The purpose of measuring serum levels of a drug is either to monitor
the toxicity of the drug or the therapeutic concentration for a particular
condition. Emergence of infections with beta-lactam-resistant
Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus sp.
has led to the frequent use of vancomycin in neonates. Vancomycin
historically has had a reputation for tox...
The purpose of measuring serum levels of a drug is either to monitor
the toxicity of the drug or the therapeutic concentration for a particular
condition. Emergence of infections with beta-lactam-resistant
Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus sp.
has led to the frequent use of vancomycin in neonates. Vancomycin
historically has had a reputation for toxicity. Many of its original
adverse reactions, including ototoxicity and nephrotoxicity, were probably
due impurities in the formulation.[1] Now, that a more purified form is
available, these adverse reactions are uncommon; however, concomitant
administration with aminoglycosides or other nephrotoxins may increase the
risk of toxicity.[2]
Effective drug therapy is measured by response, not by achievement of a
particular circulating drug concentration. Because the association between
vancomycin peak concentrations and toxicity is poor, some have recommended
measuring trough concentration only [3] as your study is clearly
documenting, but others have suggested not measuring any concentrations in
the majority of children with normal renal function.[4]
However, in critically ill premature neonates, poor glomerular filtration
rate with prematurity and compromised cardiovascular function, it remains
prudent to measure both peak and trough concentrations in those with poor
or changing renal function. Caution must be exercised when other
nephrotoxic or ototoxic drugs such as aminoglycisides are administered
concurrently.[5] In your study, you have not mentioned about the
concomittent use of aminoglycoside.
References
(1) Baillie GR, Neal D. Vancomycin ototoxicity and nephrotoxicity. A
review. Med Toxicol Adv Drug Exp 1988;3:376-386.
(2) Rybak MJ, Albrecht LM, Boike SC, Chandrasekar PH. Nephrotoxicity of
vancomycin, alone and with an aminoglycoside. J Antimicrob Chemother
1990;25:679-687.
(4) Thomas MP, Steele RW. Monitoring serum vancomycin concentrations in
children. Is it necessary? Pediatr Infect Dis J 1998;17:351-352.
(5) Moellering RC, Krogstad DJ, and Greenblatt DJ. Vancomycin therapy in
patients with impaired renal function: a nomogram for dosage. Ann Intern
Med 1981;94:343-346.
As well emphasized by Koppen et al,[1] congenital pulmonary
arteriovenous malformation presenting in the neonatal period is an
exceedingly rare anomaly, perhaps underdiagnosed. The index of suspition
should be high if appropriate treatment is to be offered to these babies
and, unfortunately, this was not the case in a 6-day-old patient seen by
us 7 years ago.[2] Adding to the severe hypoxaemia, o...
As well emphasized by Koppen et al,[1] congenital pulmonary
arteriovenous malformation presenting in the neonatal period is an
exceedingly rare anomaly, perhaps underdiagnosed. The index of suspition
should be high if appropriate treatment is to be offered to these babies
and, unfortunately, this was not the case in a 6-day-old patient seen by
us 7 years ago.[2] Adding to the severe hypoxaemia, our case had isolated
left ventricular overload demonstrated by the EKG and 2D-echo, which
should have raised the strong possibility of a right to left shunt. Our
index of suspition was moderate but not enough for the patient, despite
attempted cardiac catheterization.
This case should, in our view, be added to the other 12 mentioned by
Koppen and so far reported in the literature. Also,this is perhaps the
youngest patient reported and awareness of this possibility should be
useful for the neonatologist.
Fernando Amaral
UNAERP Medical School
References
(1) S Koppen, CRW Korver, M Dalinghaus, CJJ Westermann. Neonatal pulmonary
arteriovenous malformation in hereditary haemorrhagic telangiectasia. Arch
Dis Child Fetal Neonatal 2002; 87:F226-F227.
(2) Amaral FTV, Félix PR, Granzotti JA, Rugolo LMS, Bernardes TA,
Nunes MA. Fístula arteriovenosa pulmonar maciça. Causa rara,
potencialmente curável de hipóxia neonatal. Arq Bras Cardiol 1995; 66:353-
355.
