We welcome the coverage given to the major, and potentially fatal, problem
of medication errors within managed health care.[1] We disagree however
with the key message that MEDICATION ERRORS ARE UNCOMMON. They are
endemic, extremely common, overlooked and often ignored.
Observational studies of medicine administration within hospitals in
the United Kingdom report an error rate of 3% to 8%.[2] In
co...
We welcome the coverage given to the major, and potentially fatal, problem
of medication errors within managed health care.[1] We disagree however
with the key message that MEDICATION ERRORS ARE UNCOMMON. They are
endemic, extremely common, overlooked and often ignored.
Observational studies of medicine administration within hospitals in
the United Kingdom report an error rate of 3% to 8%.[2] In
contrast Ross et al report 195 errors, collated from a mandatory error
reporting policy, in 65 months.[1] While mandatory reporting is a
commendable principle, the reality remains that the majority of healthcare
professionals will not report errors, and the majority of medication
errors, will not be reported.
Reasons for lack of reporting among nursing
staff include confusion regarding the definition of drug errors and the
appropriate action to take when they occurred, fear of disciplinary
action, loss of clinical confidence and variation in managerial response.[3]
Voluntary, non-punitive error reporting programmes have been
advocated as the most effective way to promote candid disclosure of
medical error.[4]
Unless we are aware of what errors occur, we cannot expect to implement an
appropriate system fix.
We would suggest that the occurrence of 3 errors/month, represents a
tremendous under-reporting of the extent of medication error.[1] If
patient through put totalled 335,835 patient bed-days, and we assume that
each day the average patient received 6 doses of medicine, an error rate
of 5%, suggests that a more realistic interpretation of the extent
of the error iceberg is an incidence of greater than 100,000.
The conclusion therefore that medication errors are uncommon is
unfortunately not true. The reality is that REPORTED MEDICATION ERRORS ARE
UNCOMMON.
Neil A Caldwell
Principal Pharmacist/Lecturer
Wirral Hospital NHS Trust/Liverpool John Moores University
Don K Hughes
Principal Pharmacist Clinical Services/Honorary Lecturer
Wirral Hospital NHS Trust/Liverpool John Moores University
References
(1) Ross LM, Wallace J, Paton JY. Medication errors in a paediatric
teaching hospital in the UK: five years operational experience. Arch Dis Child 2000;83:492-7.
(2) Barber N, Dean B. The incidence of medication errors and ways to reduce
them. Clinical Risk 1998;4:103-6.
(3) Gladstone J. Drug administration errors: a study into the factors
underlying the occurrence and reporting of drug errors in a district
general hospital. Journal of Advanced Nursing 1995;22:628-37.
(4) Cohen MR. Why error reporting systems should be voluntary. BMJ 2000;320:728-9.
We read with interest the article by Kerr et al "An association
between sudden infant death syndrome (SIDS)
and Helicobacter pylori infection". While the proportion
of samples positive for H pylori DNA were significantly higher in the
SIDS group compared with the control group, the findings need to be
interpreted with caution.
PCR is a useful tool for detection of DNA. It is, however,
evidence...
We read with interest the article by Kerr et al "An association
between sudden infant death syndrome (SIDS)
and Helicobacter pylori infection". While the proportion
of samples positive for H pylori DNA were significantly higher in the
SIDS group compared with the control group, the findings need to be
interpreted with caution.
PCR is a useful tool for detection of DNA. It is, however,
evidence that the DNA of the organism is present, not evidence that the
organisms were alive or caused disease. Culture, microscopy, serological
evidence or histological evidence of inflammatory or immune responses are
needed to support the hypothesis that the bacteria were involved with
pathological processes, not just transient contamination of the infant
with DNA from non-viable bacteria.
There are several points that detract from the paper:
In relation to the findings reported:
1. Only the PCR assays provided positive evidence. In contrast to other
studies reported as abstracts,
microscopic examination of the stained sections did
not find any evidence of H pylori. This discrepancy needs to be
explained. There were no serological data to support the PCR findings and
no data from histological examinations to provide evidence that the
bacteria were causing
infection or that inflammatory responses had been elicited.
