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Recent eLetters

Displaying 1-10 letters out of 83 published

  1. Pulse oximetry in Children - consider variant haemoglobin.

    We read with interest the recent review by Sinha et al[1] regarding physiological background, technological basis and limitations of pulse oximetry. The factors listed by the authors that may affect the accuracy of pulse oximetry include motion artifact, inadequate perfusion, nail polish, and high-ambient infrared light.

    We would like to add to that list structural variants of haemoglobin. Over 1,000 variant haemoglobins have been described [2], and while the majority are not associated with abnormal SpO2 readings, a reduced SpO2 may in some instances be the main finding associated with variant haemoglobin. Variant haemoglobins with low SpO2 as measured by pulse oximetry may be associated with either reduced SaO2 or normal SaO2, as measured by arterial blood gas analysis, as reviewed by Verhovsek et al [3].

    The finding of an unexplained reduced SpO2 can give rise to extensive cardiopulmonary investigations. Diagnosis of variant hemoglobin should be considered early on in the investigation of patients who are found to have unexpectedly low oxygen saturation but do not have clinical evidence of cardiopulmonary disease. Arterial blood gas analysis (which may in some cases of variant haemoglobin show a normal SaO2) or the simple expedient of carrying out pulse oximetry on parents (as haemoglobin variants are autosomally transmitted) may direct investigations towards a haemoglobin variant and spare the patient unnecessary cardiopulmonary investigations. Furthermore, with the increasing recommendations for use of pulse oximetry as a screening tool for detecting congenital heart disease [4], it is worth remembering haemoglobin variants as potential cause of unexplained low SpO2.

    Conflict of Interest:

    None declared

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  2. Let`s not forget CSF lactate

    The authors have done an impressive task by taking us through the physiological and biochemical basis and the clinical value of serum/blood lactate. However, I was hopeful that they would touch on CSF lactate as an important investigation tool, not only useful for paediatric neurologists but for general paediatricians alike.

    Lumbar puncture (LP) is commonly performed as part of the evaluation process of a child with suspected meningitis. In two meta-analyses, elevated CSF lactate was found to be a good indicator that can differentiate between bacterial meningitis and viral meningitis.(1) Interestingly, its diagnostic accuracy was better than CSF white cell count, glucose and protein.(1) The test is cheap, widely-available and the result is usually available by the time you get your other biochemical results back. A word of caution though: the sensitivity of the test declines significantly in those who had antibiotics pre-treatment.

    Other less common causes of elevated CSF lactate include: encephalitis, other cerebral inflammatory conditions, mitochondrial diseases, Menkes disease, LP within 72 hrs after a seizure (2), biotinidase deficiency and stroke.(2)

    References: 1. Brouwer MC, Thwaites GE, Tunkel AR, et al. Dilemmas in the diagnosis of acute community-acquired bacterial meningitis. Lancet 2012;10;380(9854):1684-92.

    2. Chow SL, Rooney ZJ, Cleary MA, et al. The significance of elevated CSF lactate. Arch Dis Child 2005;90:1188-1189.

    Conflict of Interest:

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  3. Re:Epilepsy-related Tongue biting as another cause for recurrent oral ulcers

    Thank you for identifying another cause of mouth ulcers for consideration in this specific group of patients. You highlight the point that in children with poorly controlled seizures, ulcers will resolve by achieving seizure control if they are related to tongue-biting, thereby avoiding unnecessary investigation for an alternative cause.

    Conflict of Interest:

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  4. Epilepsy-related Tongue biting as another cause for recurrent oral ulcers

    Sascha Meyer (MD), Isabel Oster (MD), Sylvia Peterlini (MD), Ludwig Gortner (MD, Professor), Georg Kutschke (MD)

    Dear Sir and Madam,

    We read with interest the 15 minute consultation on recurrent oral ulceration in a child by Le Doare et al. (1). In their report, the authors provide a wide range of differential diagnoses that may lead recurrent oral ulcerations (1).