We read with interest the findings of Evans et al. concerning the changes in middle cerebral artery (MCA) haemodynamics over the first two days after birth in preterm infants.[1]
Evans et al. demonstrated a significant change in several Doppler
velocity measures in the MCA, including systolic, diastolic and mean
velocity, pulsatility index and velocity time integral, during days 1 and...
We read with interest the findings of Evans et al. concerning the changes in middle cerebral artery (MCA) haemodynamics over the first two days after birth in preterm infants.[1]
Evans et al. demonstrated a significant change in several Doppler
velocity measures in the MCA, including systolic, diastolic and mean
velocity, pulsatility index and velocity time integral, during days 1 and
2 after birth in a cohort of preterm infants. Blood flow (F), blood
pressure (P) and vascular resistance (R) are closely related (F = P / R),
and resistance changes are a function of changing vessel calibre. The
authors attempted to measure MCA diameter, but because measurements were
inaccurate the authors did not attempt to calculate values for MCA blood
flow.
Our own studies of cerebral haemodynamics, using near infrared
spectroscopy, supports the view of Evans et al. that there are significant
changes in cerebral blood flow over the first 36 hours after birth. The
demographic details of our cohort were similar to the one studied by Evans
et al., with 36 infants of mean (±SD) gestation 26±2 weeks and mean birth
weight 929±250g. We found that a significant increase in cerebral blood
flow between days 1 and 2 was accompanied by a significant decrease in
cerebral fractional oxygen extraction (FOE). High cerebral FOE may protect
the brain from hypoxic-ischaemic injury, a potential consequence of
reduced cerebral blood flow.
The results presented by Evans et al. give an insight into the complex
relationships that exist within a dynamic fluid system. Systemic blood
pressure was closely related to MCA mean velocity, but not estimated MCA
diameter, thus implying that cerebral blood flow would vary independently
of systemic blood pressure because of changes in cerebrovascular
resistance. Our own observations have produced similar results. Cerebral
FOE, which is expected to increase as cerebral blood flow decreases, is
not related to mean arterial blood pressure.[2] There is, however, a
significant relationship between cerebral FOE and left ventricular output,
which is a major determinant of central blood flow.[2] This latter
finding is in agreement with the observation of Evans et al. that SVC flow,
also related to central blood flow, was significantly associated with
estimated MCA diameter.
Evans et al. remind us that velocity is not the same as flow. Their
observations, and our own, stress the importance of vascular resistance in
mediating the relationship between blood pressure and blood flow. In the
sick preterm infant, the presence of an adequate mean arterial blood
pressure, often achieved using pharmacological methods, although
reassuring, does not guarantee the presence of good central blood flow,
nor the adequate perfusion of the end-organs, including the brain.
References
(1) Evans NJ, Kluckow M, Simmons M,et al. Which to measure, systemic or
organ blood flow? Middle cerebral artery and superior vena cava flow in
very preterm infants. Arch Dis Child Fetal Neonatal Ed 2002;87:F181-F184.
(2) Kissack CM, Garr R, Wardle SP et al. Cardiac output, blood pressure and
cerebral oxygen extraction in very low birthweight infants. Arch Dis Child
2001;84(Suppl I):A33
Having recently reviewed the case notes of babies readmitted to
hospital in the first 10 days of life (over a 1 year period), we firmly
agree with the views expressed by Laing and Wong.[1] The incidence of
documented hypernatraemic dehydration secondary to the failure of
lactation in Bristol is 1.7 per 1000 live births much higher than that
described by Oddie et al. [2] in the Northern Region (2.5...
Having recently reviewed the case notes of babies readmitted to
hospital in the first 10 days of life (over a 1 year period), we firmly
agree with the views expressed by Laing and Wong.[1] The incidence of
documented hypernatraemic dehydration secondary to the failure of
lactation in Bristol is 1.7 per 1000 live births much higher than that
described by Oddie et al. [2] in the Northern Region (2.5 per 10,000 live
births). In addition only 50% of infants readmitted with weight loss of
<10% had a plasma sodium concentration measured. The true incidence of
hypernatraemic dehydration secondary to lactation problems in Bristol
could thus be as high 3.4 per 1000 live births. Our estimate could be an
underestimate as our study looked only at infants readmitted within 10
days(Oddie et al looked at infants readmitted up to one month of age) and
due to failure of recognition of this condition.