2. The proportion of PCR positive samples among SIDS infants (88%) was
significantly larger than that among controls (12.5%). The possibility of
contamination was not addressed for SIDS or the positive control case.
There was no demonstration by molecular methods that the DNA detected was
from different strains. H pylori strains show great genetic variability
and previous studies demonstrated that most individuals carry unique
strains. Isolates from different individuals that appear to be genetically
identical are those obtained only from close contacts, usually within a
family.
The interpretation of the epidemiological data for H pylori and
socioeconomic factors was not assessed in relation to incidence of SIDS
among different ethnic groups.
In Britain, white families in lower socioeconomic groups have more
evidence of H pylori infections and more SIDS. If the data for incidence
of infections with H pylori is assessed for ethnic groups and SIDS, this
parallel breaks down. The incidence of seropositivity for H pylori among
Bangladeshi women in the UK ranges from 66% among women born abroad to
81% among women born in the UK [Banatvala et al, 1995]; however, the
incidence of SIDS in Bangladeshi families was the lowest in Britain
(0.3%) [Balarajan et al, 1989]. A similar trend was observed in the
United States; seropositivity for H pylori is 61% among Hispanics and
26.2% among non-Hispanic whites [Everhart et al, 2000]. In the paper
quoted in the manuscript, the incidence of seropositivity was similar for
Hispanic and black groups and both were significantly higher than that of
non-Hispanic whites [Malaty et al, 1992]. The SIDS rates per 100,000
for US populations were 5.1 for blacks, 1.3 for Hispanics and 1.2 for non-Hispanic whites [Nelson, 1996]. This evidence questions the assumptions
made by the authors.
While there is increasing evidence for other hypotheses that SIDS
might be triggered by inflammatory responses to infection [Vege and
Rognum, 1999; Raza and Blackwell, 1999; Forsyth, 1999], there is no
physiological or histological evidence to support the hypothesis that
urease in the lung of the infants is causing increased levels of ammonia
in the blood (see detailed assessment of pathology of SIDS in relation to
this hypothesis below). Animal models [Pattison et al, 1998a,b] do not
reflect the combination of genetic, environmental and developmental
factors associated with SIDS, and results from animal studies must be
interpreted with extreme caution when extrapolated to the human infant.
H pylori infection does not fit the common bacterial hypothesis, a
mathematical model which accurately predicted the age range for SIDS
[Morris, 1999]. According to the model, 50% of infants should acquire the
bacteria during the first 50 days of life. While 19% of Gambian children
were positive for the C13 urea breath test by 3 months of age [Thomas et
al, 1999], in industrialised countries the evidence is that H pylori
infection in infants under 1 year of age is much lower. Among 67 Belgian
children born to seropositive mothers, only 1 (1.5%) had a positive breath
test by the age of 12-15 months. [Blecker et al, 1994]. Among Finnish
children 10.6% had IgG to H pylori at birth, but the antibodies
disappeared in all but one child before the age of 7 months and there were
no seroconversions in these children. The Finnish study concluded that
maternal seropositivity is not a straight forward risk factor for
acquiring H pylori infection [Ashorn et al, 1996].
The oral/oral route of transmission is suggested to be the route by
which infants acquire H. pylori, mainly by vomit [Leung et al, 1999]. H
pylori has been cultured from one of four vomit samples from children
and detected by PCR in two of four culture negative samples. There is
much stronger direct (culture) evidence for transmission from mother to
child of other bacterial species implicated in SIDS [Blackwell et al,
1999a].
The pathogenic mechanism proposed for the role of ammonia cannot be
substantiated by the available evidence:
a. There are no acute changes in the upper respiratory tree or lungs
consistent with inflammatory responses to H pylori.
b. The presence of ammonia in the lower respiratory tree would initiate a
bronchospasm which should produce clinical features such as wheezing
which has not been reported by parents of SIDS infants. This type of
reaction should be demonstrable histologically by muscular, glandular and
secretory changes identified by microscopy.
c. If ammonia is present in excess in the blood as a proximate cause of
death, this should be demonstrable in blood samples and vitreous fluid,
and there is no evidence for this.
d. The liver in SIDS cases shows no abnormality and had it been acutely
affected by an influx of ammonia, there should be changes.
e. Ammonia in excess leads to cerebral changes of an acute type and none
have been demonstrated.
f. If the ammonia is postulated as a cause of petechiae in the lungs due
to local damage, this does not account for the presence of petechiae in
the thymus and pericardium.
