatric
resuscitation education experience in Spain.
The Spanish Paediatric and
Neonatal Resuscitation Working Group (SPNRWG) was created in 1992 with the
aim to generate and publish, in Spanish, paediatric and neonatal
resuscitation guidelines, following the international consensus and the
European Resuscitation Council recommendations. The first guidelines were
published in 1995 [2,3] and they were updated in 1999 and 2000 [4-7]. In
addition, the main objective of our group was to define, organise and
carry on paediatric resuscitation courses in our country. This task has
included the release of diverse teaching material: handbooks for teachers
and students, a paediatric basic life support video aimed at lay
persons, slide collections for every type of course, and a bank of
multiple-choice questions [8,9]. The SPNRWG has developed several types of
paediatric courses (one day basic life support course, one day basic life
support plus bag-mask ventilation course, one day neonatal life support
course, three days advanced life support course, one day basic life
support instructor course, two and a half days advanced life support
instructor course, and one day re-training life support course). These
courses were carried out since 1994. Nowadays, there are more than 40
local paediatric resuscitation education working groups in all the regions
of our country and each year they organise more than 70 advanced life
support courses accounting about 2000 students (paediatricians,
paediatrics residents, anaesthetists, intensive care physicians, emergency
physicians, paediatric nurses and emergency nurses), as well as numerous
basic life support courses for lay people. In our knowledge, Spain is the
European country with more experience in paediatric resuscitation teaching
and with a more structured development of the formation. The main aspects
of our educational experience have been previously analysed and published
[10-13].
In recent years, our group has participated in the generation of
the European Paediatric Life Support (EPLS) Course, really a “course of
consensus” that gathers the experiences of all the European paediatric
resuscitation working groups. This course should be a very effective tool
to spread the teaching of paediatric life support all over Europe in an
homogeneous and standardised way, under the recommendations of the
European Resuscitation Council, and could be the basis for the development
of other courses that expand the scope of the EPLS course modules (eg.
Neonatal Resuscitation, Paediatric Trauma, Difficult Airway, Arrhythmias
in children, Special situations, Stabilisation and Transport, Ethics in
paediatric resuscitation).
Jesús López-Herce and Angel Carrillo Álvarez
Paediatric Intensive Care Unit. Gregorio Marañón University Hospital. Madrid. Spain.
Spanish Paediatric and Neonatal Resuscitation Working Group
References
(1) Jewkes F, Phillips B. Resuscitation training of paediatricians.
Arch Dis Child 2003;88:118-121.
(2) Calvo C, Delgado MA, García L, López-Herce J, Loscertales M,
Rodríguez A, Tormo C. Normas de reanimación cardiopulmonar básica y
avanzada en pediatría (1ª parte). An Esp Pediatr
1995;43:245-251
(3) Calvo C, Delgado MA, García L, López-Herce J, Loscertales M,
Rodríguez A, Tormo C. Normas de reanimación cardiopulmonar básica y
avanzada en pediatría (2ª parte). An Esp Pediatr
1995;43:323-334.
(4) López-Herce J, Carrillo A y Grupo Español de Reanimación Cardiopulmonar
Pediátrica y Neonatal. Recomendaciones de Reanimación Cardiopulmonar
Pediátrica y Neonatal (I). An Esp Pediatr 1999;51:305-312.
(5) Calvo C, Rodriguez A, López-Herce J, Manrique I y Grupo Español de
Reanimación Cardiopulmonar Pediátrica y Neonatal. Recomendaciones de
Reanimación Cardiopulmonar Pediátrica y Neonatal (II). Reanimación
cardiopulmonar básica en pediatría. An Esp Pediatr 1999;51:409-416.
(6) Carrillo A,Delgado MA, López-Herce J y Grupo Español de Reanimación
Cardiopulmonar Pediátrica y Neonatal. Recomendaciones de Reanimación
Cardiopulmonar Pediátrica y Neonatal (III).Reanimación cardiopulmonar
avanzada en pediatría. An Esp Pediatr 1999;51:551-564.