Laing and Wong [1] have proposed weighing all infants when the
Guthrie blood samples are taken to identify those infants at risk of
dehydration. We believe that this is too late as in many areas this occurs
on days 7 or on day 10 with hand-over of care to the health visitor. We
have already described a series of babies with hypernatraemic dehydration
where all presented to hospital before day 7.[3]
The case has been made correctly [1, Newman] that newborn
hypernatraemia is due to failure of successful feeding. While we agree
that careful examination, observation of the infant while feeding etc may
identify these babies we would dispute that this is currently universally
possible. Due to midwifery shortages, postnatal wards are short staffed,
community midwives are fully stretched and many women are discharged
within a few hours of delivering. If a midwifery home visit does not
coincide with a feed the mother’s assessment of feeding is assumed to be
correct (as indeed it usually is). Weighing will reassure most mothers
that their baby is following the normal pattern of loss followed by gain.
Identification of excessive weight loss should prompt the health
professional to examine the baby for evidence of illness and carefully
observe breast-feeding technique. These mother-baby dyads could then be
given additional support and advice in the community and thus successfully
establish feeding. In our experience once the baby has become ill and
required readmission to hospital the mother is reluctant to continue to
attempt to breast-feed.
There continues to be confusion regarding the best way to manage this
problem [1, Smith]. It should be remembered that these babies have normal
guts and are suffering from starvation. If the infant is not shocked the
rehydration can safely occur using enteral fluids – expressed breast milk
or a breast milk substitute. Serum sodium should initially be measured six
hourly and the volume of milk altered to ensure a slow return to
normality.
We believe we need to foster a greater awareness of this problem and
weigh the babies at risk around day 5 if we are to prevent tragedies from
a common condition affecting otherwise well babies.
References
(1) Hypernatraemia in the first few days: is the incidence rising?
Laing IA, Wong M. Arch Dis Child 2002;87:F158-161.
(2) Hypernatraemic dehydration and breast feeding: a population study.
Oddie S, Richmond S, Coulthard M. Arch Dis Child 2001;85:318-20.
(3) Hypernatraemia: why bother weighing breast fed babies? Harding D,
Cairns P, Gupta S, Cowan F. Arch Dis Child Fetal Neonatal Ed 2001; 85:
F145.
We read the article by Dr Perry et al. on ultrasound of the thyroid
gland in the newborn: normative data with great interest.[1] In this study
on the measurements of the thyroid volumes in the newborn, there are many
discrepancies with the normative data described by previous studies. And
also the results of this study try to change widely accepted criteria. In
my opinion, this may cause confusio...
We read the article by Dr Perry et al. on ultrasound of the thyroid
gland in the newborn: normative data with great interest.[1] In this study
on the measurements of the thyroid volumes in the newborn, there are many
discrepancies with the normative data described by previous studies. And
also the results of this study try to change widely accepted criteria. In
my opinion, this may cause confusion about the size of the thyroid gland
in the newborn.
The thyroid volume of newborns found in this study was not similar to that
reported by several authors. Chanoine et al. [2] reported that in Belgium,
median thyroid volume in newborns was 0.84 (0.38) ml, Klingmuller et al. [3]
reported that in Germany, mean thyroid volume was 1.1 (0.6) Boehles et al.[4] reported that in Germany, median thyroid volume was 0.61 ml, Glinoer et al. [5] reported that in Belgium, mean (SD) thyroid volume was 1.05 (0.34) et al. [6] reported that in USA term euthyroid neonates had a
thyroid gland volume ranging between 0.47 and 1.43 ml, Liesenkoetter et al.[7] reported that in Germany, mean thyroid volume was 0.7 ml, and Hnikova
et al. [8] reported that in Czech Rep, mean thyroid volume was 0.60 ml,
Tajtakova et al 9 reported that in Slovakia, mean (SD) thyroid volume was
0.6 (0.2) ml.