There is evidence to explain how risk factors could contribute to
susceptibility of infants to infectious agents to triggering the series
of events leading to SIDS [Blackwell et al, 1999b]; however, that
presented for H pylori needs to be substantiated by more than one method
and testable hypotheses proposed to explain how these bacteria might
contribute to the series of events that lead to SIDS.
CC Blackwell, PhD, FRCPath DSc
DM Weir, MD FRCPE
A Busuttil, MD, DMJ FRCPath FRCP
References
Ashorn M, Miettinen A, Ruuska T, et al.
Seroepidemiological study of Helicobacter pylori infection in infancy. Arch Dis Child Fetal Neonatal Ed 1996; F141-2.
Balarajan R, Raleigh VS, Botting B. Sudden infant death
syndrome and post neonatal mortality in immigrants in England and Wales.
BMJ 1989;298: 716-20.
Banatvala N, Clements L, Abdi Y, et al. Migration and Helicobacter pylori seroprevalence:
Bangladeshi migrants in the UK. J Infect 1995;31:133-5.
Blackwell CC, Mackenzie DAC, James VS, et al. Toxigenic bacteria and SIDS:
nasopharyngeal flora in the first year of life. FEMS Immunol Med Microbiol 1999;25:51-8.
Blackwell CC, Weir DM, Busuttil A. Infection, inflammation
and sleep: more pieces to the puzzle of sudden infant death syndrome
(SIDS). APMIS 1999;107:455-73.
Blecker U, Lanciers S, Keppens E, Vandenplas Y. Evolution of
Helicobacter pylori positivity in infants born from positive mothers. J Pediatr Gastorenterol Nutr 1994;19:87-90.
Everhart JE, Kruszon-Moran D, Perez-Perez GI, et al. Seroprevalence and ethnic differences in Helicobacter
pylori infection among adults in the United States. J Infect Dis 2000;181:1359-63.
Forsyth KD. Immune and inflammatory responses in sudden infant
death syndrome. FEMS Immunol Med Microbiol 1999;25:79-84.
Leung WK, Siu KL, Kwok CK, et al. Isolation of Helicobacter pylori from vomitus in children and its
implication in gastro-oral transmission. Am J Gastroenterol 1999;94:2881-4.
Malaty HM, Evans DG, Evans DJ, Graham, DY. Helicobacter
pylori in Hispanics: comparison with blacks and whites of similar age and
socioeconomic class. Gastroenterology 1992;103:813-16.
Morris JA. The common bacterial toxins hypothesis of sudden infant
death syndrome. FEMS Immunol Med Microbiol 1999;25:11-18.
Nelson T. Sudden infant death syndrome and child care practices.
Lammar Offset Pringing, Ltd. Hong Kong, 1996.
Pattison CP, Marshall BJ, Scott LW, et al. Proposwed link between Helicobacter pylori and sudden infant death
syndrome (SIDS): possible pathogenic mechanisms in an animal model. I. Effects of intratracheal urease. Gastroenterology 1998;114:G3689.
Pattison CP, Scott LW, Herndon B, Willsie SK. Proposed link
between Helicobacer pylori and SIDS: possible pathogenic mechanisms in an
animal model. II. Effects of intratracheal urease after pretreatment with
intravenous IL-1b. Ibid.
Raza MW, Blackwell CC. Sudden infant death syndrome: virus
infections and cytokines FEMS Immunol Med Microbiol 1999;25: 85-96. Gastroenterology 1998;114:G3690.
Thomas JF, Dale A, Harding M, et al. Helicobacter pylori colonization in early life. Pediatric Res
1999;45:218-23.
Vege A, Rognum TO. Inflammatory responses in sudden infant death
syndrome: past and present views. FEMS Immunol Med Microbiol 1999;25:67-78.
Xylitol is now available in America in health food stores and via the
internet. Parents of children with recurrent ear infection are making
their own syrup with xylitol granules or purchasing supplements that
contain it. They can also obtain xylitol nasal sprays. Research is needed
on the minimum dose that is effective but as more parents discover the
benefits the use of xylitol will increase.