(7) Burón E, Paisán L y Grupo Español de Reanimación Cardiopulmonar
Pediátrica y Neonatal. Recomendaciones de Reanimación Cardiopulmonar
Pediátrica y Neonatal (IV).Reanimación del recién nacido. An Esp Pediatr
1999;51:717-722.
(8) Grupo Español de RCP Pediátrica y Neonatal. Manual de Reanimación
cardiopulmonar básica en niños. Alhulia, Salobreña. 2000.
(9) Grupo Español de RCP Pediátrica y Neonatal. Manual de Reanimación
cardiopulmonar avanzada pediátrica y neonatal. Publimed, Madrid, 2000.
(10) Carrillo A, López-Herce J, Moral R, Sancho L. Enseñanza de la
reanimación cardiopulmonar básica pediátrica en la Licenciatura de
Medicina y Cirugía. An Esp Pediatr 1999;50:571-575.
(11) López-Herce J, Carrillo A, Sancho L, Moral R, Bustinza A, Seriñá C.
Pediatric basic and advanced life support courses: first experience in
Spain. Resuscitation 1996;33:43-48.
(12) López-Herce J, Carrillo A, Sancho L, Seriñá C, Bustinza A,
Merello C, Moral R. Conocimientos teóricos de reanimación cardiopulmonar
de los médicos residentes de pediatría y cirugía pediátrica. An Esp
Pediatr 1995;43:257-260.
(13) López-Herce J, Carrillo A, Rodríguez A, Calvo C, Delgado MA, Spanish
Working Group on Paediatric and neonatal Cardiopulmonary Resuscitation.
Paediatric life support instructors courses in Spain. Resuscitation
1999;41:205-209
We have interest in the case of pulmonary hypertension (PHT) with B.
pertussis infection, described in paper of Casano et al.[1] We think the Bordetella heat-labile toxin (HLT) or dermonecrotic toxin may
have a role of the PHT. The toxin causes contraction of various smooth
muscles.[2,3] Endoh et al. suggested that an increase of the perfusion
pressure was induced in perfused lung of guinea p...
We have interest in the case of pulmonary hypertension (PHT) with B.
pertussis infection, described in paper of Casano et al.[1] We think the Bordetella heat-labile toxin (HLT) or dermonecrotic toxin may
have a role of the PHT. The toxin causes contraction of various smooth
muscles.[2,3] Endoh et al. suggested that an increase of the perfusion
pressure was induced in perfused lung of guinea pigs by HLT.[4] The data
was similar to the case described by Casano et al. [1] It may be necessary
to study HLT for prevention of PHT.
References
(1) Casano P, Pons Odena M, Cambra FJ et al. Bordetella pertussis infection
causing pulmonary hypertension. Arch Dis Child 2002;86:453.
(2) Endoh M, Nagai M, Nakase Y. Contractile action of heat-labile toxin of
Bordetella parapertussis on aortic smooth muscles of pigs. Microbiol
Immunol 1988;35:755-767.
(3) Endoh M, Nakase Y. Mechanism of action of Bordetella heat-labile toxin
on vascular smooth muscle strips and cells. Tokai J Exp Clin Med
1988;13 Suppl l:193-202.
(4) Endoh M, Nagai M, Nakase Y. Effect of Bordetella heat-labile toxin on
perfused lung preparations of guinea pigs. Microbiol Immunol 1986;30:1239-1246.
We note the concern of Arkwright and colleagues [1] that the young
infants described in our recent report [2] might have co-existing severe
combined immunodeficiency (SCID). This possibility was, indeed,
considered by our haematological and intensive care teams, but was not
found to be the case, because:
(i) on the day of admission, the infant had
already recovered from the initial...
We note the concern of Arkwright and colleagues [1] that the young
infants described in our recent report [2] might have co-existing severe
combined immunodeficiency (SCID). This possibility was, indeed,
considered by our haematological and intensive care teams, but was not
found to be the case, because:
(i) on the day of admission, the infant had
already recovered from the initial upper respiratory tract infection and
was apyrexial. He was thriving and did not have chronic diarrhoea.