The thyroid volumes of newborns found in these studies were similar. It is
known that mean values and upper limits appear to differ according to
iodine intake and urinary iodine. Thus, in newborns of iodine supplemented
mothers the upper limit was 1.4 ml (Glinoer et al5 1994) and 1.6 ml
(Liesenkoetter et al. [7] 1995). However, the upper limit of thyroid volumes
in newborns is 1.5 ml (Chanoine et al. [2]) and this cut off point is widely
accepted. In Scotland, UK, term neonates were found to have a mean (SD)
thyroid gland volume of 1.63 (0.37) ml by Peery et al. and this value is
definitely high.
In 1992, most European countries, with the exceptions of Switzerland,
Austria, Great Britain, and most Scandinavian countries, were still
affected by mild to moderate degrees of iodine deficiency 10 (Delange F).
Turkey has long been known, as a mild to moderate iodine deficiency area
according to the figures obtained from previous epidemiological studies.
Kurtoglu et al. [11] reported that in the Central Anatolia (Kayseri) of
Turkey, mean (SD) thyroid volume of the term newborn was 1.26 (0.36) ml.
After the national salt iodization program, again in the same region they
reported that mean (SD) thyroid volume was 0.99 (0.79) ml 12 In the second
study they also reported that the median values of urinary iodine in
mothers and their babies on the 5th day after delivery were 30.20 (range
3.20-171.50) and 23.80 (3.20-95.30) g/L, respectively. These
urinary iodine values in mothers and their babies represents that Kayseri
still is an area of moderate iodine deficiency.
Urinary iodine level is an indicator to assess the present iodine intake.
There is an agreement that causal urine samples from a representative
fraction of the population provide accurate information on the status of
the iodine nutrition. In this study, urinary iodine excretion in the
mothers and their babies were not studied.
As a conclusion, there is a discrepancy between the normative data in this
study and the data those reported in studies from the other countries
using the same volumetric calculations and it is not clear the status of
iodine nutrition in Scotland (urinary iodine excretion were not measured
in this study). Because of these two reasons, this study of thyroid size
in normal newborn babies is far from to be a normative data for other
centers performing neonatal ultrasonography.
References
(1) Perry RJ, Hollman AS, Wood AM, Donaldson MD. Ultrasound of the
thyroid gland in the newborn: normative data. Arch Dis Child Fetal
Neonatal Ed 2002;87:F209-11.
(2) Chanoine JP, Toppet V, Lagasse R, Spehl M, Delange F. Determination of
thyroid volume by ultrasound from the neonatal period to late adolescence.
Eur J Pediatr 1991;150:395-9.
(3) Klingmuller V, Fiedler C, Otten A. Characteristics of thyroid sonography
in infants and children. Radiologe 1992;32:320-6.
(4) Boehles H, Aschenbrenner M, Roth M, von Loewenich V, Ball F, Usadel KH.
Development of thyroid gland volume during the first 3 months of life in
breast-fed versus iodine-supplemented and iodine-free formula-fed infants.
Clin Investig 1993;71:13-20.
(5) Glinoer D, De Nayer P, Delange F,et al. A randomized trial for the
treatment of mild iodine deficiency during pregnancy: maternal and
neonatal effects. J Clin Endocrinol Metab 1995;80:258-69.
(6) Vade A, Gottschalk ME, Yetter EM, Subbaiah P. Sonographic measurements
of the neonatal thyroid gland. J Ultrasound Med 1997;16:395-9.
(7) Liesenkotter KP, Gopel W, Bogner U, Stach B, Gruters A. Earliest
prevention of endemic goiter by iodine supplementation during pregnancy.
Eur J Endocrinol 1996;134:443-8.
(8) Hnikova O, Zikmund J, Janeckova M. The thyroid and iodine In: Nauman J,
Glinoer D, Braverman LE, Hostalek U (Ed) Results of a preventive approach
to iodine deficiency in newborns from a mild deficiency region. Stuttgart:
Schattauer, 1996:193.
(9) Tajtakova M, Capova J, Bires J, Sebokova E, Petrovicova J. Thyroid
volume, urinary and milk iodine in mothers after delivery and their
newborns in iodine-replete country. Endocr Regul 1999;33:9-15.