    In our opinion, it is important to take into consideration other causes for oral ulcers in children - most importantly recurrent seizures (2, 3). This is of great importance because in addition to local treatment and use of a bite guard, administration of anti-epileptic drugs is of utmost importance. This medical problem is illustrated in Fig. 1 and Fig. 2.

    With kind regards

    Sascha Meyer, Isabel Oster, Sylvia Peterlini, Ludwig Gortner, Georg Kutschke

    University Children`s Hospital of Saarlnd 66421 Homburg Germany

    References: 1) Le Doare K, Hullah E, Challacombe S, Menson E. Fifteen-minute consultation: a structured approach to the management of recurrent oral ulceration in a child. Arch Dis Child Educ Pract Ed. 2013 Sep 19. doi: 10.1136/archdischild-2013-304471. [Epub ahead of print]. 2) Cerqueira DF, Vieira AS, Maia LC, Sweet E. Severe tongue injury in an adolescent with epilepsy: a case report. Spec Care Dentist. 2007 Jul- Aug;27(4):154-7. 3) Sanders BJ, Weddell JA, Dodge NN. Managing patients who have seizure disorders: dental and medical issues. J Am Dent Assoc. 1995 Dec;126(12):1641-7.

    Figure 1: Multiple oral and tongue ulcers in a 2-year-old-girl

    Figure 2: Sleep EEG recording demonstrating generalized seizure activity accompanied by a short episode of myoclonus, increased oral muscular tone, and bleeding from the oral cavity

    Conflict of Interest:

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  5. Re: Question 2 -NeurofibromatosisType1

    Dear Editor, We read with interest the article by Peter A Lio et. al. (1). With regards to question no.2, the authors have rightly pointed out that Neurofibromatosis Type 1 (NF1) is the most likely diagnosis.

    Once the diagnosis of NF1 is confirmed, an affected individual should have a thorough initial assessment with particular attention to features of NF1, a physical examination with particular attention to the skin, skeleton, cardiovascular system & neurological systems, ophthalmologic evaluation including slit lamp examination and developmental assessment in children.

    Ongoing surveillance should include annual physical examination comprising regular blood pressure monitoring, annual head circumference monitoring (rapid increase might indicate tumour or hydrocephalus, annual ophthalmologic examination (including fundoscopy and visual fields) until age 7, regular developmental and growth assessment.Further investigations as indicated.

    However, we are aware that presently in this child's case only one criteria for diagnosis is met. As the diagnosis of NF1 has major implications for the child and the family, we would be interested in finding out whether one should confirm the diagnosis at this stage with genetic test and start the surveillance process as per the guidelines (2) or should one wait for the second major criteria to appear?

    Reference: 1. Peter A Lio, Kachiu C Lee. Brown birthmarks. Arch Dis Child Educ Pract Ed 2013;98:171-172 2. Ferner RE, Huson SM, Thomas N, et al. Guidelines for the diagnosis and management of individuals with neurofibromatosis 1. J Med Genet 2007;44:81 -88

    Conflict of Interest:

    None declared

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  6. How to adjust for case-mix when comparing outcomes across healthcare providers

    We welcome Santhakumaran's article (1) describing some of the problems and misunderstandings that can arise when adjusting for case-mix differences between hospitals. In our recent paper (2) we quantified the bias that is likely to arise when comparing standardised mortality ratios (SMRs) between one neonatal unit and another. In our paper it was shown that, using actual observed differences in case-mix, even if two neonatal units were performing identically for each patient group the ratio of their SMRs could range from 0.79 to 1.68.

    However, this is not to say that the SMR has no role when reporting of clinical outcomes. First, when case-mix differences are small the likely bias that occurs when comparing two SMRs is also likely to be small. Second, the value of the SMR can indicate where intervention (e.g. training, guidelines) may be the most beneficial. For example, with Santhakumaran's two hypothetical neonatal units (Table 1 (1)) it seems entirely reasonable for the hypothetical manager to conclude that prioritizing intervention in unit A (the unit with the highest SMR) would result in improved outcomes for more patients than would the same intervention in unit B, since there are more deaths in unit A than in unit B.