Cervical lymph nodes were palpable on examination and chest radiograph
showed a moderate size thymus; (ii) there was no family history of SCID or
inborn errors of metabolism; (iii) the serum immunoglobulin pattern before
methylprednisolone and intravenous immunoglobulin (IVIG) treatment was
normal [serum IgG, IgA and IgM concentrations were 7.1g/L (normal range
2.1-7.7 g/L), 0.50 g/L (normal range 0.05 ¡V 0.40 g/L) and 0.60 g/L
(normal range 0.15 ¡V 0.70 g/L), respectively]; (iv) the absolute
lymphocyte count on admission was also within the normal range for his age
[9.0 x 109/L (normal range 4.0 ¡V 13.5 x 109/L, mean 7.3 x 109/L)]. As
lymphopenia is present in almost all patients with SCID from the time of
birth, the absolute lymphocyte count is considered to be the single most
reliable screening diagnostic test of this condition.[3] In view of
absence of the clinical features of SCID, normal absolute lymphocyte count
and normal serum immunoglobulin profile; analysis of lymphocyte subset
was, therefore, not considered necessary.
Although autoimmune disorders have been documented in
immunodeficiency diseases, it is a very rare initial presentation in
patients with SCID.[4] A recent report further suggested that the use of
corticosteroids, IVIG and rituximab were ineffective in halting the
haemolytic process in an 11-month old girl with SCID.[4] This finding was
in sharp contrast to the favourable response observed in our patient
without SCID.[2]
Nosocomial and opportunistic infections are common in infants
requiring intensive care. Our infant became immunocompromised only after
receiving high dose corticosteorids and anti B cell immunotherapy, and
contracted the infections 20 days after commencement of immunosuppressive
treatment. Respiratory syncytial virus pneumonia was likely to be
acquired from the mother who had flu-like symptoms at the time, and
candida septicaemia was secondary to indwelling long lines sepsis.
Whilst we agreed with Arkwright et al that SCID is a medical
emergency, there were no clinical or laboratory features in our patient
suggestive of this diagnosis. The Lady Pao Children's Cancer Centre at
Prince of Wales Hospital is a specialist bone marrow transplant centre in
Hong Kong. Anti B cell targeted immunotherapy (rituximab) is a
potentially useful therapeutic tool for treatment of refractory autoimmune
haemolytic anaemia.[2,5]
References
(1) Arkwright PD, Abinum M, Cant AJ. Severe autoimmune haemolytic anaemia in an infant: watch out for SCID! [electronic response to Ng PC et al. Anti B cell targeted immunotherapy for treatment of refractory autoimmune haemolytic anaemia in a young infant] archdischild 2003 http://adc.bmjjournals.com/cgi/eletters/archdischild;88/4/337#452
(2) Ng PC, Lee KKM, Lo AFC, Li CK, Fok TF. Anti B cell targeted immunotherapy for treatment of refractory autoimmune haemolytic anaemia in
a young infant. Arch Dis Child 2003;88:337-9.
(3) Gossage DL, Buckley RH. Prevalence of lymphocytopenia in severe
combined immunodeficiency. N Engl J Med 1990;323:1422-3.
(4) Nowak-Wegrzyn A, King KE, Shirey RS, Chen AR, McDonough C,
Lederman HM. Fetal warm autoimmune hemolytic anaemia resulting from IgM
autoagglutinins in an infant with severe combined immunodeficiency. J
Pediatr Hematol Oncol 2001;23:250-2.
(5) Quartier P, Brethon B, Philippet P, et al. Treatment of childhood
autoimmune haemolytic anaemia with rituximab. Lancet 2001;358:1511-3.
We thank Colver, MacDougall and Cant for their response to our
paper.[1] The message underpinning our paper was that severe
allergic reactions to foods are not as uncommon as MacDougall et al. suggested.[2] However, we are not comparing like with like and
the problem lies in the definition of a severe food reaction.
MacDougall et al. only identified the extreme end of the clinical
s...