(10) Delange F. Iodine deficiency in Europe and its consequences: an update.
Eur J Nucl Med 2002;29:S404–S416.
(11) Kurtoglu S, Covut IE, Kendirci M, Uzum K, Durak AC, Kýrýs A. Normal
thyroid volume of children in Turkey: Pilot study in Kayseri province. IDD
Newslett 1995;11: 41-42.
(12) Kurtoglu S, Akcakus M, Kocaoglu C, et al. Iodine Deficiency in Pregnant
Women, and Their Neonates in the Central Anatolia (Kayseri) of Turkey.
Turkish J Pediatr (In press)
We are grateful to colleagues for their comments on our annotation.[1]
We would stress that we merely abstracted the views of others so any
criticisms (apart from our brevity) will be of the lawyers, doctors,
nurses, physiotherapists and parents who contributed to the Royal
Commission Report. We found it to be systematic, rational and objective.
We strongly refute any suggestion that any of t...
We are grateful to colleagues for their comments on our annotation.[1]
We would stress that we merely abstracted the views of others so any
criticisms (apart from our brevity) will be of the lawyers, doctors,
nurses, physiotherapists and parents who contributed to the Royal
Commission Report. We found it to be systematic, rational and objective.
We strongly refute any suggestion that any of the New Zealand
professionals should be criticised let alone made scapegoats (witness our
final paragraph). We are puzzled that Drs Rosenbloom and Ryan discount
the quoted witness statements of the parents and involved clinicians. The
lawyers and doctors are clear that the physiotherapy and nursing practices
did occur and that the levels of head shaking were not monitored.
We are concerned with infant brain injuries not lung disease and
consider this to be topical. We share colleagues’ concern at the need to
base opinions on speculative presumption extrapolated from animal or
accident research and are aware of the limited evidence that identifies
the minimal forces needed to cause shaken brain damage in neonates or
older infants. We found the reported experiences to be a helpful insight.
We are delighted that Dr Rushton (eLetter) has taken this opportunity
to state he thought vigorous chest physiotherapy without supporting the
head was responsible for the porencephalic lesions and to
inform of his pivotal involvement in advising New Zealand colleagues. We
understand there were earlier concerns that publishing the speculation
about physiotherapy would open liability to litigation. Lawyers might
consider the inference that fear of litigation led to suppression of
information that might have prevented the New Zealand deaths and the
dilemma facing clinicians who reported the cerebral implications of
vigorous physiotherapy. Dr Knight reports (eLetter) their unit has been
‘subject to a long official public inquiry, law suits and had twenty
medical, nursing and physiotherapy staff investigated by registration
authorities, lasting 8 years.’
We do not accept criticisms of inaccurate references. The Cochrane
review we both cited was last updated in 1997. There has been an updated
review this year (dealing with lung not brain disease), which was
unavailable to the editors or us at the time of submission. Dr Knight
(eLetter) states there was no change in the vigour of chest physiotherapy
from 1985 until the end of 1994 but he co-authored the paper [2] we cited
that states that there was no policy to support the head during chest
physiotherapy and no data on the extent the head moved during
physiotherapy whether given by nurses or physiotherapists. The Royal
Commission Report found no record of the vigour of chest percussion and
understood there was considerable variation with no standardisation of
training.
We recommend interested colleagues to read this Report and the
publications of Knight and Harding et al before dismissing the possibility
that vigorous chest physiotherapy without supporting the head may cause
brain injuries in certain circumstances.
References
(1) Williams AN, Sunderland R, Neonatal shaken baby syndrome: an
aetiological view from Down Under. Arch Dis Child 2002;87:F29-30
(2) Knight DB, Bevan CJ, Harding JE, et al. Chest physiotherapy and
porencephalic lesions in very preterm infants. J Paediatr Child Health
2001;37:554–8.
It is difficult to define what is suboptimal care in some situations. For example a borderline Cardiotocograph can be interpreted differently by different individuals.
Secondly, although not mentioned in the article, it would be interesting to know how the all case notes for the study were acquired. The number of infants with neonatal encephalopathy might be more than 49. It is possibl...
It is difficult to define what is suboptimal care in some situations. For example a borderline Cardiotocograph can be interpreted differently by different individuals.