    1 Santhakumaran S. How to adjust for case-mix when comparing outcomes across healthcare providers Arch Dis Child Educ Pract Ed Published Online First: 30 September 2013 doi:10.1136/archdischild-2013-303940

    2 Evans TA, Seaton SE, Manktelow BN. Quantifying the potential bias when directly comparing standardised mortality ratios for in-unit neonatal mortality. PLoS ONE 8(4):e61237

    Conflict of Interest:

    None declared

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  7. Early-onset headache does not predict poor long term headache disability

    I read with interest the "Fifteen minute consultation: headache in children under 5 years of age" recently published online. It would also be worth remembering and will be reassuring to all of us to know that although some characteristics of early-onset headache can be different from that of late-onset headaches for e.g. shorter duration, the overall impact of the headache on the school performance and learning and clinical severity do not significantly differ from the later.

    In other words, early-onset of headaches does not necessarily imply poorer long term headache disability or harmful aetiology. (1)

    Reference: 1. Ravid S, Gordon S, Schiff Aet. al. Headache in Children: Young Age at Onset Does Not Imply a Harmful Etiology or Predict a Harsh Headache Disability. Journal of Child Neurology2013: 28(7) 857-862

    Conflict of Interest:

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  8. 'Benign Enlargement of Subarachnoid Space (BESS)'- an important differential for large head

    I read with interest "The Fifteen-minute consultation on the infant with a large head" published recently by Arnab Seal. Clinicians should also be aware of 'Benign Enlargement of Subarachnoid Space (BESS)'. It is described under various names in literature including benign extra-axial collections of infancy, external hydrocephalus, subdural effusions, etc (1). It presents in infancy with rapid enlarged of head circumference on the background of normal development. It should be differentiated from isolated or familial macrocephaly as the head circumference is normal at birth followed by rapid growth in infancy crossing more than 2 centiles. Hence although it would fall in category E (figure 2) neuroimaging (Computed tomography (CT)/Magnetic resonance imaging (MRI) head) would be required to rule out any intracranial pathology and establish the diagnosis. In the majority of cases there is a positive family history of macrocephaly, thus can be misdiagnosed as familial macrocephaly if neuroimaging is not undertaken. The anterior fontanelle is enlarged along with enlargement of fronto- parietal subarachnoid space. There is no associated brain atrophy or signs of raised intracranial pressure. As the name indicates it is completely benign condition and no surgical intervention is required. This condition is self-limiting with spontaneous resolution usually by 2 years of age. Although the macrocephaly may persist it plateaus by 2 years of age and associated with resolution of subarachnoid space as the child grow older (1). It is important to monitor the head growth and developmental progress. If there is any deviation from normal in neuro-development or there is persistence of rapid head growth beyond 2 years of age further evaluation is required to exclude other intracranial pathologies (2). In summary, clinicians should consider BESS in any infant presenting with rapid head growth and normal development. This is a benign self-limiting condition and no surgical intervention is required.

    Conflict of Interest:

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  9. Whether a head is 'abnormally' large depends on the growth chart used

    The Fifteen-minute consultation on the infant with a large head just published on line (1) has one major weakness: no mention of which chart the child's head is compared to. Comparison with representative Belgian, Norwegian (2) and British data (3) has shown that European infants' heads appear large compared to the WHO standards. We have undertaken further analyses of the data from the Southampton Women's Survey used for our previous paper (3) and these suggest that, out of 1731 healthy infants aged 6 months, 3.3% have a head circumference (HC) above the WHO 99.6th centile and half of these (1.8% of all infants) will also have crossed 2 or more centile spaces upwards since birth. Reassuringly, between 6 and 12 months there was much less centile crossing and only 5 infants (0.3% of all infants) move further upwards by more than the equivalent of one centile space (0.67SD). It is probably these latter children who should be investigated further.