We thank Colver, MacDougall and Cant for their response to our
paper.[1] The message underpinning our paper was that severe
allergic reactions to foods are not as uncommon as MacDougall et al. suggested.[2] However, we are not comparing like with like and
the problem lies in the definition of a severe food reaction.
MacDougall et al. only identified the extreme end of the clinical
spectrum (children who have suffered cardio-respiratory arrest,
received at least 2 doses of epinephrine (adrenaline), a fluid
bolus, inotropic support or at least 2 doses of nebulised
bronchodilator- all unvalidated and unreferenced outcome
measures). Having set the threshold for inclusion so high, it is
hardly surprising that the incidence of this extreme outcome is so
low. What was the authors’ purpose in identifying this extreme
population? If it was reassurance about the low incidence of life-
threatening reactions, then it should be appreciated that in a
recent American series [3] 8/10 children who died of food allergy
had previously reacted to the food that caused the fatality. Also, in
a UK survey, 21/92 (23%) of peanut allergic patients with a history
of a mild reaction subsequently had a severe reaction to peanut.[4] MacDougall’s data should not be used to dilute care given to
children with less severe food allergy.
MacDougall et al. have failed to identify the much larger
population, of the most interest to paediatricians, allergists and
parents i.e. children who have suffered a less extreme but still
severe food allergy reaction (or anaphylaxis) characterised by
airway narrowing.[5] It is important to identify and study this large
group as there is no consensus on how they should be managed.
We have shown that intervention with a structured management
plan, incorporating assessment of severity, avoidance advice and
tailored medication for self treatment, together with a patient-held
treatment plan, reduces the risk and severity of further reactions, in
both adults and children.[6]
It is clear that the British Paediatric Surveillance Unit (BPSU)
survey missed children referred to allergy centres, not run by
paediatricians. MacDougall et al. studied only inpatient
admissions and not outpatient referrals. It is erroneous to assume
that children referred to an allergy clinic would have been seen by
a paediatrician. We look after over 790 outpatient referrals of
children with nut allergy, 218 (29%) have had reactions involving
respiratory symptoms and 58 (8%) severe dyspnoea and collapse.
This number would be much larger is all foods were considered,
and this effect is repeated for other allergy centres around the
country. These children with severe reactions are derived from
approximately 1/30th of the UK population. The majority were
referred directly from their general practitioner and have had no
contact with a paediatrician and therefore would not have been
notified to the BPSU. The fact that the number of inpatient
admissions in MacDougall's paper matched that from a previous
survey is irrelevant, as neither considers the large number of
children who present to allergy out-patient clinics via their general
practitioner.
We present data to estimate the incidence of those severe
reactions that were missed by MacDougall’s paper, using a
different and more appropriate definition of severity. We compare
them to MacDougall’s estimate of 0.19 severe food reactions per
100,000 children per year. We have data from 791 children with
nut allergy, 58 of whom had at least one severe nut induced
reaction and the data were collected over six years, giving an
incidence of at least 1.93 severe reactions per 100,000 children
per year for nut allergy alone: a figure 10 fold higher than
MacDougall’s data for all food allergy. This estimate is a minimum,
as each child has had at least one severe reaction (possibly more)
and is for nut allergy alone, rather than all food allergies.
The estimate of the incidence of deaths due to food allergy
produced by MacDougall et al. is an underestimate, as the authors
did not consider asthmatic deaths, where no allergenic cause was
suspected and we thank Colver for acknowledging this. There are
sixty fold more deaths due to asthma, than those identified as due
to a severe food reaction by MacDougall et al. If only a few of
these were due to food allergy, it would alter the figures
dramatically.
Colver has citied Bock’s important series of fatal food reactions,[3]
which showed 80% (8/10) of deaths in under 16 year olds were
due to peanuts or nuts, the youngest being 2 years old. It is not
clear, however, why we should be reassured by MacDougall’s
finding of no peanut allergy induced deaths in children under 13
years. Do the authors not consider tree nut allergy induced deaths
in 2 year olds, or peanut allergy induced deaths in 14-16 year olds
relevant?