Secondly, although not mentioned in the article, it would be interesting to know how the all case notes for the study were acquired. The number of infants with neonatal encephalopathy might be more than 49. It is possible to include all deaths and stillbirths in a region but it may not be the case with encephalopathic infants.
Finally, because the outcome of these studies can be anticipated from the outset, there is scope for harsher judgement on the quality of care provided.
I am grateful to Laing and Wong for raising once again the issue of
hypernatraemic dehydration in the first few days of life.[1] However, I
think it is important to remember that hypernatraemic dehydration, like
anaemia, is a sign of disease not a diagnosis in itself. A low haemoglobin
concentration in blood can be caused by a large number of different
pathological and physiological processes. Hypern...
I am grateful to Laing and Wong for raising once again the issue of
hypernatraemic dehydration in the first few days of life.[1] However, I
think it is important to remember that hypernatraemic dehydration, like
anaemia, is a sign of disease not a diagnosis in itself. A low haemoglobin
concentration in blood can be caused by a large number of different
pathological and physiological processes. Hypernatraemic dehydration
should be seen in the same light.
Laing and Wong’s article describes two situations in which a child
can be found to exhibit the typical biochemical and clinical features of
hypernatraemic dehydration, i.e. weight loss and hypernatraemia. The first
mentioned is associated with gastroenteritis in a bottle fed infant,
commonly a few weeks old and the second is seen in ‘breastfed’ infants in
the first few days of life. The hypernatraemia associated with these
situations is caused by different problems with water balance – in neither
is the problem an increased intake of sodium. In the infant with diarrhoea
there is an excess loss of water and in the ‘breastfed’ baby an
insufficient intake of water.
In discussing hypernatraemic dehydration in association with
diarrhoea in young infants Laing and Wong refer to a paper by Chambers and
and Steel [2] where attention is drawn to the slightly increased
concentration of sodium in artificial milk mixed incorrectly by parents.
This is a red herring. The excess sodium concentration of the artificial
milk mixed incorrectly by the mothers reached a maximum of 59 mmol/L with
a mean of 37.2 mol/L. Those who believe that this concentration of sodium
could be responsible for hypernatraemic dehydration should remember that
the concentration of sodium in the standard oral rehydration solutions in
use in this country is 60 mmol/L (Dioralyte®, Dioralyte Relief®,
Rehidrat®), or in one case 50 mmol/L (Electrolade®) and that the WHO
formulation for oral rehydration solution contains 90 mmol/L of sodium.
In fact the cause of this association of hypernatraemic dehydration
with diarrhoea is the continued feeding with artificial milk after the
onset of diarrhoea. The intestinal hurry associated with gastroenteritis
results in the delivery of a solution rich in protein and complex
carbohydrates to the colon which, after digestion by colonic bacteria,
produces a considerable osmotic load in the colon which in turn results in
the production of voluminous stool low in sodium.[3] The result is
hypernatraemic dehydration due to excessive water loss. Those who require
further discussion of this hypothesis are advised to read the excellent
paper by Hirschhorn.[3]
The second situation relates to the title of the piece namely,
hypernatraemic dehydration in the first few days of life in association
with ‘breastfeeding’. Though the breast milk produced, in very small
quantities, by the mothers of these children is often found to contain a
high concentration of sodium, this has nothing to do with their
hypernatraemic state. As Jack Newman so eloquently puts it in his
electronic response to Laing and Wong, these babies are not dehydrated
because they are breastfed but because they are only pretending to
breastfeed. They are, in fact, starving. This is amply illustrated by the
case described in Oddie et al of a ‘bottle fed’ baby admitted at six days
of age with hypernatraemic dehydration whose dehydration had nothing to do
with the bottle milk being ‘fed’ to her but was caused by the fact that
she had oesophageal atresia. Hypernatraemic dehydration is frequently seen
in the elderly and the mentally handicapped when their need for basic
care, and presumably a regular intake of water, is neglected. [5,6,7]
Hypernatraemic dehydration is a sign of illness not a diagnosis. It
is commonly caused by excess water loss or by insufficient water intake
either alone or in combination. It is almost never the result of excess
sodium intake which would result in retention of water and an increase in
body weight, though this would obviously require intact thirst mechanisms
and access to sufficient water.