Dr Nathwani has highlighted an important area in relation to training
and child health surveillance. Once we are clear about what we need to do,
the next step is to (further) develop a competent workforce to provide the
service as prescribed. To date, most Districts have interpreted RCGP (Royal College of General Practitioners) and
BPA (British Paediatric Association; pre Royal College) guidance locally in or...
Dr Nathwani has highlighted an important area in relation to training
and child health surveillance. Once we are clear about what we need to do,
the next step is to (further) develop a competent workforce to provide the
service as prescribed. To date, most Districts have interpreted RCGP (Royal College of General Practitioners) and
BPA (British Paediatric Association; pre Royal College) guidance locally in order to assure themselves of
competence. What he is really asking is whether this is effective?
I would
support the development of a set of nationally agreed competencies in this
programme which can be reliably and accurately tested. This can act as the
"gold standard" against which any training programme might be measured no
matter what the individual local arrangements are for training.
I hope the message from this letter is not that paediatricians in
district hospitals stop doing research. The challenge is to allow an
environment in which clinical research can flourish.
Pedley et al[1] raise concerns about the risk of upper airway trauma
resulting from the use of cuffed endotracheal tubes (ETT)
in paediatric airway management and indicate that they prefer to avoid the
use of cuffed tubes in the acute management of
children with meningococcal disease.
Experience from neonatal intensive care, paediatric anaesthesia and
paediatric intensive care indicate that...
Pedley et al[1] raise concerns about the risk of upper airway trauma
resulting from the use of cuffed endotracheal tubes (ETT)
in paediatric airway management and indicate that they prefer to avoid the
use of cuffed tubes in the acute management of
children with meningococcal disease.
Experience from neonatal intensive care, paediatric anaesthesia and
paediatric intensive care indicate that tightly fitting ETTs
cause upper airway trauma, manifest as post-extubation stridor or later
subglottic stenosis.[2][3] For this reason, the correct
sized ETT should always be selected and placed in the airway with
meticulous care in order to avoid
these problems.
Appropriately sized, cuffed ETTs are probably not associated with
immediate post-extubation problems or longer-term
complications.[3-5] In addition, there are a number of advantages in using
cuffed tubes: they virtually eliminate the need to
repeat laryngoscopy and intubation, which is traumatic to the airway[5];
they reduce environmental contamination with inhaled
drugs,[5] such as anaesthetics and nitric oxide; and the use of cuffed
ETTs allows high pressure ventilation without
necessitating change to a well-fitting ETT.[4]
In meningococcal disease pulmonary oedema is common as a result of
capillary leakiness and high positive end expiratory
pressures (PEEP) may be necessary in order to maintain oxygenation. With
an uncuffed ETT, it is not uncommon for a child
with this disease to require reintubation in order to treat pulmonary
oedema, with risk of associated airway complications and
more serious acute decompensation during the procedure. In our recent
experience with over 550 children ventilated for meningococcal disease we
have frequently used cuffed endotracheal tubes and
are not aware of any airway trauma that has specifically resulted from
their use. In those patients who do not develop severe
gas exchange problems we leave the cuff deflated.
On the other hand, in the context of meningococcal disease, we have
observed many occasions when uncuffed tubes have
been changed to facilitate a rise in PEEP following development of
pulmonary oedema, resulting in haemodynamic or
respiratory decompensation. If cuffed ETTs are not available, it may be
better to put a bigger or tighter tube in the trachea, with
risk of airway trauma, rather than facing a situation of an emergency tube
change, which can be life-threatening in an
unventilatable patient
with pulmonary oedema.
Correctly used, cuffed ETTs may be no more traumatic to the airway
than uncuffed tubes and may greatly facilitate ventilatory
management in pulmonary oedema.