Finally, we agree that the issues surrounding provision of
adrenaline autoinjectors require good data on the clinical features
and natural history of nut allergy. However, to consider adrenaline
autoinjectors in isolation is missing the point. The provision of
adrenaline autoinjectors should be seen in the broader context of
a comprehensive management plan for all children with food
allergy. Children with mild food allergy reactions can go on to
have more severe reactions.[4] We have shown that enrolment of
children with nut allergy of all severities in such a management
plan, consisting of repeated specialist advice on allergen
avoidance, together with tailored medication including oral
antihistamine with or without inhaled adrenaline or injectable
adrenaline, results in reduced number and severity of further
reactions.[6] Colver has emphasised the efficacy of this treatment
plan in children, by highlighting that only three adults (aged 27-41
years) and no children had further severe reactions.
References
(1) Clark AT, Ewan PW. Food allergy in childhood: Have the
dangers been underestimated? Arch Dis Child 2003;88:79-81.
(2) MacDougall CF, Cant AJ, Colver AF. How dangerous is food
allergy in childhood? The incidence of severe and fatal allergic
reactions across the UK and Ireland. Arch Dis Child 2002:86:236-239.
(3) Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to
anaphylactic reactions to foods. J Allergy Clin Immunol
2001;107:191-3.
(4) Hourihane JO’B, Kilburn SA, Dean P, Warner JO. Clinical
characteristics of peanut allergy. Clin Exp Allergy 1997;27:634-9.
(5) Project team of the Resuscitation Council, UK. Emergency
medical treatment of anaphylactic reactions. J Accid Emerg Med 1999;16:243-7.
(6) Ewan PW, Clark AT. Long-term prospective observational study
of patients with peanut and nut allergy after participation in a
management plan. Lancet 2001;357:111-15.
We wish to highlight our concerns on the interpretation of the case report
presented by Ng and colleagues.[1] An 8 week old infant boy who presents
with a fever, pallor, jaundice and hepatosplenomegaly and goes on to
develop fulminant RSV bronchiolitis and disseminated Candidiasis from
which he dies strongly suggests that severe combined immunodeficiency
(SCID) as the underlying diagnosis. We and others...
We wish to highlight our concerns on the interpretation of the case report
presented by Ng and colleagues.[1] An 8 week old infant boy who presents
with a fever, pallor, jaundice and hepatosplenomegaly and goes on to
develop fulminant RSV bronchiolitis and disseminated Candidiasis from
which he dies strongly suggests that severe combined immunodeficiency
(SCID) as the underlying diagnosis. We and others have seen a number of
cases of severe "autoimmune" haemolytic anaemic as a presenting feature of
SCID.[2,3] This clinical presentation is an emergency, and after
confirming the underlying diagnosis by lymphocyte subset and serum
immunoglobulin analysis (not commented on in this report), children where
SCID is confirmed require urgent transfer to a specialist paediatric bone
marrow transplantation unit and treatment of the infection which has
precipitated the haemolysis. Despite the most aggressive medical support,
many of these infants will die, as in this case.
In such cases, the message for the paediatrician should certainly not
be to use steroid and rituximab alone which as the authors admit will only
hasten the demise of the child.
Peter D. Arkwright
Academic Unit of Child Health, Booth Hall Children's Hospital
Manchester, M9 7AA, UK
Mario Abinun
Northern Supra-regional Bone Marrow Transplantation Unit for SCID
Newcastle, General Hospital, Westgate Rd Newcastle Upon Tyne, NE4 6BE, UK
Andrew J. Cant
Northern Supra-regional Bone Marrow Transplantation Unit for SCID
Newcastle, General Hospital, Westgate Rd Newcastle Upon Tyne, NE4 6BE, UK
References
(1) Ng PC, Lee KKM, Lo AFC, Li CK, Fok TF. Anti B cell targeted
immunotherapy
for treatment of refractory autoimmune haemolytic anaemia in a young
infant. Arch Dis Child 2003;88:337-339.
(2) Elhasid R, Bergman R, Etzioni A. Autoimmunity in severe combined
immunodeficiency (SCID). Blood 2002;100:2677-8.