    If compared to the previous UK 1990 growth chart only around 0.5% of children will have a head circumference above the 99.6th, but it should be born in mind that compared to the UK 1990 UK more infants' heads appear small. After the age of 6 months between 5-8% of children have heads below the UK1990 2nd centile (3) and our further analyses of the latter data3 suggest that by 6 months of age 17% of healthy infants will have crossed 2 or more centile spaces downwards compared to the UK 1990 reference.

    So the growth chart you choose makes a huge difference: make sure you know which one is being referred to!

    Reference List

    (1) Seal A. Fifteen-minute consultation on the infant with a large head. Arch Dis Child Educ Pract Ed 2013. (2) Juliusson PB, Roelants M, Hoppenbrouwers K, Hauspie R, Bjerknes R. Growth of Belgian and Norwegian children compared to the WHO growth standards: prevalence below -2 and above +2 SD and the effect of breastfeeding. Arch Dis Child 2011; 96(10):916-921. (3) Wright CM, Inskip HM, Godfrey K, Williams AF, Ong KK. Monitoring head size and growth using the new UK-WHO growth standard. Arch Dis Child 2011; 96(4):386-388.

    Conflict of Interest:

    I am academic lead for the RCPCH growth chart group that published the new UK-wHO growth charts

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  10. The two fundamental caveats of IGRAs

    The reservations exepressed about the interpretation of interferon gamma release assays(IGRAs)(1)are underpinned by the following observations:- IGRAs do not reliably identify subjects with active tuberculosis(even in the context of culture positive disease)(2), as shown by a study where 45 subjects received a diagnosis of active tuberculosis characterised, in 37 of those subjects, by positive cultures for mycobacterium tuberculosis(MTB). Nevertheless, in 17 of the 45 patients with a final diagnosis of active tuberculosis the IGRA test was negative(2). This means that, in that study,the spectrum of 17 negative IGRA tests included, at a bare minimum, at least eight patients with culture positive tuberculosis. The suboptimal sensitivity of IGRAs is compounded by apparently spontaneous reversion from positive to negative test status(3)(4), and also by apparently spontaneous by conversion from negative to positive test status(3)(4). This state of affairs has implications for recognition and management of latent tuberculosis, not only in the context of low disease prevalence(3), but also in the context of high disease prevalence(4). In the former context, an American study utilised IGRAs to screen 3,234 individuals considered to be at low risk of mycobacterium tuberculosis infection, including low risk of infection in the remote past. Of these, 2,819 tested unequivocally negative, 218 tested unequivocally positive, and 177 yielded indeterminate tests per manufaturer's criteria. On retesting 13(9%) of initially negative tests converted to positive, and 15(7%) of initially positive tests reverted to negative test status using the manufacturer's cut-off value(3). In the context of high disease prevalence a review was published which included evaluation of in-subject variability of IGRAs in India and in South Africa. In the Indian context, over a 2 weeks period, 2 of 14 health care workers experienced reversion from positive to negative test status. In the South African study, over a 3 week period, 7 of 26 helth care workers experienced either a conversion or a reversion. In both the Indian and the South African studies subjects who experienced either reversion or conversion had initial values close to the cut-off point(4). These observations(2)(3)(4) should serve as fundamental caveats to the use of IGRAs in clinical practice. References (1) Pollock L., Roy RB., Kampmann B How to use: interferon gamma release assays for tuberculosis Education and Practice 2013;98:99-105 (2)Dewan PK., Grinsdale J., Kawamura M Low sensitivity of a whole blood interferon gamma release assay for detection of active tuberculosis Clinical Infectious Diseases 2007;44:69-73 (3) Metcalfe JZ., Cattamanchi A., McCulloch CE et al Test variability of the QuabtiFERON-TB-Gold in-Tube assay in clinical practice Am J Respir Crit Care Med 2013;187:206-2011 (4) van Zyl Smit RN., Zwerling A., Dheda K., Pai M Within-subject variability of interferon-gamma assay results for tuberculosis and boosting effect of tuberculin skin testing: A systematic review PLoS ONE 2009;4:e8517

    Conflict of Interest:

    None declared

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