Andrew J Pollard
Simon Nadel
Nilesh Mehta
Claudine De Munter
Joseph Britto
Parviz Habibi
Michael Levin
Paediatric Intensive Care Unit Department of Paediatrics
Imperial College School of Medicine St Mary's Hospital, London W2 1NY, UK
Address for Correspondence:
Dr Andrew J Pollard
Division of Infectious and Immunologic Disease
British Columbia’s Children’s Hospital
British Columbia Research Institute for Children's & Women's Health
950, West 28th Avenue, Room 375
Vancouver, BC V5Z 4H4, Canada
References
(1) Pedley D, Finlay L, Johnston M. Are cuffed endotracheal tubes really indicated in the management of meningococcal disease? Arch Dis Child [Rapid Response] 20 November 2000. http://adc.bmjjournals.com/cgi/eletters/archdischild;80/3/290#EL2
(2) Lee KW, Templeton JJ, Dougal RM. Tracheal tube size and post-
intubation croup in children, Anesthesiology 1980;53:S325.
(3) Koka BV, Jeon IS, Andre JM, MacKay I, Smith RM. Postintubation
croup in children. Anesth Analg Curr Res 1997;56:501-5.
(4) Deakers TW, Reynolds G, Stretton M, Newth CJL. Cuffed
endotracheal tubes in pediatric intensive care. J Pediatr
1994;125:57-62.
(5) Khine HH, Corddry DH, Kettrick, RG, Martin TM, McCloskey JJ, Rose
JB, Theroux MC, Zagnoev M. Comparison of
cuffed and uncuffed endotracheal tubes in young children during general
anaesthesia. Anesthesiology 1997;86:627-31.
This paper[1] on the role of a coordinator in child health
surveillance/promotion (CHS) is both opportune and timely given the degree
of interest generated in preventive healthcare for a variety of reasons.
Blair has brilliantly summarised the activities covered by the programme
that needs coordinating. One aspect which needs to be highlighted further
is the area of training.
This paper[1] on the role of a coordinator in child health
surveillance/promotion (CHS) is both opportune and timely given the degree
of interest generated in preventive healthcare for a variety of reasons.
Blair has brilliantly summarised the activities covered by the programme
that needs coordinating. One aspect which needs to be highlighted further
is the area of training.
The author has quite rightly pointed out that with the 1990 NHS Act,
the provision of the preschool programme is generally delivered by primary
health care teams including general practitioners (GPs) and health
visitors. Most districts have a clear process of GP accreditation to
deliver CHS in practice based on the national guidance[2] in place since
1990. This paper does not offer clear guidance on the need for
reaccreditation and continuing professional development (CPD). In 1997,
there were some discussions at the college level to draft updated guidance
on the processes for accrediation and CPD. Unfortunately the discussions
never concluded. In view of clinical governance it may be timely to
reconvene these discussions as training and update programmes for the
primary health care teams are critical to the success of CHS. In the
absence of national guidance individual health authorities tend to produce
(or not produce) their own local guidelines which tend to be of variable
effectiveness (personal experience).
References
(1) Blair M, The need for and the role of a coordinator in child
health surveillance/promotion. Arch Dis Child 2001;84:1-5.
(2) "Training and accreditation of General Practitioners in Child Health Surveillance" (October 1991) - Guidelines by the British Paediatric Association, GMSC and RCGP.
Bad news is called bad news because it is … bad news. To be told
that their child has cerebral palsy is devastating for parents and it is
naïve to expect parents to be anything other than deeply distressed.
Baird et al interviewed parents to ask their views and feelings about
how the bad news was broken to them.[1] Firstly, there are two sides to
every story. They did not interview the doctors...
Bad news is called bad news because it is … bad news. To be told
that their child has cerebral palsy is devastating for parents and it is
naïve to expect parents to be anything other than deeply distressed.
Baird et al interviewed parents to ask their views and feelings about
how the bad news was broken to them.[1] Firstly, there are two sides to
every story. They did not interview the doctors involved. As Bill
Dobyns, the eminent geneticist writes, “When parents first hear that their
child has a serious problem they are often not ready to understand or
accept it. In this situation there is no good way to give the news. I
have on several occasions heard professional friends give the most
compassionate discussion I could image only to hear later they were
‘insensitive’ and so on.”[2]
Articles about breaking bad news inevitably
do not take account of the ‘arousal gap’ – parents are in a heightened
state of arousal so that every word, gesture or silence is given a meaning
far beyond its intention.[3] Nor do the authors seem to show an
understanding of the grieving process. Very few parents are honest enough
to admit at this stage – or ever – what and who it is they are really
angry with: they are angry with the child, themselves, God, life, etc; they feel guilty about that anger.