(3)Arkwright PD, Abinun M, Cant AJ. Redefining autoimmunity in primary
immunodeficiency diseases. Blood 2002;100:2678-9.
Dr Anand still refuses to quote our work accurately there was of course a difference between those preterm children who had received ventilatory support and those who had not, but this difference was almost entirely explained, in multiple regression, by birthweight. Hence their
conclusions largely support our 1989 study.
Dr Anand still refuses to quote our work accurately there was of course a difference between those preterm children who had received ventilatory support and those who had not, but this difference was almost entirely explained, in multiple regression, by birthweight. Hence their
conclusions largely support our 1989 study.
Yours faithfully
Professor Michael Silverman
Department of Child Health
Faculty of Medicine & Biological Sciences
Robert Kilpatrick Clinical Sciences Building
Leicester Royal Infirmary
Dear Editor
With great interest we read the recent case report by Wachowski et al. about bronchiolitis obliterans organising pneumonia associated with Mycoplasma pneumoniae infection in a 10 year old boy.[1]
We recently investigated a similar case of community-acquired M. pneumoniae infection in a non-immunocompromised 12-year-old girl with fatal outcome. The girl was seen by her general practit...
Dear Editor
We read with great interest the paper by Yilmaz HL and colleagues on amitraz poisoning and its epidemiology, clinical features, management, and preventive strategies.[1]
We wish to raise some matters not discussed in the paper. First, clinical features are depending on ingested dose. Dose for intoxication estimated by the authors is 89.2 and 163 mg/kg. But, amitraz is sold as 12.5% solution and u...
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
Wraige et al describe three children suffering from idiopathic intracranial hypertension (IIH) in the absence of papilloedema [1]. MRI findings in two cases along with an initial symptomatic improvement following lumbar puncture support the diagnosis. In the third case MRI scan was normal and the child's headaches did not respond to lumbar puncture or Acetazolamide. In all three cases CSF...
Dear Editor
We have read the interesting paper by F Jewkes and B Phillips about resuscitation training of paediatricians [1]. In our opinion, the authors have made a description focused on the development of teaching in paediatric resuscitation in United Kingdom, with some but incomplete reference to the correspondent activities in other countries. In this sense, we would like to contribute with a summary of the...
Dear Editor
We have interest in the case of pulmonary hypertension (PHT) with B. pertussis infection, described in paper of Casano et al.[1] We think the Bordetella heat-labile toxin (HLT) or dermonecrotic toxin may have a role of the PHT. The toxin causes contraction of various smooth muscles.[2,3] Endoh et al. suggested that an increase of the perfusion pressure was induced in perfused lung of guinea p...
Dear Editor
We note the concern of Arkwright and colleagues [1] that the young infants described in our recent report [2] might have co-existing severe combined immunodeficiency (SCID). This possibility was, indeed, considered by our haematological and intensive care teams, but was not found to be the case, because:
(i) on the day of admission, the infant had already recovered from the initial...
Dear Editor
We thank Colver, MacDougall and Cant for their response to our paper.[1] The message underpinning our paper was that severe allergic reactions to foods are not as uncommon as MacDougall et al. suggested.[2] However, we are not comparing like with like and the problem lies in the definition of a severe food reaction. MacDougall et al. only identified the extreme end of the clinical s...
Dear Editor
We wish to highlight our concerns on the interpretation of the case report presented by Ng and colleagues.[1] An 8 week old infant boy who presents with a fever, pallor, jaundice and hepatosplenomegaly and goes on to develop fulminant RSV bronchiolitis and disseminated Candidiasis from which he dies strongly suggests that severe combined immunodeficiency (SCID) as the underlying diagnosis. We and others...
Dear Editor
Dr Anand still refuses to quote our work accurately there was of course a difference between those preterm children who had received ventilatory support and those who had not, but this difference was almost entirely explained, in multiple regression, by birthweight. Hence their conclusions largely support our 1989 study.
Yours faithfully
Professor Michael Silverman
...
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