Sam Richmond
References
(1) Laing IA, Wong CM, Hypernatraemia in the first few days: is the
incidence rising? Arch Dis Child Fetal Neonatal Ed 2002; 87: F158-F162.
(2) Chambers TL, Steel AE. Concentrated milk feeds and their relation
to hypernatraemic dehydration in infants. Arch Dis Child 1975; 50: 610-5.
(3) Hirschhorn N. The treatment of acute diarrhea in children. An
historical and physiological perspective. Amer J Clin Nutrition 1980; 33:
637-63.
(4) Oddie S, Richmond S, Coulthard M. Hypernatraemic dehydration and
breastfeeding: a population study. Arch Dis Child 2001; 85: 318-20.
(6) Miller PD, Krebs RA, Neal BJ. McIntyre DO. Hypodipsia in geriatric
patients. Am J Med 1982; 73: 354-6.
(7) Himmelstein DU, Jones AA, Woolhandler S. Hypernatremic dehydration
in nursing home patients: an indicator of neglect. J Am Geriatr Soc 1983;31: 466-71.
These findimgs go strongly in favour of the dictum not to interfere
with "mother nature". Also it goes to prove that one must "treat the
patient not the biochemistry"
It helps us who may not have access to good biochemistry and
monitoring apart from clinical in managinr our newborns.
I have read the recent lead article in the Archives, Laing and Wong.[1] I wish to point out that dehydration in the first few days does not occur in breastfed babies. If the babies were breastfeeding, they wouldn't get dehydrated. It occurs in babies who are only pretending to breastfeed. But unfortunately, this is altogether too common, babies leaving hospital only pretending to breastfeed.
I have read the recent lead article in the Archives, Laing and Wong.[1] I wish to point out that dehydration in the first few days does not occur in breastfed babies. If the babies were breastfeeding, they wouldn't get dehydrated. It occurs in babies who are only pretending to breastfeed. But unfortunately, this is altogether too common, babies leaving hospital only pretending to breastfeed.
The problem is not that babies are not being weighed frequently enough in the first few days after birth, but rather that hospital staff, in general, have not the training or the skills or the time, perhaps, to help mothers with breastfeeding and to know when a baby is not breastfeeding well. So mothers go home thinking the baby is breastfeeding when he is not. And the mothers are also not given the information about how to know the baby is getting milk, what to expect from urine output, bowel movements and so on. Instead, mothers are told to wake the baby up every three hours in order to feed the baby. But a baby who feeds well, will wake up when he is hungry. And if the baby feeds so poorly he is going to get dehydrated, there is no point in waking a baby up every 3 hours so he gets nothing 8 times a day instead of nothing 5 times a day, say.
We are so fixated on numbers and weighing that we do not really look at babies on the breast and make sure they are latched on and feeding well. Because, in fact, observation of the baby at the breast can tell you if the baby is getting milk or not. It's simple, yet paediatricians and family physicians rarely watch the baby at the breast, at least partly because they haven't a clue what to look for. A baby can be seen to be getting milk at the breast even on day one of life, if the observer knows what to look for. Babies are being readmitted to the hospital with severe dehydration because we don't know how to help mothers with breastfeeding. Sometimes these babies die. Sometimes they end up with severe neurological sequelae. Yet, very little effort is being made, it seems, to help doctors and nurses understand how breastfeeding works. Even the latest training too often emphasizes frequency of going to the breast, length of time on the breast, percentage weight loss as something worthwhile, when, in fact, this information is useless. Hospital staff nurses need to help mothers get a good latch (but they need to know how to achieve this), they need to observe the feeding and teach the mother how to know the baby is getting milk (but they need to know this first themselves, don't they?). If the mothers knew how to know the baby was getting milk, they would come back for help before it was too late. Ask the paediatricians.
What is the normal stool pattern of the baby doing well on the breast? Most don't know. What are the worrisome signs? Most don't know. Is a baby who is passing only meconium on day 4 okay? Most don't know.