Secondly, Baird recommends that junior doctors are not present at the
time of disclosure. I disagree. I hold a regular ‘hand over’ clinic with
the neonatologist and a physiotherapist where these diagnoses are often
confirmed and/or disclosed. The physiotherapist is not necessarily the
one who has been or will be seeing the child, but represents her
colleagues at the clinic and is an experienced and valued member of the
team. A junior doctor from SCBU is also present. It is important that
the junior medical staff see a variety of styles of delivering bad news
and, equally importantly, a variety of responses from the parents.
Thirdly, the authors suggest that one obstacle to progress may be
senior staff believing they know how to break bad news. The implication
is that any doctor who does not go along with the guidelines recommended
in the article is being obstructive and arrogant. I admit I think I do
know how to break bad news but do not regard myself as an ‘obstacle’. I
run several joint clinics with colleagues from other paediatric and
related disciplines: these act as ongoing peer review on this and many
other aspects of our practice for both the consultants present.
Dr Charles Essex
Consultant Neurodevelopmental Paediatrician
Child Development Unit
Gulson Hospital, Coventry CV1 2HR, UK
References
(1) Baird G, McConachie H, Scrutton D. Parents’ perception of
disclosure of the diagnosis of cerebral palsy. Arch Dis Child 2000;83:475-80.
(2) Dobyns W. Lissencephaly : Frequently asked questions. http://www.lissencephaly.org/medical/doctor/index.htm
(3) Metcalfe D. Doctors and patients should be fellow travellers. BMJ 1998;316:1892-3.
We welcome the coverage given to the major, and potentially fatal, problem of medication errors within managed health care.[1] We disagree however with the key message that MEDICATION ERRORS ARE UNCOMMON. They are endemic, extremely common, overlooked and often ignored.
Observational studies of medicine administration within hospitals in the United Kingdom report an error rate of 3% to 8%.[2] In co...
We read with interest the article by Kerr et al "An association between sudden infant death syndrome (SIDS) and Helicobacter pylori infection". While the proportion of samples positive for H pylori DNA were significantly higher in the SIDS group compared with the control group, the findings need to be interpreted with caution.
PCR is a useful tool for detection of DNA. It is, however, evidence...
Xylitol is now available in America in health food stores and via the internet. Parents of children with recurrent ear infection are making their own syrup with xylitol granules or purchasing supplements that contain it. They can also obtain xylitol nasal sprays. Research is needed on the minimum dose that is effective but as more parents discover the benefits the use of xylitol will increase.
Dr Nathwani has highlighted an important area in relation to training and child health surveillance. Once we are clear about what we need to do, the next step is to (further) develop a competent workforce to provide the service as prescribed. To date, most Districts have interpreted RCGP (Royal College of General Practitioners) and BPA (British Paediatric Association; pre Royal College) guidance locally in or...
I hope the message from this letter is not that paediatricians in district hospitals stop doing research. The challenge is to allow an environment in which clinical research can flourish.
Dear Editor,
Pedley et al[1] raise concerns about the risk of upper airway trauma resulting from the use of cuffed endotracheal tubes (ETT) in paediatric airway management and indicate that they prefer to avoid the use of cuffed tubes in the acute management of children with meningococcal disease.
Experience from neonatal intensive care, paediatric anaesthesia and paediatric intensive care indicate that...
This paper[1] on the role of a coordinator in child health surveillance/promotion (CHS) is both opportune and timely given the degree of interest generated in preventive healthcare for a variety of reasons. Blair has brilliantly summarised the activities covered by the programme that needs coordinating. One aspect which needs to be highlighted further is the area of training.
The author has quite r...
Bad news is called bad news because it is … bad news. To be told that their child has cerebral palsy is devastating for parents and it is naïve to expect parents to be anything other than deeply distressed.
Baird et al interviewed parents to ask their views and feelings about how the bad news was broken to them.[1] Firstly, there are two sides to every story. They did not interview the doctors...
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