If one depends on a scale in the physician's office and compares it to the hospital weight, one can go dangerously wrong. Either urging supplementation for a baby who doesn't need it, or reassuring oneself and the mother that all is well, when it isn't. The ignorance of how breastfeeding works, and the lack of support in North America and Western Europe (with few exceptions), boggles the mind. Undoubtedly, this article will be picked up by the press, and yet another series of television programmes, radio talk shows will start discussing hypernatremic dehydration and thousands more women will be frightened out of breastfeeding their babies. A real shame.
Jack Newman, MD, FRCPC
Breastfeeding Clinic
St. Michael's Hospital
Toronto, Ontario
Reference
(1) Laing IA, Wong CM, Hypernatremic dehydration the first few days: is the incidence rising? Arch Dis Child Fetal Neonatol Ed 2002;87:F158-F162.
Dear Editor
The purpose of measuring serum levels of a drug is either to monitor the toxicity of the drug or the therapeutic concentration for a particular condition. Emergence of infections with beta-lactam-resistant Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus sp. has led to the frequent use of vancomycin in neonates. Vancomycin historically has had a reputation for tox...
Dear Editor
As well emphasized by Koppen et al,[1] congenital pulmonary arteriovenous malformation presenting in the neonatal period is an exceedingly rare anomaly, perhaps underdiagnosed. The index of suspition should be high if appropriate treatment is to be offered to these babies and, unfortunately, this was not the case in a 6-day-old patient seen by us 7 years ago.[2] Adding to the severe hypoxaemia, o...
Dear Editor
We read with interest the findings of Evans et al. concerning the changes in middle cerebral artery (MCA) haemodynamics over the first two days after birth in preterm infants.[1]
Evans et al. demonstrated a significant change in several Doppler velocity measures in the MCA, including systolic, diastolic and mean velocity, pulsatility index and velocity time integral, during days 1 and...
Dear Editor
Having recently reviewed the case notes of babies readmitted to hospital in the first 10 days of life (over a 1 year period), we firmly agree with the views expressed by Laing and Wong.[1] The incidence of documented hypernatraemic dehydration secondary to the failure of lactation in Bristol is 1.7 per 1000 live births much higher than that described by Oddie et al. [2] in the Northern Region (2.5...
Dear Editor
We read the article by Dr Perry et al. on ultrasound of the thyroid gland in the newborn: normative data with great interest.[1] In this study on the measurements of the thyroid volumes in the newborn, there are many discrepancies with the normative data described by previous studies. And also the results of this study try to change widely accepted criteria. In my opinion, this may cause confusio...
Dear Editor
We are grateful to colleagues for their comments on our annotation.[1] We would stress that we merely abstracted the views of others so any criticisms (apart from our brevity) will be of the lawyers, doctors, nurses, physiotherapists and parents who contributed to the Royal Commission Report. We found it to be systematic, rational and objective.
We strongly refute any suggestion that any of t...
Dear Editor
It is difficult to define what is suboptimal care in some situations. For example a borderline Cardiotocograph can be interpreted differently by different individuals.
Secondly, although not mentioned in the article, it would be interesting to know how the all case notes for the study were acquired. The number of infants with neonatal encephalopathy might be more than 49. It is possibl...
Dear Editor
I am grateful to Laing and Wong for raising once again the issue of hypernatraemic dehydration in the first few days of life.[1] However, I think it is important to remember that hypernatraemic dehydration, like anaemia, is a sign of disease not a diagnosis in itself. A low haemoglobin concentration in blood can be caused by a large number of different pathological and physiological processes. Hypern...
Dear Editor
These findimgs go strongly in favour of the dictum not to interfere with "mother nature". Also it goes to prove that one must "treat the patient not the biochemistry"
It helps us who may not have access to good biochemistry and monitoring apart from clinical in managinr our newborns.
Well done!
Dear Editor
I have read the recent lead article in the Archives, Laing and Wong.[1] I wish to point out that dehydration in the first few days does not occur in breastfed babies. If the babies were breastfeeding, they wouldn't get dehydrated. It occurs in babies who are only pretending to breastfeed. But unfortunately, this is altogether too common, babies leaving hospital only pretending to breastfeed.
The...
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